Array ( [0] => Array ( [ArticleId] => 82 [Create_Time] => 2020-12-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202106/20210617051035.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10031/10031.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10031/10031.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10031/10031_cover.png [JournalsId] => 5 [Title] => Exploration of Immunology: challenging knowledge, developing curiosity and transforming passion into discovery [Abstract] => [AbstractComplete] => [Names] => Dominique J Charron, Reem Al-Daccak [Doi] => 10.37349/ei.2021.00001 [Published] => April 30, 2021 [Viewed] => 2970 [Downloaded] => 62 [Subject] => Editorial [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00001 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:1–3 [Recommend] => 0 [Keywords] => [DetailTitle] => [DetailUrl] => [Id] => 10031 [ris] => https://www.explorationpub.com/uploads/Article/A10031/b2dce66bbffb0c0eb1e650d474b86935.ris [bib] => https://www.explorationpub.com/uploads/Article/A10031/4ba8d17d1afe155bee7f88c47b29ff32.bib [ens] => [Cited] => 0 [Cited_Time] => 2021-02-01 [CitethisArticle] => Charron DJ, Al-Daccak R. Exploration of immunology: challenging knowledge, developing curiosity and transforming passion into discovery. Explor Immunol. 2021;1:1-3. https://doi.org/10.37349/ei.2021.00001 [Jindex] => 1 [CName] => Dominique JCharron, [CEmail] => d.charron.sls@gmail.com, [Ris_Time] => 0000-00-00 00:00:00 [Bib_Time] => 0000-00-00 00:00:00 [KeysWordContens] => Exploration of Immunology: challenging knowledge, developing curiosity and transforming passion into discovery,,,Dominique J Charron, Reem Al-Daccak [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [1] => Array ( [ArticleId] => 109 [Create_Time] => 2021-03-02 [zipUrl] => https://www.explorationpub.com/uploads/zip/202106/20210617051200.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10032/10032.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10032/10032.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10032/10032_cover.png [JournalsId] => 5 [Title] => The role of interleukin-24 in atopic dermatitis [Abstract] => Atopic dermatitis (AD) is characterized by skin barrier disruption, type 2 immune dysregulation, chronic pruritus, and abnormal colonization by Staphylococcus aureus (S. aureus). Tapinarof, an aryl [AbstractComplete] =>

Atopic dermatitis (AD) is characterized by skin barrier disruption, type 2 immune dysregulation, chronic pruritus, and abnormal colonization by Staphylococcus aureus (S. aureus). Tapinarof, an aryl hydrocarbon receptor modulator, has been demonstrated to attenuate the development of AD in clinical studies. Recently, we found that tapinarof upregulated the expression of filaggrin and loricrin, which are essential proteins in skin barrier functions. Paradoxically, tapinarof induced interleukin (IL)-24 secretion by normal human keratinocytes. IL-24 is produced by T helper 2 lymphocytes and keratinocytes following stimulation by type 2 cytokines, and IL-24 is upregulated in the skin of patients with AD. Furthermore, IL-24 contributes to skin barrier disruption and hyperplasia in AD, and it may exacerbate skin inflammatory responses, itch, and S. aureus infection. In this review, we summarized the current findings regarding the detrimental role of IL-24 in AD, thereby suggesting that co-treatment of tapinarof with therapeutics that block IL-24 signaling may represent a promising strategy for managing AD.

[Names] => Yen Hai Vu ... Gaku Tsuji [Doi] => 10.37349/ei.2021.00002 [Published] => April 30, 2021 [Viewed] => 5638 [Downloaded] => 200 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00002 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 42 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:4–15 [Recommend] => 0 [Keywords] => Atopic dermatitis, interleukin-24, aryl hydrocarbon receptor, tapinarof, Janus kinase inhibitor, dupilumab [DetailTitle] => Cross Talk Among Skin Cells and Immune Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/42 [Id] => 10032 [ris] => https://www.explorationpub.com/uploads/Article/A10032/c49a7ab0cad63db4e521d3655c3f8a21.ris [bib] => https://www.explorationpub.com/uploads/Article/A10032/ff90f3d9dd0dba33a4f685305c8ebd5e.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Vu YH, Furue M, Tsuji G. The role of interleukin-24 in atopic dermatitis. Explor Immunol. 2021;1:4-15. https://doi.org/10.37349/ei.2021.00002 [Jindex] => 1 [CName] => MasutakaFurue, [CEmail] => furue@dermatol.med.kyushu-u.ac.jp, [Ris_Time] => 0000-00-00 00:00:00 [Bib_Time] => 0000-00-00 00:00:00 [KeysWordContens] => The role of interleukin-24 in atopic dermatitis, Atopic dermatitis, interleukin-24, aryl hydrocarbon receptor, tapinarof, Janus kinase inhibitor, dupilumab, Atopic dermatitis (AD) is characterized by skin barrier disruption, type 2 immune dysregulation, chronic pruritus, and abnormal colonization by Staphylococcus aureus (S. aureus). Tapinarof, an aryl hydrocarbon receptor modulator, has been demonstrated to attenuate the development of AD in clinical studies. Recently, we found that tapinarof upregulated the expression of filaggrin and loricrin, which are essential proteins in skin barrier functions. Paradoxically, tapinarof induced interleukin (IL)-24 secretion by normal human keratinocytes. IL-24 is produced by T helper 2 lymphocytes and keratinocytes following stimulation by type 2 cytokines, and IL-24 is upregulated in the skin of patients with AD. Furthermore, IL-24 contributes to skin barrier disruption and hyperplasia in AD, and it may exacerbate skin inflammatory responses, itch, and S. aureus infection. In this review, we summarized the current findings regarding the detrimental role of IL-24 in AD, thereby suggesting that co-treatment of tapinarof with therapeutics that block IL-24 signaling may represent a promising strategy for managing AD. ,Yen Hai Vu ... Gaku Tsuji [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [2] => Array ( [ArticleId] => 118 [Create_Time] => 2021-03-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202106/20210617051411.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10033/10033.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10033/10033.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10033/10033_cover.png [JournalsId] => 5 [Title] => In silico investigation of binding affinities between human leukocyte antigen class I molecules and SARS-CoV-2 virus spike and ORF1ab proteins [Abstract] => Aim: The novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019, a global pandemic. There is hence an urgent need for effective approaches to [AbstractComplete] =>

Aim:

The novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019, a global pandemic. There is hence an urgent need for effective approaches to understand the mechanism of viral interaction with immune cells that lead to viral elimination and subsequent long-term immunity. The first, immediate response to the viral infection involves mobilization of native immunity and human leukocyte antigen (HLA) class I mechanisms to kill infected cells and eliminate the virus. The second line of defense involves the activation of HLA class II system for the production of antibodies against the virus which will add to the elimination of the virus and prevent future infections. In a previous study, investigated the relations between SARS-CoV-2 spike glycoprotein (S protein) and HLA class II alleles were investigaed; here report on the relations of the S protein and the open reading frame 1ab (ORF1ab) of SARS-CoV-2 to HLA class I alleles.

Methods:

An in silico sliding window approach was used to determine exhaustively the binding affinities of linear epitopes of 10 amino acid length (10-mers) to each of 61 common (global frequency ≥ 0.01) HLA class I molecules (17, 24 and 20 from gene loci A, B and C, respectively). A total of 8,354 epitopes were analyzed; 1,263 from the S protein and 7,091 from ORF1ab.

Results:

HLA-A genes were the most effective at binding SARS-CoV-2 epitopes for both spike and ORF1ab proteins. Good binding affinities were found for all three genes and were distributed throughout the length of the S protein and ORF1ab polyprotein sequence.

Conclusions:

Common HLA class I molecules, as a population, are very well suited to binding with high affinity to SARS-CoV-2 spike and ORF1ab proteins and hence should be effective in aiding the early elimination of the virus.

[Names] => Spyros A. Charonis ... Apostolos P. Georgopoulos [Doi] => 10.37349/ei.2021.00003 [Published] => April 30, 2021 [Viewed] => 2244 [Downloaded] => 50 [Subject] => Original Article [Year] => 2021 [CiteUrl] => [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:16–26 [Recommend] => 0 [Keywords] => ORF1ab, SARS-CoV-2, SARS-CoV-2 spike glycoprotein protein, human leukocyte antigen class I, in silico investigation [DetailTitle] => [DetailUrl] => [Id] => 10033 [ris] => https://www.explorationpub.com/uploads/Article/A10033/1fdde522c7d3ed6c2f77cdd1ad636c20.ris [bib] => https://www.explorationpub.com/uploads/Article/A10033/2ea723abaabddab118005efe50c63f15.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Charonis SA, Tsilibary EP, Georgopoulos AP. In silico investigation of binding affinities between human leukocyte antigen class I molecules and SARS-CoV-2 virus spike and ORF1ab proteins. Explor Immunol. 2021;1:16-26. https://doi.org/10.37349/ei.2021.00003 [Jindex] => 1 [CName] => Apostolos P.Georgopoulos, [CEmail] => omega@umn.edu, [Ris_Time] => 0000-00-00 00:00:00 [Bib_Time] => 0000-00-00 00:00:00 [KeysWordContens] => In silico investigation of binding affinities between human leukocyte antigen class I molecules and SARS-CoV-2 virus spike and ORF1ab proteins, ORF1ab, SARS-CoV-2, SARS-CoV-2 spike glycoprotein protein, human leukocyte antigen class I, in silico investigation, Aim: The novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019, a global pandemic. There is hence an urgent need for effective approaches to understand the mechanism of viral interaction with immune cells that lead to viral elimination and subsequent long-term immunity. The first, immediate response to the viral infection involves mobilization of native immunity and human leukocyte antigen (HLA) class I mechanisms to kill infected cells and eliminate the virus. The second line of defense involves the activation of HLA class II system for the production of antibodies against the virus which will add to the elimination of the virus and prevent future infections. In a previous study, investigated the relations between SARS-CoV-2 spike glycoprotein (S protein) and HLA class II alleles were investigaed; here report on the relations of the S protein and the open reading frame 1ab (ORF1ab) of SARS-CoV-2 to HLA class I alleles. Methods: An in silico sliding window approach was used to determine exhaustively the binding affinities of linear epitopes of 10 amino acid length (10-mers) to each of 61 common (global frequency ≥ 0.01) HLA class I molecules (17, 24 and 20 from gene loci A, B and C, respectively). A total of 8,354 epitopes were analyzed; 1,263 from the S protein and 7,091 from ORF1ab. Results: HLA-A genes were the most effective at binding SARS-CoV-2 epitopes for both spike and ORF1ab proteins. Good binding affinities were found for all three genes and were distributed throughout the length of the S protein and ORF1ab polyprotein sequence. Conclusions: Common HLA class I molecules, as a population, are very well suited to binding with high affinity to SARS-CoV-2 spike and ORF1ab proteins and hence should be effective in aiding the early elimination of the virus. ,Spyros A. Charonis ... Apostolos P. Georgopoulos [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [3] => Array ( [ArticleId] => 121 [Create_Time] => 2021-04-20 [zipUrl] => https://www.explorationpub.com/uploads/zip/202106/20210617051439.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10034/10034.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10034/10034.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10034/10034-cover.png [JournalsId] => 5 [Title] => Correlation of N-glycan dynamics and interaction network with allosteric antigen binding and Fc receptor recognition [Abstract] => Aim: Fragment crystallizable (Fc) glycans modulate Fc conformations and functions, and glycan may also regulate antigen recognition. In the antibody drug development, glycosylation patterns affect a [AbstractComplete] =>

Aim:

Fragment crystallizable (Fc) glycans modulate Fc conformations and functions, and glycan may also regulate antigen recognition. In the antibody drug development, glycosylation patterns affect antibody drug characteristics and quality control. In order to provide a global feature of N-glycan interactions in response to antigen and Fc receptor bindings, the interactions among Fc N-glycans and N-glycans’ interaction with Fc CH2 and CH3 domains have been studied.

Methods:

Molecular dynamics simulations were used to generate conformation ensembles of free antibody, antibody-antigen complex, antibody-human Fc-gamma-receptor-I (hFcγRI) and antibody-antigen-hFcγRI, the hydrogen bonds and radial distance distribution involving N-glycans carbohydrate chains have been analyzed.

Results:

Two important interaction patterns have been observed. The first is the strong but non-specific interactions between two carbohydrate chains in free antibody. Secondly, it has been found that N-glycans carbohydrate chains can directly interact with CH3 domain in free antibody, and that the distance distribution between carbohydrate chains and CH3 domain clearly differentiate the free antibody, antibody-antigen complex, antibody-hFcγRI complex, and final antibody-antigen-hFcγRI complex.

Conclusions:

N-glycans partially acts as allosteric sensor and respond to antigen and hFcγRI binding.

[Names] => Buyong Ma [Doi] => 10.37349/ei.2021.00004 [Published] => April 30, 2021 [Viewed] => 1640 [Downloaded] => 31 [Subject] => Original Article [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00004 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:27–36 [Recommend] => 0 [Keywords] => Antigen recognition, molecular dynamics simulations, allosteric, glycan, Fc receptor binding, antibody drug [DetailTitle] => [DetailUrl] => [Id] => 10034 [ris] => https://www.explorationpub.com/uploads/Article/A10034/cd46dfa934f7bf39b1b554afbbda5e6b.ris [bib] => https://www.explorationpub.com/uploads/Article/A10034/12efb18401cf74ccfe81f20774d06adf.bib [ens] => [Cited] => 2 [Cited_Time] => 2024-04-26 [CitethisArticle] => Ma B. Correlation of N-glycan dynamics and interaction network with allosteric antigen binding and Fc receptor recognition. Explor Immunol. 2021;1:27-36. https://doi.org/10.37349/ei.2021.00004 [Jindex] => 1 [CName] => BuyongMa, [CEmail] => mabuyong@sjtu.edu.cn, [Ris_Time] => 0000-00-00 00:00:00 [Bib_Time] => 0000-00-00 00:00:00 [KeysWordContens] => Correlation of N-glycan dynamics and interaction network with allosteric antigen binding and Fc receptor recognition, Antigen recognition, molecular dynamics simulations, allosteric, glycan, Fc receptor binding, antibody drug, Aim: Fragment crystallizable (Fc) glycans modulate Fc conformations and functions, and glycan may also regulate antigen recognition. In the antibody drug development, glycosylation patterns affect antibody drug characteristics and quality control. In order to provide a global feature of N-glycan interactions in response to antigen and Fc receptor bindings, the interactions among Fc N-glycans and N-glycans’ interaction with Fc CH2 and CH3 domains have been studied. Methods: Molecular dynamics simulations were used to generate conformation ensembles of free antibody, antibody-antigen complex, antibody-human Fc-gamma-receptor-I (hFcγRI) and antibody-antigen-hFcγRI, the hydrogen bonds and radial distance distribution involving N-glycans carbohydrate chains have been analyzed. Results: Two important interaction patterns have been observed. The first is the strong but non-specific interactions between two carbohydrate chains in free antibody. Secondly, it has been found that N-glycans carbohydrate chains can directly interact with CH3 domain in free antibody, and that the distance distribution between carbohydrate chains and CH3 domain clearly differentiate the free antibody, antibody-antigen complex, antibody-hFcγRI complex, and final antibody-antigen-hFcγRI complex. Conclusions: N-glycans partially acts as allosteric sensor and respond to antigen and hFcγRI binding. ,Buyong Ma [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [4] => Array ( [ArticleId] => 125 [Create_Time] => 2021-04-27 [zipUrl] => https://www.explorationpub.com/uploads/zip/202106/20210617051500.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10035/10035.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10035/10035.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10035/10035_cover.png [JournalsId] => 5 [Title] => Interleukin-22 and keratinocytes; pathogenic implications in skin inflammation [Abstract] => Interleukin (IL)-22 is produced from immune cells such as T helper (Th)22 cells, Th17/22 cells, and group 3 innate lymphoid cells. IL-22 signals via the IL-22 receptor 1 (IL-22R1) and the IL-10 rece [AbstractComplete] =>

Interleukin (IL)-22 is produced from immune cells such as T helper (Th)22 cells, Th17/22 cells, and group 3 innate lymphoid cells. IL-22 signals via the IL-22 receptor 1 (IL-22R1) and the IL-10 receptor 2 (IL-10R2). As the IL-22R1/IL-10R2 heterodimer is preferentially expressed on border tissue between the host and the environment, IL-22 is believed to be involved in border defense. Epidermal keratinocytes are the first-line skin barrier and express IL-22R1/IL-10R2. IL-22 increases keratinocyte proliferation but inhibits differentiation. Aryl hydrocarbon receptor (AHR) is a chemical sensor and an essential transcription factor for IL-22 production. In addition, AHR also upregulates the production of barrier-related proteins such as filaggrin in keratinocytes, suggesting a pivotal role for the AHR-IL-22 axis in regulating the physiological skin barrier. Although IL-22 signatures are elevated in atopic dermatitis and psoriasis, their pathogenic and/or protective implications are not fully understood.

[Names] => Masutaka Furue, Mihoko Furue [Doi] => 10.37349/ei.2021.00005 [Published] => April 30, 2021 [Viewed] => 3148 [Downloaded] => 129 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00005 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 42 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:37–47 [Recommend] => 0 [Keywords] => IL-22, IL-22 receptor, aryl hydrocarbon receptor, skin barrier, keratinocyte, atopic dermatitis, psoriasis [DetailTitle] => Cross Talk Among Skin Cells and Immune Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/42 [Id] => 10035 [ris] => https://www.explorationpub.com/uploads/Article/A10035/bd5bac42f58cc0b493bfc8a5e14546bd.ris [bib] => https://www.explorationpub.com/uploads/Article/A10035/1d55ed758e74413843b3f3958d954f2e.bib [ens] => [Cited] => 2 [Cited_Time] => 2024-04-26 [CitethisArticle] => Furue M, Furue M. Interleukin-22 and keratinocytes; pathogenic implications in skin inflammation. Explor Immunol. 2021;1:37-47. https://doi.org/10.37349/ei.2021.00005 [Jindex] => 1 [CName] => MasutakaFurue, [CEmail] => furuemasutaka00@yahoo.co.jp, [Ris_Time] => 0000-00-00 00:00:00 [Bib_Time] => 0000-00-00 00:00:00 [KeysWordContens] => Interleukin-22 and keratinocytes; pathogenic implications in skin inflammation, IL-22, IL-22 receptor, aryl hydrocarbon receptor, skin barrier, keratinocyte, atopic dermatitis, psoriasis, Interleukin (IL)-22 is produced from immune cells such as T helper (Th)22 cells, Th17/22 cells, and group 3 innate lymphoid cells. IL-22 signals via the IL-22 receptor 1 (IL-22R1) and the IL-10 receptor 2 (IL-10R2). As the IL-22R1/IL-10R2 heterodimer is preferentially expressed on border tissue between the host and the environment, IL-22 is believed to be involved in border defense. Epidermal keratinocytes are the first-line skin barrier and express IL-22R1/IL-10R2. IL-22 increases keratinocyte proliferation but inhibits differentiation. Aryl hydrocarbon receptor (AHR) is a chemical sensor and an essential transcription factor for IL-22 production. In addition, AHR also upregulates the production of barrier-related proteins such as filaggrin in keratinocytes, suggesting a pivotal role for the AHR-IL-22 axis in regulating the physiological skin barrier. Although IL-22 signatures are elevated in atopic dermatitis and psoriasis, their pathogenic and/or protective implications are not fully understood. ,Masutaka Furue, Mihoko Furue [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [5] => Array ( [ArticleId] => 131 [Create_Time] => 2021-04-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202106/20210617051527.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10036/10036.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10036/10036.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10036/10036_cover.png [JournalsId] => 5 [Title] => Immunology of biodegradable nanoparticles: a brief overview on a wide growing field [Abstract] => Immunity is continuously evolving by evolutionary mechanisms shaped by pathogenic stimuli of different kinds. Man-made nanomaterials (NMs) have been developed in the last decades and represent a nov [AbstractComplete] =>

Immunity is continuously evolving by evolutionary mechanisms shaped by pathogenic stimuli of different kinds. Man-made nanomaterials (NMs) have been developed in the last decades and represent a novel challenge for our immune system, especially when applied to medical science. Toxicological studies of such nanoparticles (NPs) revealed that size, shape, and surface chemistry are key parameters to understand their noxious effects on cellular mechanisms. Less is known on the immune reactions to NMs since prolonged exposure data are not so detailed as the results for acute administration. The importance of immunity to biocompatible NPs is underlined by their increasing use as drug or gene delivery carriers in common pharmaceutical preparations and vaccines. In the latter case, the immunomodulatory properties of NMs allow their use also as efficient adjuvants to enhance the innate immune response. In the current manuscript, the authors discuss the main concepts in this fast-growing field by restricting our view to NMs with consolidated application in biomedicine.

[Names] => Anissa Pisani, Giuseppe Bardi [Doi] => 10.37349/ei.2021.00006 [Published] => April 30, 2021 [Viewed] => 3975 [Downloaded] => 226 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00006 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:48–60 [Recommend] => 0 [Keywords] => Immune system, nanoparticles, inflammation, cytokines, protein corona [DetailTitle] => [DetailUrl] => [Id] => 10036 [ris] => https://www.explorationpub.com/uploads/Article/A10036/22ffebcfbf7927e799ce7fa358c07894.ris [bib] => https://www.explorationpub.com/uploads/Article/A10036/ade721fa3e231cbee3ffbbb0dc45bbe0.bib [ens] => [Cited] => 5 [Cited_Time] => 2024-04-25 [CitethisArticle] => Pisani A, Bardi G. Immunology of biodegradable nanoparticles: a brief overview on a wide growing field. Explor Immunol. 2021;1:48-60. https://doi.org/10.37349/ei.2021.00006 [Jindex] => 1 [CName] => GiuseppeBardi, [CEmail] => giuseppe.bardi@iit.it, [Ris_Time] => 0000-00-00 00:00:00 [Bib_Time] => 0000-00-00 00:00:00 [KeysWordContens] => Immunology of biodegradable nanoparticles: a brief overview on a wide growing field, Immune system, nanoparticles, inflammation, cytokines, protein corona, Immunity is continuously evolving by evolutionary mechanisms shaped by pathogenic stimuli of different kinds. Man-made nanomaterials (NMs) have been developed in the last decades and represent a novel challenge for our immune system, especially when applied to medical science. Toxicological studies of such nanoparticles (NPs) revealed that size, shape, and surface chemistry are key parameters to understand their noxious effects on cellular mechanisms. Less is known on the immune reactions to NMs since prolonged exposure data are not so detailed as the results for acute administration. The importance of immunity to biocompatible NPs is underlined by their increasing use as drug or gene delivery carriers in common pharmaceutical preparations and vaccines. In the latter case, the immunomodulatory properties of NMs allow their use also as efficient adjuvants to enhance the innate immune response. In the current manuscript, the authors discuss the main concepts in this fast-growing field by restricting our view to NMs with consolidated application in biomedicine. ,Anissa Pisani, Giuseppe Bardi [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [6] => Array ( [ArticleId] => 142 [Create_Time] => 2021-07-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230612085659.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10037/10037.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10037/10037.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10037/10037_cover.png [JournalsId] => 5 [Title] => Immunopathogenesis of severe acute respiratory syndrome coronavirus-2: evolving knowledge and its current status [Abstract] => As the severe acute respiratory syndrome coronavirus (SARS-CoV)-2 is a new virus, the current knowledge on the immunopathogenesis of this newly emerged SARS-CoV-2 is beginning to unravel with intens [AbstractComplete] =>

As the severe acute respiratory syndrome coronavirus (SARS-CoV)-2 is a new virus, the current knowledge on the immunopathogenesis of this newly emerged SARS-CoV-2 is beginning to unravel with intensive ongoing global research efforts. Although a plethora of new studies have been published in a short space of time describing how the virus causes disease and incurs insults on the host immune system and the underlying immunopathogenic mechanisms remain to be elucidated. Thus, the discussion in this review is based on the most current knowledge on the immunopathogenesis of SARS-CoV-2 that has emerged in the past 12 months. The main objective is to shed light on the most current concepts in immunopathological aspects of the lung, bloodstream, and brain caused by the SARS-CoV-2, which has led to the current pandemic resulting in > 100 million infections and > 2 million deaths, and ongoing.

[Names] => Nitin Saksena ... Monica Miranda-Saksena [Doi] => 10.37349/ei.2021.00007 [Published] => June 30, 2021 [Viewed] => 2543 [Downloaded] => 78 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00007 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:61–79 [Recommend] => 0 [Keywords] => Coronavirus disease 2019, severe acute respiratory syndrome coronavirus 2, immunopathology, viral infection, acute respiratory distress syndrome, cytokine storm, immunopathogenesis [DetailTitle] => [DetailUrl] => [Id] => 10037 [ris] => https://www.explorationpub.com/uploads/Article/A10037/227e412c5c49e830036a8ba853d4f007.ris [bib] => https://www.explorationpub.com/uploads/Article/A10037/60bb225b24a5521bdbb8b6ef0aefed4b.bib [ens] => [Cited] => 3 [Cited_Time] => 2024-04-25 [CitethisArticle] => Saksena N, Bonam SR, Miranda-Saksena M. Immunopathogenesis of severe acute respiratory syndrome coronavirus-2: evolving knowledge and its current status. Explor Immunol. 2021;1:61-79. https://doi.org/10.37349/ei.2021.00007 [Jindex] => 1 [CName] => NitinSaksena, [CEmail] => nitin.saksena@bigpond.com, [Ris_Time] => 0000-00-00 00:00:00 [Bib_Time] => 0000-00-00 00:00:00 [KeysWordContens] => Immunopathogenesis of severe acute respiratory syndrome coronavirus-2: evolving knowledge and its current status, Coronavirus disease 2019, severe acute respiratory syndrome coronavirus 2, immunopathology, viral infection, acute respiratory distress syndrome, cytokine storm, immunopathogenesis, As the severe acute respiratory syndrome coronavirus (SARS-CoV)-2 is a new virus, the current knowledge on the immunopathogenesis of this newly emerged SARS-CoV-2 is beginning to unravel with intensive ongoing global research efforts. Although a plethora of new studies have been published in a short space of time describing how the virus causes disease and incurs insults on the host immune system and the underlying immunopathogenic mechanisms remain to be elucidated. Thus, the discussion in this review is based on the most current knowledge on the immunopathogenesis of SARS-CoV-2 that has emerged in the past 12 months. The main objective is to shed light on the most current concepts in immunopathological aspects of the lung, bloodstream, and brain caused by the SARS-CoV-2, which has led to the current pandemic resulting in > 100 million infections and > 2 million deaths, and ongoing. ,Nitin Saksena ... Monica Miranda-Saksena [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [7] => Array ( [ArticleId] => 143 [Create_Time] => 2021-07-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202107/20210701061201.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10038/10038.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10038/10038.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10038/10038_cover.png [JournalsId] => 5 [Title] => L-arginine as a novel target for clinical intervention in inflammatory bowel disease [Abstract] => Arginase-1 (Arg1) and the inducible nitric oxide synthase 2 (NOS2) compete for the common substrate L-arginine, semi-essential amino acid, and central intestinal metabolite. Both enzymes exhibit var [AbstractComplete] =>

Arginase-1 (Arg1) and the inducible nitric oxide synthase 2 (NOS2) compete for the common substrate L-arginine, semi-essential amino acid, and central intestinal metabolite. Both enzymes exhibit various, sometimes opposing effects on immune responses, tissue regeneration, or microbial growth and replication. In sub-mucosal tissues of patients suffering from inflammatory bowel disease (IBD), similar as in experimental colitis, the expression and activity of both enzymes, Arg1 and NOS2 are more prominent than in respective controls. Accordingly, the metabolism of L-arginine is altered in IBD patients. Thus, L-arginine represents a promising medical target for clinical intervention in these devastating diseases. Previous studies primarily focused on the host side of L-arginine metabolism. Initial reports using Arg1 inhibitors generated conflicting results in murine colitis models. Subsequently, only the generation of conditional Arg1 knockout mice allowed reliable functional analyses of Arg1 and the L-arginine metabolism in the immune system. Utilizing cell-specific conditional Arg1 knockouts, we have recently reported that Arg1, surprisingly, hampered the resolution of experimental colitis due to the restriction of the intraluminal availability of L-arginine. Reduced levels of L-arginine restrained the compositional diversity of the intestinal microbiota and subsequently the mutual metabolism between the microbiota and the host. Thus, the intraluminal microbiota represents a potential therapeutic target for L-arginine metabolism aside from host-dependent L-arginine consumption.

[Names] => Björn Nüse, Jochen Mattner [Doi] => 10.37349/ei.2021.00008 [Published] => June 30, 2021 [Viewed] => 2858 [Downloaded] => 95 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00008 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:80–89 [Recommend] => 0 [Keywords] => Arginase-1, L-arginine, inflammatory bowel disease, colitis, gut microbiota, intestinal metabolism [DetailTitle] => [DetailUrl] => [Id] => 10038 [ris] => https://www.explorationpub.com/uploads/Article/A10038/c3c8b028bc484af2f0c2d143c97d68b5.ris [bib] => https://www.explorationpub.com/uploads/Article/A10038/c4ed9794141f8b3688447dce66d2cda9.bib [ens] => [Cited] => 3 [Cited_Time] => 2024-04-25 [CitethisArticle] => Cite this article: Nüse B, Mattner J. L-arginine as a novel target for clinical intervention in inflammatory bowel disease. Explor Immunol. 2021;1:80-9. https://doi.org/10.37349/ei.2021.00008 [Jindex] => 1 [CName] => JochenMattner, [CEmail] => Jochen.Mattner@uk-erlangen.de, [Ris_Time] => 0000-00-00 00:00:00 [Bib_Time] => 0000-00-00 00:00:00 [KeysWordContens] => L-arginine as a novel target for clinical intervention in inflammatory bowel disease, Arginase-1, L-arginine, inflammatory bowel disease, colitis, gut microbiota, intestinal metabolism, Arginase-1 (Arg1) and the inducible nitric oxide synthase 2 (NOS2) compete for the common substrate L-arginine, semi-essential amino acid, and central intestinal metabolite. Both enzymes exhibit various, sometimes opposing effects on immune responses, tissue regeneration, or microbial growth and replication. In sub-mucosal tissues of patients suffering from inflammatory bowel disease (IBD), similar as in experimental colitis, the expression and activity of both enzymes, Arg1 and NOS2 are more prominent than in respective controls. Accordingly, the metabolism of L-arginine is altered in IBD patients. Thus, L-arginine represents a promising medical target for clinical intervention in these devastating diseases. Previous studies primarily focused on the host side of L-arginine metabolism. Initial reports using Arg1 inhibitors generated conflicting results in murine colitis models. Subsequently, only the generation of conditional Arg1 knockout mice allowed reliable functional analyses of Arg1 and the L-arginine metabolism in the immune system. Utilizing cell-specific conditional Arg1 knockouts, we have recently reported that Arg1, surprisingly, hampered the resolution of experimental colitis due to the restriction of the intraluminal availability of L-arginine. Reduced levels of L-arginine restrained the compositional diversity of the intestinal microbiota and subsequently the mutual metabolism between the microbiota and the host. Thus, the intraluminal microbiota represents a potential therapeutic target for L-arginine metabolism aside from host-dependent L-arginine consumption. ,Björn Nüse, Jochen Mattner [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [8] => Array ( [ArticleId] => 151 [Create_Time] => 2021-07-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230612091241.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10039/10039.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10039/10039.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10039/10039_cover.png [JournalsId] => 5 [Title] => Vitamin D and immunomodulation in the skin: a useful affirmative nexus [Abstract] => Skin is the largest organ of the body having multifunctional activities. It has a dynamic cellular network with unique immunologic properties to maintain defensive actions, photoprotection, immune r [AbstractComplete] =>

Skin is the largest organ of the body having multifunctional activities. It has a dynamic cellular network with unique immunologic properties to maintain defensive actions, photoprotection, immune response, inflammation, tolerogenic capacity, wound healing, etc. The immune cells of the skin exhibit distinct properties. They can synthesize active vitamin D [1,24(OH)2D3] and express vitamin D receptors. Any difficulties in the cutaneous immune system cause skin diseases (psoriasis, vitiligo, atopic dermatitis, skin carcinoma, and others). Vitamin D is an essential factor, exhibits immunomodulatory effects by regulating dendritic cells’ maturation, lymphocytes’ functions, and cytokine production. More specifically, vitamin D acts as an immune balancing agent, inhibits the exaggeration of immunostimulation. This vitamin suppresses T-helper 1 and T-helper 17 cell formation decreases inflammatory cytokines release and promotes the maturation of regulatory T cells and interleukin 10 secretion. The deficiency of this vitamin promotes the occurrence of immunoreactive disorders. Administration of vitamin D or its analogs is the therapeutic choice for the treatment of several skin diseases.

[Names] => Saptadip Samanta [Doi] => 10.37349/ei.2021.00009 [Published] => June 30, 2021 [Viewed] => 3208 [Downloaded] => 93 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/e1.2021.00009 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 42 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:90–111 [Recommend] => 0 [Keywords] => Vitamin D, skin, immunomodulation, cytokines, anti-inflammatory effects, calcipotriol [DetailTitle] => Cross Talk Among Skin Cells and Immune Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/42 [Id] => 10039 [ris] => https://www.explorationpub.com/uploads/Article/A10039/029c8c206354c4c492b6a46f99a61c06.ris [bib] => https://www.explorationpub.com/uploads/Article/A10039/d06a625b7cbb9497b93548a04aa2f9cc.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Samanta S. Vitamin D and immunomodulation in the skin: a useful affirmative nexus. Explor Immunol. 2021;1:90-111. https://doi.org/10.37349/ei.2021.00009 [Jindex] => 1 [CName] => SaptadipSamanta, [CEmail] => saptadip174@gmail.com, [Ris_Time] => 0000-00-00 00:00:00 [Bib_Time] => 0000-00-00 00:00:00 [KeysWordContens] => Vitamin D and immunomodulation in the skin: a useful affirmative nexus, Vitamin D, skin, immunomodulation, cytokines, anti-inflammatory effects, calcipotriol, Skin is the largest organ of the body having multifunctional activities. It has a dynamic cellular network with unique immunologic properties to maintain defensive actions, photoprotection, immune response, inflammation, tolerogenic capacity, wound healing, etc. The immune cells of the skin exhibit distinct properties. They can synthesize active vitamin D [1,24(OH)2D3] and express vitamin D receptors. Any difficulties in the cutaneous immune system cause skin diseases (psoriasis, vitiligo, atopic dermatitis, skin carcinoma, and others). Vitamin D is an essential factor, exhibits immunomodulatory effects by regulating dendritic cells’ maturation, lymphocytes’ functions, and cytokine production. More specifically, vitamin D acts as an immune balancing agent, inhibits the exaggeration of immunostimulation. This vitamin suppresses T-helper 1 and T-helper 17 cell formation decreases inflammatory cytokines release and promotes the maturation of regulatory T cells and interleukin 10 secretion. The deficiency of this vitamin promotes the occurrence of immunoreactive disorders. Administration of vitamin D or its analogs is the therapeutic choice for the treatment of several skin diseases. ,Saptadip Samanta [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [9] => Array ( [ArticleId] => 153 [Create_Time] => 2021-07-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230612091519.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100310/100310.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100310/100310.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100310/100310_cover.png [JournalsId] => 5 [Title] => Interplay between mesenchymal stromal cells and immune system: clinical applications in immune-related diseases [Abstract] => Mesenchymal stromal cells (MSCs) are a mesodermal stem cell population, with known self-renewal and multilineage differentiation properties. In the last century, MSCs have been widely used in regene [AbstractComplete] =>

Mesenchymal stromal cells (MSCs) are a mesodermal stem cell population, with known self-renewal and multilineage differentiation properties. In the last century, MSCs have been widely used in regenerative medicine and tissue engineering approaches. MSCs initially were isolated from bone marrow aspirates, but currently have been identified in a great number of tissues of the human body. Besides their utilization in regenerative medicine, MSCs possess significant immunoregulatory/immunosuppressive properties, through interaction with the cells of innate and adaptive immunity. MSCs can exert their immunomodulatory properties with either cell-cell contact or via paracrine secretion of molecules, such as cytokines, growth factors and chemokines. Of particular importance, the MSCs’ immunomodulatory properties are explored as promising therapeutic strategies in immune-related disorders, such as autoimmune diseases, graft versus host disease, cancer. MSCs may also have an additional impact on coronavirus disease-19 (COVID-19), by attenuating the severe symptoms of this disorder. Nowadays, a great number of clinical trials, of MSC-mediated therapies are evaluated for their therapeutic potential. In this review, the current knowledge on cellular and molecular mechanisms involved in MSC-mediated immunomodulation were highlighted. Also, the most important aspects, regarding their potential application in immune-related diseases, will be highlighted. The broad application of MSCs has emerged their role as key immunomodulatory players, therefore their utilization in many disease situations is full of possibilities for future clinical treatment.

[Names] => Panagiotis Mallis ... Catherine Stavropoulos Giokas [Doi] => 10.37349/ei.2021.00010 [Published] => June 30, 2021 [Viewed] => 3763 [Downloaded] => 80 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00010 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:112–139 [Recommend] => 0 [Keywords] => Mesenchymal stromal cells, immunomodulation, adaptive immunity, graft versus host disease, autoimmune disorders, COVID-19 [DetailTitle] => [DetailUrl] => [Id] => 100310 [ris] => https://www.explorationpub.com/uploads/Article/A100310/fc06f1393f5350c5da3f696f1f5166f5.ris [bib] => https://www.explorationpub.com/uploads/Article/A100310/02f0fcc8dbf1d1d3d54747c239add575.bib [ens] => [Cited] => 5 [Cited_Time] => 2024-04-25 [CitethisArticle] => Mallis P, Michalopoulos E, Chatzistamatiou T, Giokas CS. Interplay between mesenchymal stromal cells and immune system: clinical applications in immune-related diseases. Explor Immunol. 2021;1:112-39. https://doi.org/10.37349/ei.2021.00010 [Jindex] => 1 [CName] => PanagiotisMallis, [CEmail] => pmallis@bioacademy.gr, [Ris_Time] => 0000-00-00 00:00:00 [Bib_Time] => 0000-00-00 00:00:00 [KeysWordContens] => Interplay between mesenchymal stromal cells and immune system: clinical applications in immune-related diseases, Mesenchymal stromal cells, immunomodulation, adaptive immunity, graft versus host disease, autoimmune disorders, COVID-19, Mesenchymal stromal cells (MSCs) are a mesodermal stem cell population, with known self-renewal and multilineage differentiation properties. In the last century, MSCs have been widely used in regenerative medicine and tissue engineering approaches. MSCs initially were isolated from bone marrow aspirates, but currently have been identified in a great number of tissues of the human body. Besides their utilization in regenerative medicine, MSCs possess significant immunoregulatory/immunosuppressive properties, through interaction with the cells of innate and adaptive immunity. MSCs can exert their immunomodulatory properties with either cell-cell contact or via paracrine secretion of molecules, such as cytokines, growth factors and chemokines. Of particular importance, the MSCs’ immunomodulatory properties are explored as promising therapeutic strategies in immune-related disorders, such as autoimmune diseases, graft versus host disease, cancer. MSCs may also have an additional impact on coronavirus disease-19 (COVID-19), by attenuating the severe symptoms of this disorder. Nowadays, a great number of clinical trials, of MSC-mediated therapies are evaluated for their therapeutic potential. In this review, the current knowledge on cellular and molecular mechanisms involved in MSC-mediated immunomodulation were highlighted. Also, the most important aspects, regarding their potential application in immune-related diseases, will be highlighted. The broad application of MSCs has emerged their role as key immunomodulatory players, therefore their utilization in many disease situations is full of possibilities for future clinical treatment. ,Panagiotis Mallis ... Catherine Stavropoulos Giokas [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [10] => Array ( [ArticleId] => 170 [Create_Time] => 2021-09-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230612091719.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100311/100311.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100311/100311.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100311/100311_cover.png [JournalsId] => 5 [Title] => Severe acute respiratory syndrome coronavirus 2 targeted antibodies cocktail and B cell receptor interplay: interventions to trigger vaccine development [Abstract] => Coronavirus disease-2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus (SARS-CoV)-2 spread globally and creates an alarming situation. Following the SARS-CoV-2 paradigm, therape [AbstractComplete] =>

Coronavirus disease-2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus (SARS-CoV)-2 spread globally and creates an alarming situation. Following the SARS-CoV-2 paradigm, therapeutic efficacy is achieved via repurposing several antiviral, antibacterial, and antimalarial drugs. Innate and adaptive immune cells work close to combat infection through the intricate production of antibodies (Abs) and inflammatory cytokines. As an essential component of the immune system, Abs play an important role in eliminating viruses and maintaining homeostasis. B lymphocytes (B cells) are effector cells, stringent to produce neutralizing Abs to combat infection. After recognizing SARS-CoV-2 antigens by a surface receptor called B cell receptors (BCRs) on the plasma membrane, the BCRs transmembrane signal transduction and immune activation results in Ab production and development of immune memory. Thus, it ensures that plasma B cells can quickly start an intricate immune response to generate efficient protective Abs to clear the pathogen. Nevertheless, considering therapeutic challenges in the context of the new coronavirus pandemic, this review addresses the molecular mechanism of the immune activation and function of novel SARS-CoV-2 specific B cells in the production of SARS-CoV-2 specific Abs. Additionally, these studies highlighted the Ab-mediated pathogenesis, the intriguing role of nano-scale signaling subunits, non-structural proteins during COVID-19 infection, and structural insights of SARS-CoV-2 specific Abs.

[Names] => Kabeer Haneef ... Zainab Fatima [Doi] => 10.37349/ei.2021.00011 [Published] => August 31, 2021 [Viewed] => 1885 [Downloaded] => 71 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00011 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 47 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:140–154 [Recommend] => 0 [Keywords] => Severe acute respiratory syndrome coronavirus 2, humoral immunity, B cell receptor, vaccine production, adaptive immunity, antibody pathogenesis, cytokine responses, non-structural protein [DetailTitle] => Vaccine-induced Immune Responses Against SARS-CoV-2 Infections [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/47 [Id] => 100311 [ris] => https://www.explorationpub.com/uploads/Article/A100311/ca4fbb3e39ddcc178de216facf7a78c7.ris [bib] => https://www.explorationpub.com/uploads/Article/A100311/ce1ed194ab6c3307aec3c92f75f70544.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Haneef K, Saleem R, Iqbal Khan MS, Adeyinka OS, Banday S, Asghar MU, et al. Severe acute respiratory syndrome coronavirus 2 targeted antibodies cocktail and B cell receptor interplay: interventions to trigger vaccine development. Explor Immunol. 2021;1:140-54. https://doi.org/10.37349/ei.2021.00011 [Jindex] => 1 [CName] => KabeerHaneef,RabiaSaleem, [CEmail] => Kabeerhaneef16@gmail.com,Kabeerhaneef16@gmail.com, [Ris_Time] => 2021-09-01 01:47:18 [Bib_Time] => 2021-09-01 01:47:18 [KeysWordContens] => Severe acute respiratory syndrome coronavirus 2 targeted antibodies cocktail and B cell receptor interplay: interventions to trigger vaccine development, Severe acute respiratory syndrome coronavirus 2, humoral immunity, B cell receptor, vaccine production, adaptive immunity, antibody pathogenesis, cytokine responses, non-structural protein, Coronavirus disease-2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus (SARS-CoV)-2 spread globally and creates an alarming situation. Following the SARS-CoV-2 paradigm, therapeutic efficacy is achieved via repurposing several antiviral, antibacterial, and antimalarial drugs. Innate and adaptive immune cells work close to combat infection through the intricate production of antibodies (Abs) and inflammatory cytokines. As an essential component of the immune system, Abs play an important role in eliminating viruses and maintaining homeostasis. B lymphocytes (B cells) are effector cells, stringent to produce neutralizing Abs to combat infection. After recognizing SARS-CoV-2 antigens by a surface receptor called B cell receptors (BCRs) on the plasma membrane, the BCRs transmembrane signal transduction and immune activation results in Ab production and development of immune memory. Thus, it ensures that plasma B cells can quickly start an intricate immune response to generate efficient protective Abs to clear the pathogen. Nevertheless, considering therapeutic challenges in the context of the new coronavirus pandemic, this review addresses the molecular mechanism of the immune activation and function of novel SARS-CoV-2 specific B cells in the production of SARS-CoV-2 specific Abs. Additionally, these studies highlighted the Ab-mediated pathogenesis, the intriguing role of nano-scale signaling subunits, non-structural proteins during COVID-19 infection, and structural insights of SARS-CoV-2 specific Abs. ,Kabeer Haneef ... Zainab Fatima [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [11] => Array ( [ArticleId] => 171 [Create_Time] => 2021-09-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202109/20210902051758.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100313/100313.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100313/100313.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100313/100313_cover.png [JournalsId] => 5 [Title] => Immunosuppressive microenvironment in oral cancer: implications for cancer immunotherapy [Abstract] => Head and neck squamous cell carcinoma (HNSCC) is a relatively widespread cancer with high mortality rates. Many patients with locally advanced disease are treated with combinations of surgery, radia [AbstractComplete] =>

Head and neck squamous cell carcinoma (HNSCC) is a relatively widespread cancer with high mortality rates. Many patients with locally advanced disease are treated with combinations of surgery, radiation, and chemotherapy, while others are considered incurable and develop recurrent/metastatic (R/M) disease. Despite these treatment modalities, the 5-year survival rate of HNSCC has remained at 50% due to limited treatment options in patients with recurrent disease. Immunotherapy has been shown to induce durable responses in R/M patients, but only a minority of patients currently respond. A major hurdle in tumor immunotherapy is identifying the non-responders and markers to predict resistance in patients who at first responded to the therapy. In HNSCC patients, the tumor microenvironment (TME) assumes a vital role to either diminish or augment immune responses. There is an urgent need for extensive studies to be undertaken to better understand how tumor cells escape immune surveillance and resist immune attack. In this review, the impact of TME on the efficiency of immunotherapy, addressing the factors that mediate therapy resistance are highlighted. The composition of the TME encompassing the immunosuppressive cells including myeloid-derived suppressor cell (MDSC), regulatory T cells (Treg), mesenchymal stem cell (MSC), cancer-associated fibroblast (CAF), and tumor-associated macrophages (TAMs) and intrinsic factors like hypoxia, reactive oxygen species (ROS), extracellular matrix (ECM), angiogenesis, and epithelial-mesenchymal transition (EMT), how this debilitates immunosurveillance, and also discuss existing and potential strategies aimed at targeting these cellular and molecular TME components are reviewed. Understanding the interactions between the TME and immunotherapy is not only important in dissevering the mechanisms of action of immunosuppression but also offers scope for developing newer strategies to improve the competence of current immunotherapies.

[Names] => Shalini K. Sureshbabu ... Shubhada V. Chiplunkar [Doi] => 10.37349/ei.2021.00013 [Published] => August 31, 2021 [Viewed] => 2534 [Downloaded] => 113 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00013 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:166–198 [Recommend] => 0 [Keywords] => Head and neck squamous cell carcinoma, tumor microenvironment, immunosuppressive network, immunotherapy, checkpoint inhibitors, adoptive transfer of T cells, vaccines [DetailTitle] => [DetailUrl] => [Id] => 100313 [ris] => https://www.explorationpub.com/uploads/Article/A100313/1be853893375efcfc8c781fd3d5bee51.ris [bib] => https://www.explorationpub.com/uploads/Article/A100313/1a46d6478165edd29f5616e3b64b4f82.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-25 [CitethisArticle] => SureshBabu SK, Godbole JH, Vaibhaw A, Chiplunkar SV. Immunosuppressive microenvironment in oral cancer: implications for cancer immunotherapy. Explor Immunol. 2021;1:166-98. https://doi.org/10.37349/ei.2021.00013 [Jindex] => 1 [CName] => Shubhada V.Chiplunkar, [CEmail] => shubhachiplunkar@gmail.com, [Ris_Time] => 0000-00-00 00:00:00 [Bib_Time] => 0000-00-00 00:00:00 [KeysWordContens] => Immunosuppressive microenvironment in oral cancer: implications for cancer immunotherapy, Head and neck squamous cell carcinoma, tumor microenvironment, immunosuppressive network, immunotherapy, checkpoint inhibitors, adoptive transfer of T cells, vaccines, Head and neck squamous cell carcinoma (HNSCC) is a relatively widespread cancer with high mortality rates. Many patients with locally advanced disease are treated with combinations of surgery, radiation, and chemotherapy, while others are considered incurable and develop recurrent/metastatic (R/M) disease. Despite these treatment modalities, the 5-year survival rate of HNSCC has remained at 50% due to limited treatment options in patients with recurrent disease. Immunotherapy has been shown to induce durable responses in R/M patients, but only a minority of patients currently respond. A major hurdle in tumor immunotherapy is identifying the non-responders and markers to predict resistance in patients who at first responded to the therapy. In HNSCC patients, the tumor microenvironment (TME) assumes a vital role to either diminish or augment immune responses. There is an urgent need for extensive studies to be undertaken to better understand how tumor cells escape immune surveillance and resist immune attack. In this review, the impact of TME on the efficiency of immunotherapy, addressing the factors that mediate therapy resistance are highlighted. The composition of the TME encompassing the immunosuppressive cells including myeloid-derived suppressor cell (MDSC), regulatory T cells (Treg), mesenchymal stem cell (MSC), cancer-associated fibroblast (CAF), and tumor-associated macrophages (TAMs) and intrinsic factors like hypoxia, reactive oxygen species (ROS), extracellular matrix (ECM), angiogenesis, and epithelial-mesenchymal transition (EMT), how this debilitates immunosurveillance, and also discuss existing and potential strategies aimed at targeting these cellular and molecular TME components are reviewed. Understanding the interactions between the TME and immunotherapy is not only important in dissevering the mechanisms of action of immunosuppression but also offers scope for developing newer strategies to improve the competence of current immunotherapies. ,Shalini K. Sureshbabu ... Shubhada V. Chiplunkar [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [12] => Array ( [ArticleId] => 172 [Create_Time] => 2021-09-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230615074832.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100314/100314.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100314/100314.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100314/100314_cover.png [JournalsId] => 5 [Title] => The protective immunity induced by SARS-CoV-2 infection and vaccination: a critical appraisal [Abstract] => Understanding the interactions of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) with humans is deeply grounded in immunology, from the diagnosis to pathogenesis, from the clinical pre [AbstractComplete] =>

Understanding the interactions of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) with humans is deeply grounded in immunology, from the diagnosis to pathogenesis, from the clinical presentations to the epidemiology, prevention, and treatment. However, the difficulty of capturing the complex and changeable array of immunological concepts and incorporating them into the strategies of control of the SARS-CoV-2 pandemic poses significant hindrances to establish optimal public health policies. The contribution of immunology to the control of the pandemic is to shed light on the features and mechanisms of the protective immunity elicited by SARS-CoV-2 infection and vaccines. Do they induce effective protective immunity? How? For how long? What is the effect of vaccination on individuals who were previously infected? To appropriately answer these questions, it is necessary to get rid of the outdated notion of a naïve, static, and closed immune system, which leads to misconceptions about susceptibility, specificity, immunological memory, and protective immunity. The present essay discusses these issues based on current immunological concepts.

[Names] => Eduardo Tosta [Doi] => 10.37349/ei.2021.00014 [Published] => August 31, 2021 [Viewed] => 2676 [Downloaded] => 57 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00014 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 47 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:199–225 [Recommend] => 0 [Keywords] => Protective immunity, SARS-CoV-2 infection, SARS-CoV-2 vaccines, susceptibility, specificity, immunological memory, epitope selection, adaptation, permissive immunity [DetailTitle] => Vaccine-induced Immune Responses Against SARS-CoV-2 Infections [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/47# [Id] => 100314 [ris] => https://www.explorationpub.com/uploads/Article/A100314/806e4439918be08edfc855a74aa603c8.ris [bib] => https://www.explorationpub.com/uploads/Article/A100314/71f86083f25ae8ee13267ef613eb6557.bib [ens] => [Cited] => 5 [Cited_Time] => 2024-04-26 [CitethisArticle] => Tosta E. The protective immunity induced by SARS-CoV-2 infection and vaccination: a critical appraisal. Explor Immunol. 2021;1:199-225. https://doi.org/10.37349/ei.2021.00014 [Jindex] => 1 [CName] => EduardoTosta, [CEmail] => cetosta@unb.br, [Ris_Time] => 2021-09-01 04:03:03 [Bib_Time] => 2021-09-01 04:03:03 [KeysWordContens] => The protective immunity induced by SARS-CoV-2 infection and vaccination: a critical appraisal, Protective immunity, SARS-CoV-2 infection, SARS-CoV-2 vaccines, susceptibility, specificity, immunological memory, epitope selection, adaptation, permissive immunity, Understanding the interactions of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) with humans is deeply grounded in immunology, from the diagnosis to pathogenesis, from the clinical presentations to the epidemiology, prevention, and treatment. However, the difficulty of capturing the complex and changeable array of immunological concepts and incorporating them into the strategies of control of the SARS-CoV-2 pandemic poses significant hindrances to establish optimal public health policies. The contribution of immunology to the control of the pandemic is to shed light on the features and mechanisms of the protective immunity elicited by SARS-CoV-2 infection and vaccines. Do they induce effective protective immunity? How? For how long? What is the effect of vaccination on individuals who were previously infected? To appropriately answer these questions, it is necessary to get rid of the outdated notion of a naïve, static, and closed immune system, which leads to misconceptions about susceptibility, specificity, immunological memory, and protective immunity. The present essay discusses these issues based on current immunological concepts. ,Eduardo Tosta [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [13] => Array ( [ArticleId] => 173 [Create_Time] => 2021-09-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230612091929.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100312/100312.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100312/100312.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100312/100312-cover.png [JournalsId] => 5 [Title] => Conserved envelope protein of nCoV2 as the possible target to design polytope vaccine [Abstract] => Aim: The envelope protein of novel coronavirus 2 (nCoV2) was reported to be highly conserved compared to its spike (S) protein which was shown to undergo several alterations in their amino acid seq [AbstractComplete] =>

Aim:

The envelope protein of novel coronavirus 2 (nCoV2) was reported to be highly conserved compared to its spike (S) protein which was shown to undergo several alterations in their amino acid sequences in the span of one year (2020–2021). Therefore, it is aimed to consider highly conserved structural protein of nCov2 namely envelope (E) protein to design the polytope for the formulation of the vaccine against coronavirus disease 2019 (Covid-19).

Methods:

Online in silico tools were employed to decipher the conservancy and antigenicity of E-protein of nCoV2. They are: to evaluate the molecular affinities among the chosen representatives of alpha and beta coronaviruses, the Molecular Evolutionary Genetics Analysis (MEGA) X 10.1.1 was used. Immune Epitope Database (IEDB)-NetMHCpan (ver. 4.1) tool was used to predict the epitopes of E protein binding to the frequently distributed major histocompatibility complex (MHC) I alleles. ProtParam, VaxJen, ToxinPred and AllerTop online tools were used to assess the physicochemical features, antigenicity, non-toxin and non-allergen aspects of constructed polytope. Secondary structure analysis and homology modelling validation of polytope were done using Phyre2 online tool. Discontinuous and linear epitopes of the designed polytope were predicted through IEDB Ellipro tool. Population coverage of epitopes of the polytope was performed using IEDB online tool with the frequent distribution of human leukocyte antigen (HLA) I alleles in the South Indian Asian population.

Results:

The phylogeny of envelope proteins of chosen representatives of Coronaviridae confirmed its conservancy and possible origin of nCoV2 from alpha coronaviruses through vampire CoV2. The designed polytope of E-protein was with 53 amino acid residues. The same was developed by linking with cysteine and serine (CS) residues in between epitopes.

Conclusion:

The antigenicity, non-allergen, non-toxin, homology modelling, discontinuous and linear epitopes of the designed polytope authenticate to explore the envelope protein for prophylactic measures. The epitopes of polytope were found to restrict to MHC I alleles occurring frequently among South Indian Asians.

[Names] => Krupanidhi Sreerama [Doi] => 10.37349/ei.2021.00012 [Published] => August 31, 2021 [Viewed] => 1655 [Downloaded] => 26 [Subject] => Original Article [Year] => 2021 [CiteUrl] => https://doi.org/10.37349/ei.2021.00012 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 47 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:155–165 [Recommend] => 0 [Keywords] => Severe acute respiratory syndrome novel coronavirus 2, envelope protein, polytope, vaccine design, South Indian Asians [DetailTitle] => Vaccine-induced Immune Responses Against SARS-CoV-2 Infections [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/47 [Id] => 100312 [ris] => https://www.explorationpub.com/uploads/Article/A100312/9d3b4617adb54039e0a7903b6b457e67.ris [bib] => https://www.explorationpub.com/uploads/Article/A100312/32700499c7f3fa5d2ad880cb41aed67e.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Sreerama K. Conserved envelope protein of nCoV2 as the possible target to design polytope vaccine. Explor Immunol. 2021;1:155-65. https://doi.org/10.37349/ei.2021.00012 [Jindex] => 1 [CName] => KrupanidhiSreerama, [CEmail] => krupanidhi.srirma@gmail.com, [Ris_Time] => 2021-09-03 08:01:10 [Bib_Time] => 2021-09-03 08:01:10 [KeysWordContens] => Conserved envelope protein of nCoV2 as the possible target to design polytope vaccine, Severe acute respiratory syndrome novel coronavirus 2, envelope protein, polytope, vaccine design, South Indian Asians, Aim: The envelope protein of novel coronavirus 2 (nCoV2) was reported to be highly conserved compared to its spike (S) protein which was shown to undergo several alterations in their amino acid sequences in the span of one year (2020–2021). Therefore, it is aimed to consider highly conserved structural protein of nCov2 namely envelope (E) protein to design the polytope for the formulation of the vaccine against coronavirus disease 2019 (Covid-19). Methods: Online in silico tools were employed to decipher the conservancy and antigenicity of E-protein of nCoV2. They are: to evaluate the molecular affinities among the chosen representatives of alpha and beta coronaviruses, the Molecular Evolutionary Genetics Analysis (MEGA) X 10.1.1 was used. Immune Epitope Database (IEDB)-NetMHCpan (ver. 4.1) tool was used to predict the epitopes of E protein binding to the frequently distributed major histocompatibility complex (MHC) I alleles. ProtParam, VaxJen, ToxinPred and AllerTop online tools were used to assess the physicochemical features, antigenicity, non-toxin and non-allergen aspects of constructed polytope. Secondary structure analysis and homology modelling validation of polytope were done using Phyre2 online tool. Discontinuous and linear epitopes of the designed polytope were predicted through IEDB Ellipro tool. Population coverage of epitopes of the polytope was performed using IEDB online tool with the frequent distribution of human leukocyte antigen (HLA) I alleles in the South Indian Asian population. Results: The phylogeny of envelope proteins of chosen representatives of Coronaviridae confirmed its conservancy and possible origin of nCoV2 from alpha coronaviruses through vampire CoV2. The designed polytope of E-protein was with 53 amino acid residues. The same was developed by linking with cysteine and serine (CS) residues in between epitopes. Conclusion: The antigenicity, non-allergen, non-toxin, homology modelling, discontinuous and linear epitopes of the designed polytope authenticate to explore the envelope protein for prophylactic measures. The epitopes of polytope were found to restrict to MHC I alleles occurring frequently among South Indian Asians. ,Krupanidhi Sreerama [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [14] => Array ( [ArticleId] => 174 [Create_Time] => 2021-09-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230612092245.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100315/100315.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100315/100315.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100315/100315-cover.png [JournalsId] => 5 [Title] => Macrophages and fibroblasts underpin skin immune responses [Abstract] => There are various types of skin immune responses including inflammatory skin diseases and skin malignancy. Macrophages and fibroblasts are skin resident cells that had been overlooked in terms of im [AbstractComplete] =>

There are various types of skin immune responses including inflammatory skin diseases and skin malignancy. Macrophages and fibroblasts are skin resident cells that had been overlooked in terms of immunological research targets. In this review, cross talk among macrophages, fibroblasts, and migratory immune cells in skin diseases such as atopic dermatitis (AD), contact hypersensitivity, psoriasis, systemic sclerosis, melanoma, and cutaneous T-cell lymphoma is described. Macrophages are important in AD by antigen-presenting phagocytosis, production of inflammatory cytokines, removal of apoptotic cells, and mediating clusters between dendritic cells (DCs) and T cells. They are also increased in lesional skin of psoriasis, especially in stable plaques, and an increased ratio of M1/M2 macrophages and tumor necrosis factor-α production by macrophages are essential for development of psoriasis. The progression of skin malignancy is mediated by macrophages through promotion of tumor survival pathways via expression of cytokines and growth factors, interaction with regulatory T cells (Tregs) and myeloid-derived suppressor cells, and suppression of function of tumor-infiltrating T cells by immunosuppressive cytokines and programmed death-ligand (PD-L)1. Fibroblasts play important roles in development and maintenance of AD lesions through expression of CC chemokine ligand (CCL)17, CCL11, CCL26, C-X-C motif chemokine ligand (CXCL)12, CCL19, and periostin, interacting with T helper (Th)2 cells, natural killer T (NKT) cells, DCs, and keratinocytes. They also play important roles in psoriasis, expressing interleukin (IL)-8 and vascular endothelial growth factor, production of fibronectin, and changes in the proteomic profiles. Fibroblasts have a critical role in the progression skin malignancy via expression of cytokines, suppression natural killer (NK) functions, and establishment of Th2-dominant microenvironment. Thus, cross talk among macrophages, fibroblasts, and migratory immune cells including T cells, DCs, and NK cells in skin diseases is important and those skin-resident cells are attracting therapeutic targets in the near future.

[Names] => Makoto Sugaya [Doi] => 10.37349/ei.2021.00015 [Published] => August 31, 2021 [Viewed] => 2472 [Downloaded] => 123 [Subject] => Review [Year] => 2021 [CiteUrl] => https://doi.org/10.37349/ei.2021.00015 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 42 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:226–242 [Recommend] => 0 [Keywords] => Macrophages, fibroblasts, atopic dermatitis, contact hypersensitivity, psoriasis, systemic sclerosis, melanoma, cutaneous T-cell lymphoma [DetailTitle] => Cross Talk Among Skin Cells and Immune Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/42 [Id] => 100315 [ris] => https://www.explorationpub.com/uploads/Article/A100315/dd0fac64f5ecd4cfd1eb41134b27d2d5.ris [bib] => https://www.explorationpub.com/uploads/Article/A100315/a892eb38faf8413d28840dccfe7b1c07.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Sugaya M. Macrophages and fibroblasts underpin skin immune responses. Explor Immunol. 2021;1:226-42. https://doi.org/10.37349/ei.2021.00015 [Jindex] => 1 [CName] => MakotoSugaya, [CEmail] => sugayamder@iuhw.ac.jp, [Ris_Time] => 2021-09-03 08:06:15 [Bib_Time] => 2021-09-03 08:06:15 [KeysWordContens] => Macrophages and fibroblasts underpin skin immune responses, Macrophages, fibroblasts, atopic dermatitis, contact hypersensitivity, psoriasis, systemic sclerosis, melanoma, cutaneous T-cell lymphoma, There are various types of skin immune responses including inflammatory skin diseases and skin malignancy. Macrophages and fibroblasts are skin resident cells that had been overlooked in terms of immunological research targets. In this review, cross talk among macrophages, fibroblasts, and migratory immune cells in skin diseases such as atopic dermatitis (AD), contact hypersensitivity, psoriasis, systemic sclerosis, melanoma, and cutaneous T-cell lymphoma is described. Macrophages are important in AD by antigen-presenting phagocytosis, production of inflammatory cytokines, removal of apoptotic cells, and mediating clusters between dendritic cells (DCs) and T cells. They are also increased in lesional skin of psoriasis, especially in stable plaques, and an increased ratio of M1/M2 macrophages and tumor necrosis factor-α production by macrophages are essential for development of psoriasis. The progression of skin malignancy is mediated by macrophages through promotion of tumor survival pathways via expression of cytokines and growth factors, interaction with regulatory T cells (Tregs) and myeloid-derived suppressor cells, and suppression of function of tumor-infiltrating T cells by immunosuppressive cytokines and programmed death-ligand (PD-L)1. Fibroblasts play important roles in development and maintenance of AD lesions through expression of CC chemokine ligand (CCL)17, CCL11, CCL26, C-X-C motif chemokine ligand (CXCL)12, CCL19, and periostin, interacting with T helper (Th)2 cells, natural killer T (NKT) cells, DCs, and keratinocytes. They also play important roles in psoriasis, expressing interleukin (IL)-8 and vascular endothelial growth factor, production of fibronectin, and changes in the proteomic profiles. Fibroblasts have a critical role in the progression skin malignancy via expression of cytokines, suppression natural killer (NK) functions, and establishment of Th2-dominant microenvironment. Thus, cross talk among macrophages, fibroblasts, and migratory immune cells including T cells, DCs, and NK cells in skin diseases is important and those skin-resident cells are attracting therapeutic targets in the near future. ,Makoto Sugaya [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [15] => Array ( [ArticleId] => 179 [Create_Time] => 2021-09-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202111/20211105075534.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100317/100317.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100317/100317.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100317/100317_cover.png [JournalsId] => 5 [Title] => Serum profiles of tryptophan-kynurenine pathway metabolites in psoriasis [Abstract] => Aim: Chronic inflammation is closely associated with tryptophan (TRP)-kynurenine (KYN) metabolic pathway. However, TRP-KYN pathway has not been fully elucidated in psoriasis, a systemic inflammator [AbstractComplete] =>

Aim:

Chronic inflammation is closely associated with tryptophan (TRP)-kynurenine (KYN) metabolic pathway. However, TRP-KYN pathway has not been fully elucidated in psoriasis, a systemic inflammatory disease with skin lesions and extracutaneous manifestations. Herein, we studied comprehensively serum profiles of TRP-KYN pathway metabolites in psoriatic patients (PSOs) to clarify the involvement of this pathway in the pathophysiology of psoriasis and to evaluate serum biomarkers reflecting systemic inflammation in PSOs.

Methods:

The concentrations of main TRP metabolites, TRP, KYN, 3-hydroxykynurenine (3HK), kynurenic acid (KYNA), 3-hydroxyanthranilic acid (3HAA), and anthranilic acid (AA), were determined by high-performance liquid chromatography in the sera from 65 PSOs and 35 healthy controls (HCs). The levels of these metabolites and the ratios of metabolites were compared between these subjects. The correlations between these values and the psoriasis area severity index (PASI) scores were analyzed. Skin samples from PSOs and HCs were subjected to immunohistochemical staining for kynureninase, catabolic enzyme from KYN or 3HK to downstream. Cytokine concentrations were comprehensively measured in the same samples and the correlations between the cytokine levels and TRP-KYN pathway metabolite levels were examined.

Results:

Serum TRP, KYN, and KYNA concentrations were lower and the 3HAA concentrations were higher in PSOs than in HCs. The ratios of 3HK/KYN, 3HAA/3HK, and 3HK/AA were higher in PSOs than in HCs. The AA levels and the ratio of AA/KYN were weakly positively correlated, and TRP, KYNA, and 3HK levels and the ratios of KYNA/KYN and 3HAA/AA were weakly negatively correlated with the PASI scores. The AA, KYN, and KYNA levels were positively correlated with the interferon gamma-induced protein 10 (IP-10) concentrations. Kynureninase expression was enhanced in the epidermis, both involved and uninvolved skin.

Conclusions:

Serum profiles of TRP-KYN pathway metabolites differed between PSOs and HCs. TRP-KYN pathway-associated processes, including kynureninase activation, may be involved in the pathogenesis of psoriasis, and thus serve as targets for psoriasis therapy.

[Names] => Mariko Seishima ... Kuniaki Saito [Doi] => 10.37349/ei.2021.00017 [Published] => October 31, 2021 [Viewed] => 1639 [Downloaded] => 62 [Subject] => Original Article [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00017 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 42 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:258–268 [Recommend] => 0 [Keywords] => Psoriasis, kynureninase, kynurenine metabolite, tryptophan-kynurenine pathway, indoleamine 2, 3-dioxygenase [DetailTitle] => Cross Talk Among Skin Cells and Immune Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/42 [Id] => 100317 [ris] => https://www.explorationpub.com/uploads/Article/A100317/e65390a8bfe9283436929cf5a6e0befa.ris [bib] => https://www.explorationpub.com/uploads/Article/A100317/b4b3d300d0a11d8bfbb9a423cdd625b0.bib [ens] => [Cited] => 2 [Cited_Time] => 2024-04-26 [CitethisArticle] => Seishima M, Yamamoto Y, Sakurai M, Sakai R, Fujii K, Mizutani Y, et al. Serum profiles of tryptophan-kynurenine pathway metabolites in psoriasis. Explor Immunol. 2021;1:258-68. https://doi.org/10.37349/ei.2021.00017 [Jindex] => 1 [CName] => MarikoSeishima, [CEmail] => marikoseishima@yahoo.co.jp, [Ris_Time] => 2021-11-01 03:14:17 [Bib_Time] => 2021-11-01 03:14:17 [KeysWordContens] => Serum profiles of tryptophan-kynurenine pathway metabolites in psoriasis, Psoriasis, kynureninase, kynurenine metabolite, tryptophan-kynurenine pathway, indoleamine 2, 3-dioxygenase, Aim: Chronic inflammation is closely associated with tryptophan (TRP)-kynurenine (KYN) metabolic pathway. However, TRP-KYN pathway has not been fully elucidated in psoriasis, a systemic inflammatory disease with skin lesions and extracutaneous manifestations. Herein, we studied comprehensively serum profiles of TRP-KYN pathway metabolites in psoriatic patients (PSOs) to clarify the involvement of this pathway in the pathophysiology of psoriasis and to evaluate serum biomarkers reflecting systemic inflammation in PSOs. Methods: The concentrations of main TRP metabolites, TRP, KYN, 3-hydroxykynurenine (3HK), kynurenic acid (KYNA), 3-hydroxyanthranilic acid (3HAA), and anthranilic acid (AA), were determined by high-performance liquid chromatography in the sera from 65 PSOs and 35 healthy controls (HCs). The levels of these metabolites and the ratios of metabolites were compared between these subjects. The correlations between these values and the psoriasis area severity index (PASI) scores were analyzed. Skin samples from PSOs and HCs were subjected to immunohistochemical staining for kynureninase, catabolic enzyme from KYN or 3HK to downstream. Cytokine concentrations were comprehensively measured in the same samples and the correlations between the cytokine levels and TRP-KYN pathway metabolite levels were examined. Results: Serum TRP, KYN, and KYNA concentrations were lower and the 3HAA concentrations were higher in PSOs than in HCs. The ratios of 3HK/KYN, 3HAA/3HK, and 3HK/AA were higher in PSOs than in HCs. The AA levels and the ratio of AA/KYN were weakly positively correlated, and TRP, KYNA, and 3HK levels and the ratios of KYNA/KYN and 3HAA/AA were weakly negatively correlated with the PASI scores. The AA, KYN, and KYNA levels were positively correlated with the interferon gamma-induced protein 10 (IP-10) concentrations. Kynureninase expression was enhanced in the epidermis, both involved and uninvolved skin. Conclusions: Serum profiles of TRP-KYN pathway metabolites differed between PSOs and HCs. TRP-KYN pathway-associated processes, including kynureninase activation, may be involved in the pathogenesis of psoriasis, and thus serve as targets for psoriasis therapy. ,Mariko Seishima ... Kuniaki Saito [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [16] => Array ( [ArticleId] => 180 [Create_Time] => 2021-09-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230612092415.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100316/100316.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100316/100316.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100316/100316_cover.png [JournalsId] => 5 [Title] => Immune responses induced by different vaccine platforms against coronavirus disease-19 [Abstract] => There have been significant developments in the design of nanostructured scaffolds for eliciting robust immune responses named vaccine. The technique is to produce strong immune responses is to mani [AbstractComplete] =>

There have been significant developments in the design of nanostructured scaffolds for eliciting robust immune responses named vaccine. The technique is to produce strong immune responses is to manipulate the appearance of a pathogen. Subsequently pathogens such as viruses and bacteria often demonstrate of multiple copies of ligands on their surfaces, the immune system is predominantly sensitive towards multivalent presentations of antigens. Consequently, when designing a vaccine, it is beneficial to garnish a nanostructured surface with multiple copies of an antigen so it can effectively act as an immune booster. Different methods are there for the development of the vaccine, from them most of the techniques are well developed and reported and some of in the developing state. This review focuses primarily on cellular and non-cellular vaccines, the whole cells or cellular proteins either as the source of antigens or the platform in which to deliver the antigens. Purpose of this review, understand and discussion on the various vaccine platforms which will contribute noteworthy information to vaccine research and development (R and D).

[Names] => Eknath D. Ahire, Sanjay J. Kshirsagar [Doi] => 10.37349/ei.2021.00016 [Published] => October 31, 2021 [Viewed] => 4167 [Downloaded] => 127 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00016 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 47 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:243–257 [Recommend] => 0 [Keywords] => Vaccine, platform, immune response, vaccination, development [DetailTitle] => Vaccine-induced Immune Responses Against SARS-CoV-2 Infections [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/47 [Id] => 100316 [ris] => https://www.explorationpub.com/uploads/Article/A100316/78d8bcaef5e8e7bf082c45df94a29b2a.ris [bib] => https://www.explorationpub.com/uploads/Article/A100316/232911bbdefa3f80fbba93f80596d877.bib [ens] => [Cited] => 3 [Cited_Time] => 2024-04-26 [CitethisArticle] => Ahire ED, Kshirsagar SJ. Immune responses induced by different vaccine platforms against coronavirus disease-19. Explor Immunol. 2021;1:243-57. https://doi.org/10.37349/eI.2021.00016 [Jindex] => 1 [CName] => Eknath D.Ahire, [CEmail] => eknathahire05@gmail.com, [Ris_Time] => 2021-11-01 03:15:11 [Bib_Time] => 2021-11-01 03:15:11 [KeysWordContens] => Immune responses induced by different vaccine platforms against coronavirus disease-19, Vaccine, platform, immune response, vaccination, development, There have been significant developments in the design of nanostructured scaffolds for eliciting robust immune responses named vaccine. The technique is to produce strong immune responses is to manipulate the appearance of a pathogen. Subsequently pathogens such as viruses and bacteria often demonstrate of multiple copies of ligands on their surfaces, the immune system is predominantly sensitive towards multivalent presentations of antigens. Consequently, when designing a vaccine, it is beneficial to garnish a nanostructured surface with multiple copies of an antigen so it can effectively act as an immune booster. Different methods are there for the development of the vaccine, from them most of the techniques are well developed and reported and some of in the developing state. This review focuses primarily on cellular and non-cellular vaccines, the whole cells or cellular proteins either as the source of antigens or the platform in which to deliver the antigens. Purpose of this review, understand and discussion on the various vaccine platforms which will contribute noteworthy information to vaccine research and development (R and D). ,Eknath D. Ahire, Sanjay J. Kshirsagar [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [17] => Array ( [ArticleId] => 185 [Create_Time] => 2021-10-09 [zipUrl] => https://www.explorationpub.com/uploads/zip/202303/20230302025025.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100318/100318.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100318/100318.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100318/100318_cover.png [JournalsId] => 5 [Title] => The two faces of mast cells in vitiligo pathogenesis [Abstract] => Aim: Previously, we reported increased number of T helper 17 (Th17) cells in vitiligo. However, in our recent study, tryptase and interleukin (IL)17 double positive cells which identified by polycl [AbstractComplete] =>

Aim:

Previously, we reported increased number of T helper 17 (Th17) cells in vitiligo. However, in our recent study, tryptase and interleukin (IL)17 double positive cells which identified by polyclonal anti-IL17 antibody with specificity for IL17A, B, D, F was observed, but these mast cells cannot be stained by monoclonal anti-IL17 antibody with specificity for IL17A. Therefore, this study was aimed to clarify the role of mast cells in induction and progression of vitiligo.

Methods:

Mast cells were stained with two antibodies against IL17 and one antibody against tryptase by immunofluorescent staining. Furthermore, immunoelectron microscopy (IEM) analyses were conducted using anti-tryptase. In vitro, cultured epidermal keratinocytes were treated with agents which released by mast cells. Expression levels of mRNA were analyzed by real-time polymerase chain reaction (PCR), expression of protein levels was analyzed by western blotting.

Results:

An increased number of tryptase positive mast cells was observed at the lesional skin of upper dermis in vitiligo and rhododendrol-induced leukoderma (RDIL). These mast cells showed prominent degranulation in vitiligo. Interestingly, the melanosome forming glycoprotein non-metastatic melanoma protein B (GPNMB) is downregulated in the lesional basal keratinocytes in vitiligo and mast cell tryptase contributes to this phenomenon. In addition, small interfering GPNMB RNA (siGPNMB RNA)-introduced keratinocytes increased melanocyte survival through stem cell factor (SCF) production in the melanocyte/keratinocyte co-culture system.

Conclusions:

Mast cells might be two-faced in vitiligo induction, progression, and recovery through the differential function of histamine and tryptase.

[Names] => Ichiro Katayama ... Mari Wataya-Kaneda [Doi] => 10.37349/ei.2021.00018 [Published] => October 31, 2021 [Viewed] => 1757 [Downloaded] => 73 [Subject] => Original Article [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00018 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 42 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:269–284 [Recommend] => 0 [Keywords] => Vitiligo, rhododendrol-induced leukoderma, mast cell, tryptase, interleukin 17 [DetailTitle] => Cross Talk Among Skin Cells and Immune Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/42 [Id] => 100318 [ris] => https://www.explorationpub.com/uploads/Article/A100318/281c3fabb24132eb7434d5c419dd5480.ris [bib] => https://www.explorationpub.com/uploads/Article/A100318/958d2cd3ca715b9b3bee8ea12292a24b.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Katayama I, Yang L, Takahashi A, Yang F, Wataya-Kaneda M. The two faces of mast cells in vitiligo pathogenesis. Explor Immunol. 2021;1:269-84. https://doi.org/10.37349/ei.2021.00018 [Jindex] => 1 [CName] => LingliYang, [CEmail] => yang.lingli@med.osaka-cu.ac.jp, [Ris_Time] => 2021-11-01 03:17:59 [Bib_Time] => 2021-11-01 03:17:59 [KeysWordContens] => The two faces of mast cells in vitiligo pathogenesis, Vitiligo, rhododendrol-induced leukoderma, mast cell, tryptase, interleukin 17, Aim: Previously, we reported increased number of T helper 17 (Th17) cells in vitiligo. However, in our recent study, tryptase and interleukin (IL)17 double positive cells which identified by polyclonal anti-IL17 antibody with specificity for IL17A, B, D, F was observed, but these mast cells cannot be stained by monoclonal anti-IL17 antibody with specificity for IL17A. Therefore, this study was aimed to clarify the role of mast cells in induction and progression of vitiligo. Methods: Mast cells were stained with two antibodies against IL17 and one antibody against tryptase by immunofluorescent staining. Furthermore, immunoelectron microscopy (IEM) analyses were conducted using anti-tryptase. In vitro, cultured epidermal keratinocytes were treated with agents which released by mast cells. Expression levels of mRNA were analyzed by real-time polymerase chain reaction (PCR), expression of protein levels was analyzed by western blotting. Results: An increased number of tryptase positive mast cells was observed at the lesional skin of upper dermis in vitiligo and rhododendrol-induced leukoderma (RDIL). These mast cells showed prominent degranulation in vitiligo. Interestingly, the melanosome forming glycoprotein non-metastatic melanoma protein B (GPNMB) is downregulated in the lesional basal keratinocytes in vitiligo and mast cell tryptase contributes to this phenomenon. In addition, small interfering GPNMB RNA (siGPNMB RNA)-introduced keratinocytes increased melanocyte survival through stem cell factor (SCF) production in the melanocyte/keratinocyte co-culture system. Conclusions: Mast cells might be two-faced in vitiligo induction, progression, and recovery through the differential function of histamine and tryptase. ,Ichiro Katayama ... Mari Wataya-Kaneda [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [18] => Array ( [ArticleId] => 189 [Create_Time] => 2021-10-21 [zipUrl] => https://www.explorationpub.com/uploads/zip/202201/20220107035455.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100319/100319.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100319/100319.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100319/100319-cover.png [JournalsId] => 5 [Title] => Skin and immune cells crosstalk via circadian regulations [Abstract] => Both innate and adaptive immune cells exist in the skin, predominantly in the dermis layer. Recent studies have focused on how and which circadian rhythms contribute to maintain good health. Over re [AbstractComplete] =>

Both innate and adaptive immune cells exist in the skin, predominantly in the dermis layer. Recent studies have focused on how and which circadian rhythms contribute to maintain good health. Over recent years, we have gained a better understanding of the molecular mechanisms that control biological clocks and circadian rhythms. Circadian rhythms maintain homeostasis by providing day and night information to various physiological functions of our body. However, excessively high immune system activity can lead to a risk of developing autoimmune or allergic diseases. Recently, increasing numbers of studies with human and mouse models have been conducted to investigate the mechanisms underlying circadian regulation of the skin homeostasis. In this review, circadian regulation in the skin will be discussed from different points of view. Skin is referred as the largest organ of the body and is directly exposed to the external environment, including large changes in diurnal temperature, light, and pathogens. Immune cells as well as skin cells are the ones protecting us from these stimulants. Associations of the circadian system and these cells have been revealed in many ways, however, the specific roles of the peripheral clocks in these cells remain unknown. Circadian regulation in the skin diseases is discussed specifically in atopic dermatitis and other skin allergic symptoms as well as psoriasis.

[Names] => Kanami Orihara [Doi] => 10.37349/ei.2021.00019 [Published] => October 31, 2021 [Viewed] => 2393 [Downloaded] => 116 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00019 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 42 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:285–294 [Recommend] => 0 [Keywords] => Skin, immune cells, immunity, chronobiology, circadian rhythm, body clock, homeostasis [DetailTitle] => Cross Talk Among Skin Cells and Immune Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/42 [Id] => 100319 [ris] => https://www.explorationpub.com/uploads/Article/A100319/911bbde9ebec43d624c4107fba9d8bed.ris [bib] => https://www.explorationpub.com/uploads/Article/A100319/66662c961c455b8e96c552a9be098f3d.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-26 [CitethisArticle] => Orihara K. Skin and immune cells crosstalk via circadian regulations. Explor Immunol. 2021;1:285-94. https://doi.org/10.37349/ei.2021.00019 [Jindex] => 1 [CName] => KanamiOrihara, [CEmail] => orihara.k.ab@m.titech.ac.jp, [Ris_Time] => 2021-11-02 04:01:48 [Bib_Time] => 2021-11-02 04:01:48 [KeysWordContens] => Skin and immune cells crosstalk via circadian regulations, Skin, immune cells, immunity, chronobiology, circadian rhythm, body clock, homeostasis, Both innate and adaptive immune cells exist in the skin, predominantly in the dermis layer. Recent studies have focused on how and which circadian rhythms contribute to maintain good health. Over recent years, we have gained a better understanding of the molecular mechanisms that control biological clocks and circadian rhythms. Circadian rhythms maintain homeostasis by providing day and night information to various physiological functions of our body. However, excessively high immune system activity can lead to a risk of developing autoimmune or allergic diseases. Recently, increasing numbers of studies with human and mouse models have been conducted to investigate the mechanisms underlying circadian regulation of the skin homeostasis. In this review, circadian regulation in the skin will be discussed from different points of view. Skin is referred as the largest organ of the body and is directly exposed to the external environment, including large changes in diurnal temperature, light, and pathogens. Immune cells as well as skin cells are the ones protecting us from these stimulants. Associations of the circadian system and these cells have been revealed in many ways, however, the specific roles of the peripheral clocks in these cells remain unknown. Circadian regulation in the skin diseases is discussed specifically in atopic dermatitis and other skin allergic symptoms as well as psoriasis. ,Kanami Orihara [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [19] => Array ( [ArticleId] => 202 [Create_Time] => 2021-11-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230612092747.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100320/100320.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100320/100320.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100320/100320_cover.png [JournalsId] => 5 [Title] => Viral vector-based vaccines against SARS-CoV-2 [Abstract] => Viral vectors have been frequently applied for vaccine development. It has also been the case for vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to tackle the coronavi [AbstractComplete] =>

Viral vectors have been frequently applied for vaccine development. It has also been the case for vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to tackle the coronavirus disease 2019 (COVID-19) pandemic. A multitude of different viral vectors have been mainly targeting the SARS-CoV-2 spike (S) protein as antigen. Intramuscular injection has been most commonly used, but also intranasal administration has been tested. Adenovirus vector-based vaccines are the most advanced with several vaccines receiving Emergency Use Authorization (EUA). The simian ChAdOx1 nCoV-19 vaccine applied as a prime-boost regimen has provided 62.1–90% vaccine efficacy in clinical trials. The Ad26.COV2.S vaccine requires only one immunization to provide protection against SARS-CoV-2. The rAd26-S/rAd5-S vaccine utilizes the Ad26 serotype for the prime immunization followed by a boost with the Ad5 serotype resulting in 91.2% vaccine efficacy. All adenovirus-based vaccines are used for mass vaccinations. Moreover, vaccine candidates based on vaccinia virus and lentivirus vectors have been subjected to clinical evaluation. Among self-replicating RNA viruses, vaccine vectors based on measles virus, rhabdoviruses, and alphaviruses have been engineered and tested in clinical trials. In addition to the intramuscular route of administration vaccine candidates based on influenza viruses and adenoviruses have been subjected to intranasal delivery showing antibody responses and protection against SARS-CoV-2 challenges in animal models. The detection of novel more transmissible and pathogenic SARS-CoV-2 variants added concerns about the vaccine efficacy and needs to be monitored. Moreover, the cause of recently documented rare cases of vaccine-induced immune thrombotic thrombocytopenia (VITT) must be investigated.

[Names] => Kenneth Lundstrom [Doi] => 10.37349/ei.2021.00020 [Published] => October 31, 2021 [Viewed] => 3748 [Downloaded] => 93 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00020 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 47 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:295–308 [Recommend] => 0 [Keywords] => Viral vectors, vaccines, SARS-CoV-2, COVID-19, clinical trials, protection [DetailTitle] => Vaccine-induced Immune Responses Against SARS-CoV-2 Infections [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/47 [Id] => 100320 [ris] => https://www.explorationpub.com/uploads/Article/A100320/061d9a2c26c772dc55262e07c3406e7c.ris [bib] => https://www.explorationpub.com/uploads/Article/A100320/1e1aef468b26f73ad771a1941086ddca.bib [ens] => [Cited] => 4 [Cited_Time] => 2024-04-25 [CitethisArticle] => Lundstrom K. Viral vector-based vaccines against SARS-CoV-2. Explor Immunol. 2021;1:295-308. https://doi.org/10.37349/ei.2021.00020 [Jindex] => 0 [CName] => KennethLundstrom, [CEmail] => lundstromkenneth@gmail.com, [Ris_Time] => 2021-11-01 03:56:20 [Bib_Time] => 2021-11-01 03:56:20 [KeysWordContens] => Viral vector-based vaccines against SARS-CoV-2, Viral vectors, vaccines, SARS-CoV-2, COVID-19, clinical trials, protection, Viral vectors have been frequently applied for vaccine development. It has also been the case for vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to tackle the coronavirus disease 2019 (COVID-19) pandemic. A multitude of different viral vectors have been mainly targeting the SARS-CoV-2 spike (S) protein as antigen. Intramuscular injection has been most commonly used, but also intranasal administration has been tested. Adenovirus vector-based vaccines are the most advanced with several vaccines receiving Emergency Use Authorization (EUA). The simian ChAdOx1 nCoV-19 vaccine applied as a prime-boost regimen has provided 62.1–90% vaccine efficacy in clinical trials. The Ad26.COV2.S vaccine requires only one immunization to provide protection against SARS-CoV-2. The rAd26-S/rAd5-S vaccine utilizes the Ad26 serotype for the prime immunization followed by a boost with the Ad5 serotype resulting in 91.2% vaccine efficacy. All adenovirus-based vaccines are used for mass vaccinations. Moreover, vaccine candidates based on vaccinia virus and lentivirus vectors have been subjected to clinical evaluation. Among self-replicating RNA viruses, vaccine vectors based on measles virus, rhabdoviruses, and alphaviruses have been engineered and tested in clinical trials. In addition to the intramuscular route of administration vaccine candidates based on influenza viruses and adenoviruses have been subjected to intranasal delivery showing antibody responses and protection against SARS-CoV-2 challenges in animal models. The detection of novel more transmissible and pathogenic SARS-CoV-2 variants added concerns about the vaccine efficacy and needs to be monitored. Moreover, the cause of recently documented rare cases of vaccine-induced immune thrombotic thrombocytopenia (VITT) must be investigated. ,Kenneth Lundstrom [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [20] => Array ( [ArticleId] => 207 [Create_Time] => 2021-12-13 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230612093111.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100323/100323.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100323/100323.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100323/100323-cover.png [JournalsId] => 5 [Title] => COVID-19 vaccine and immune response [Abstract] => Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; βCoV), the causative agent of coronavirus disease 2019 (COVID-19), causes severe lower respiratory tract infections and acute [AbstractComplete] =>

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; βCoV), the causative agent of coronavirus disease 2019 (COVID-19), causes severe lower respiratory tract infections and acute respiratory failure syndrome (ARDS). Deaths due to the ongoing COVID-19 pandemic for more than a year are still seen worldwide. Therefore, vaccine trials have gained importance. The discovery of the genome and protein structure of SARS-CoV-2 in a short time allowed the development of nucleic acid-based vaccines (mRNA and DNA vaccines), vector vaccines, inactivated virus vaccines, protein-based vaccines, virus-like particle vaccines, and live attenuated virus vaccines. Many companies, universities, and institutes around the world continue to develop effective vaccines against SARS-CoV-2. In this review, the structural features, classification, genome, and intracellular entry of SARS-CoV-2 coronaviruses, stimulation of the immune system and immunity, COVID-19 vaccine types, and the latest status of clinical trials of these vaccines have been reviewed.

[Names] => Sevilay Hintistan, Hatice Demirağ [Doi] => 10.37349/ei.2021.00023 [Published] => December 31, 2021 [Viewed] => 19254 [Downloaded] => 46 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00023 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 47 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:341–355 [Recommend] => 0 [Keywords] => COVID-19, vaccine, immune response [DetailTitle] => Vaccine-induced Immune Responses Against SARS-CoV-2 Infections [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/47 [Id] => 100323 [ris] => https://www.explorationpub.com/uploads/Article/A100323/34e5614b5481b527033e3c1f4360e672.ris [bib] => https://www.explorationpub.com/uploads/Article/A100323/99634c3d715cd96f6ac96e176adcee72.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Hintistan S, Demirağ H. COVID-19 vaccine and immune response. Explor Immunol. 2021;1:341-55. https://doi.org/10.37349/ei.2021.00023 [Jindex] => 0 [CName] => HaticeDemirağ, [CEmail] => hatice_etbas@hotmail.com, [Ris_Time] => 2021-12-31 05:49:22 [Bib_Time] => 2021-12-31 05:49:22 [KeysWordContens] => COVID-19 vaccine and immune response, COVID-19, vaccine, immune response, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; βCoV), the causative agent of coronavirus disease 2019 (COVID-19), causes severe lower respiratory tract infections and acute respiratory failure syndrome (ARDS). Deaths due to the ongoing COVID-19 pandemic for more than a year are still seen worldwide. Therefore, vaccine trials have gained importance. The discovery of the genome and protein structure of SARS-CoV-2 in a short time allowed the development of nucleic acid-based vaccines (mRNA and DNA vaccines), vector vaccines, inactivated virus vaccines, protein-based vaccines, virus-like particle vaccines, and live attenuated virus vaccines. Many companies, universities, and institutes around the world continue to develop effective vaccines against SARS-CoV-2. In this review, the structural features, classification, genome, and intracellular entry of SARS-CoV-2 coronaviruses, stimulation of the immune system and immunity, COVID-19 vaccine types, and the latest status of clinical trials of these vaccines have been reviewed. ,Sevilay Hintistan, Hatice Demirağ [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [21] => Array ( [ArticleId] => 211 [Create_Time] => 2021-12-13 [zipUrl] => https://www.explorationpub.com/uploads/zip/202201/20220128073802.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100322/100322.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100322/100322.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100322/100322-cover.png [JournalsId] => 5 [Title] => Preeclampsia—an immune disease? An epidemiologic narrative [Abstract] => The maternal syndrome preeclampsia is triggered by syncytiotrophoblast (STB) stress; the heterogeneity of the syndrome is caused by the different pathways leading to this STB stress. Inflammation pl [AbstractComplete] =>

The maternal syndrome preeclampsia is triggered by syncytiotrophoblast (STB) stress; the heterogeneity of the syndrome is caused by the different pathways leading to this STB stress. Inflammation plays a pivotal role in the pathogenesis of preeclampsia. While, the immune system at large is therefore intimately involved in the causation of this heterogeneous syndrome, the role of the adaptive immune system is more controversial. The classic paradigm placed preeclampsia as the disease of the nulliparous pregnant women. Up to the later part of the 20th century, human reproduction, particularly in Western societies, was characterised by a low rate of pre-marital sex, and the great majority of children being born within one stable sexual relationship. More prolonged periods of regular sexual intercourse within a stable relationship have been demonstrated to reduce the risk of preeclampsia and fetal growth restriction. Primarily animal studies have indeed shown that repetitive sperm exposure leads to partner specific mucosal tolerance. Societal changes made partner change over the reproductive period of individual women extremely common. For the adaptive immune system of multiparous women, being pregnant in a new sexual relationship (primipaternity) would represent being faced with a new “hemi-allograft”. In these pregnancies, potential couple-specific immune “maladaptation” could lead to the superficial cytotrophoblast invasion of the spiral arteries, known to be associated with early-onset preeclampsia. Having a new pregnancy in a different relationship does indeed increase the risk for this type of preeclampsia. Large epidemiologic population studies identified prolonged birth interval but not “primipaternity” as a risk factor for preeclampsia in multiparous women. This apparent contradiction is explained by the fact that the great majority of preeclampsia cases in these population studies involve term preeclampsia. In late-onset preeclampsia, the far more common phenotype of the syndrome, STB stress is not caused by lack of proper spiral artery modification, but involves maternal genetic predisposition to cardiovascular and metabolic disease, with in particular obesity/metabolic syndrome representing major players. Partner or couple specific issues are not detectable in this disease phenotype.

[Names] => Gustaaf Albert Dekker, Pierre Yves Robillard [Doi] => 10.37349/ei.2021.00022 [Published] => December 31, 2021 [Viewed] => 1809 [Downloaded] => 35 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00022 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:325–340 [Recommend] => 0 [Keywords] => Preeclampsia heterogeneous syndrome, adaptive immune system, early-onset preeclampsia [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100322 [ris] => https://www.explorationpub.com/uploads/Article/A100322/c5d158a00cf2edcf6ed3263f22e37f60.ris [bib] => https://www.explorationpub.com/uploads/Article/A100322/a96f2237cc6aa59f470d23af21a4a684.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Dekker GA, Robillard PY. Preeclampsia—an immune disease? An epidemiologic narrative. Explor Immunol. 2021;1:325-40. https://doi.org/10.37349/ei.2021.00022 [Jindex] => 0 [CName] => Gustaaf AlbertDekker, [CEmail] => gustaaf.dekker@adelaide.edu.au, [Ris_Time] => 2021-12-31 05:40:26 [Bib_Time] => 2021-12-31 05:40:26 [KeysWordContens] => Preeclampsia—an immune disease? An epidemiologic narrative, Preeclampsia heterogeneous syndrome, adaptive immune system, early-onset preeclampsia, The maternal syndrome preeclampsia is triggered by syncytiotrophoblast (STB) stress; the heterogeneity of the syndrome is caused by the different pathways leading to this STB stress. Inflammation plays a pivotal role in the pathogenesis of preeclampsia. While, the immune system at large is therefore intimately involved in the causation of this heterogeneous syndrome, the role of the adaptive immune system is more controversial. The classic paradigm placed preeclampsia as the disease of the nulliparous pregnant women. Up to the later part of the 20th century, human reproduction, particularly in Western societies, was characterised by a low rate of pre-marital sex, and the great majority of children being born within one stable sexual relationship. More prolonged periods of regular sexual intercourse within a stable relationship have been demonstrated to reduce the risk of preeclampsia and fetal growth restriction. Primarily animal studies have indeed shown that repetitive sperm exposure leads to partner specific mucosal tolerance. Societal changes made partner change over the reproductive period of individual women extremely common. For the adaptive immune system of multiparous women, being pregnant in a new sexual relationship (primipaternity) would represent being faced with a new “hemi-allograft”. In these pregnancies, potential couple-specific immune “maladaptation” could lead to the superficial cytotrophoblast invasion of the spiral arteries, known to be associated with early-onset preeclampsia. Having a new pregnancy in a different relationship does indeed increase the risk for this type of preeclampsia. Large epidemiologic population studies identified prolonged birth interval but not “primipaternity” as a risk factor for preeclampsia in multiparous women. This apparent contradiction is explained by the fact that the great majority of preeclampsia cases in these population studies involve term preeclampsia. In late-onset preeclampsia, the far more common phenotype of the syndrome, STB stress is not caused by lack of proper spiral artery modification, but involves maternal genetic predisposition to cardiovascular and metabolic disease, with in particular obesity/metabolic syndrome representing major players. Partner or couple specific issues are not detectable in this disease phenotype. ,Gustaaf Albert Dekker, Pierre Yves Robillard [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [22] => Array ( [ArticleId] => 212 [Create_Time] => 2021-12-13 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230612093007.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100321/100321.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100321/100321.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100321/100321-cover.png [JournalsId] => 5 [Title] => Immunoregulation in the testis and its implication in fertility and infections [Abstract] => The testis is designated as one of the immune previleged sites in the body and harbours a unique immunoregulatory environment, which is important for preventing an immune response against sperm anti [AbstractComplete] =>

The testis is designated as one of the immune previleged sites in the body and harbours a unique immunoregulatory environment, which is important for preventing an immune response against sperm antigens which otherwise are recognized as “foreign” by the immune system. The blood-testis barrier along with the unique immune cells repertoire and various immunoregulatory & immunosuppressive factors secreted by the Leydig cells, Sertoli cells and peritubular cells act in concert to maintain the tolerogenic environment in the testis. Abberations in immunotolerant mechanisms in the testis can lead to generation of anti-sperm antibodies that have an association with male infertility. It can also lead to inflammatory conditions of the male reproductive tract manifested as epididymitis and orchitis, generally due to bacterial or viral infections. In addition, non-infectious epididymitis and orchitis, having autoimmune origin have also been reported in males. While the immune privilege status of human testis protects the germ cells from an immune attack, it can also make the testis a succeptible reservoir for viruses such as human immunodeficiency virus-1, Zika virus and severe acute respiratory syndrome coronavirus-2, all of which have adverse consequences on male reproduction.

[Names] => Kushaan Khambata ... Satish K. Gupta [Doi] => 10.37349/ei.2021.00021 [Published] => December 31, 2021 [Viewed] => 2255 [Downloaded] => 60 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00021 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:309–324 [Recommend] => 0 [Keywords] => Blood-testis barrier, immune cells, immune previlege, infertility, anti-sperm antibody, epididymitis, orchitis, infection, autoimmunity [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100321 [ris] => https://www.explorationpub.com/uploads/Article/A100321/1a100cba433776de074b4fda42937e59.ris [bib] => https://www.explorationpub.com/uploads/Article/A100321/39853c60487697ab3080149805c6fc84.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Khambata K, Modi DN, Gupta SK. Immunoregulation in the testis and its implication in fertility and infections. Explor Immunol. 2021;1:309-24. https://doi.org/10.37349/ei.2021.00021 [Jindex] => 0 [CName] => Satish K.Gupta, [CEmail] => skgupta.nii53@gmail.com, [Ris_Time] => 2021-12-31 05:35:37 [Bib_Time] => 2021-12-31 05:35:37 [KeysWordContens] => Immunoregulation in the testis and its implication in fertility and infections, Blood-testis barrier, immune cells, immune previlege, infertility, anti-sperm antibody, epididymitis, orchitis, infection, autoimmunity, The testis is designated as one of the immune previleged sites in the body and harbours a unique immunoregulatory environment, which is important for preventing an immune response against sperm antigens which otherwise are recognized as “foreign” by the immune system. The blood-testis barrier along with the unique immune cells repertoire and various immunoregulatory & immunosuppressive factors secreted by the Leydig cells, Sertoli cells and peritubular cells act in concert to maintain the tolerogenic environment in the testis. Abberations in immunotolerant mechanisms in the testis can lead to generation of anti-sperm antibodies that have an association with male infertility. It can also lead to inflammatory conditions of the male reproductive tract manifested as epididymitis and orchitis, generally due to bacterial or viral infections. In addition, non-infectious epididymitis and orchitis, having autoimmune origin have also been reported in males. While the immune privilege status of human testis protects the germ cells from an immune attack, it can also make the testis a succeptible reservoir for viruses such as human immunodeficiency virus-1, Zika virus and severe acute respiratory syndrome coronavirus-2, all of which have adverse consequences on male reproduction. ,Kushaan Khambata ... Satish K. Gupta [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [23] => Array ( [ArticleId] => 222 [Create_Time] => 2021-12-13 [zipUrl] => https://www.explorationpub.com/uploads/zip/202305/20230520072638.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100324/100324.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100324/100324.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100324/100324_cover.png [JournalsId] => 5 [Title] => Vaccine-induced immune responses against SARS-CoV-2 infections [Abstract] => Vaccination against coronavirus disease 2019 (COVID-19) is one of the most effective tools to curb the pandemic. Multiple vaccine candidates based on different platforms are available for emergency [AbstractComplete] =>

Vaccination against coronavirus disease 2019 (COVID-19) is one of the most effective tools to curb the pandemic. Multiple vaccine candidates based on different platforms are available for emergency use presently. However, in common all the vaccines target spike protein, which is a dominant immunogen of severe acute respiratory syndrome corona virus 2 (SARS-CoV-2). Adequate immunogenicity and efficacy are demonstrated by many of the vaccines in clinical phase III trials. The emergence of the new variant of concern is believed to be associated with less susceptibility to the post-infection or post-vaccination mounted immunity. It is a global concern currently threatening the progression of the vaccination drive. Nevertheless, the results of the presently available phase III clinical trials promote COVID-19 vaccination to prevent disease severity and COVID-19 related deaths. Cross-immunity towards the new variants of concern especially against the South African variant is yet to be explored and managed adequately.

[Names] => Mandeep Garg ... Suruchi Garg [Doi] => 10.37349/ei.2021.00024 [Published] => December 31, 2021 [Viewed] => 1537 [Downloaded] => 29 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00024 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 47 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:356–373 [Recommend] => 0 [Keywords] => Severe acute respiratory syndrome corona virus 2, coronavirus disease 2019, vaccine, immune response, pandemic [DetailTitle] => Vaccine-induced Immune Responses Against SARS-CoV-2 Infections [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/47 [Id] => 100324 [ris] => https://www.explorationpub.com/uploads/Article/A100324/d1173c390176b9f14e519d89bb1b3cb9.ris [bib] => https://www.explorationpub.com/uploads/Article/A100324/5f1e1f6a3af47b36e24e26e61fd5c46f.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Garg M, Maralakunte M, Kumar Y, Bhujade H, Sehgal IP, Suri V, et al. Vaccine-induced immune responses against SARS-CoV-2 infections. Explor Immunol. 2021;1:356-73. https://doi.org/10.37349/ei.2021.00024 [Jindex] => 0 [CName] => MandeepGarg, [CEmail] => gargmandeep@hotmail.com, [Ris_Time] => 2021-12-31 10:05:07 [Bib_Time] => 2021-12-31 10:08:03 [KeysWordContens] => Vaccine-induced immune responses against SARS-CoV-2 infections, Severe acute respiratory syndrome corona virus 2, coronavirus disease 2019, vaccine, immune response, pandemic, Vaccination against coronavirus disease 2019 (COVID-19) is one of the most effective tools to curb the pandemic. Multiple vaccine candidates based on different platforms are available for emergency use presently. However, in common all the vaccines target spike protein, which is a dominant immunogen of severe acute respiratory syndrome corona virus 2 (SARS-CoV-2). Adequate immunogenicity and efficacy are demonstrated by many of the vaccines in clinical phase III trials. The emergence of the new variant of concern is believed to be associated with less susceptibility to the post-infection or post-vaccination mounted immunity. It is a global concern currently threatening the progression of the vaccination drive. Nevertheless, the results of the presently available phase III clinical trials promote COVID-19 vaccination to prevent disease severity and COVID-19 related deaths. Cross-immunity towards the new variants of concern especially against the South African variant is yet to be explored and managed adequately. ,Mandeep Garg ... Suruchi Garg [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [24] => Array ( [ArticleId] => 223 [Create_Time] => 2021-12-16 [zipUrl] => https://www.explorationpub.com/uploads/zip/202305/20230523063423.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100325/100325.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100325/100325.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100325/100325_cover.png [JournalsId] => 5 [Title] => Activation of mucosal immunity and novel prophylactic and therapeutic strategy in combating COVID-19 [Abstract] => Coronavirus disease 2019 (COVID-19) emerges as an expeditiously growing pandemic, in the human population caused by the highly transmissible RNA virus severe acute respiratory syndrome of coronaviru [AbstractComplete] =>

Coronavirus disease 2019 (COVID-19) emerges as an expeditiously growing pandemic, in the human population caused by the highly transmissible RNA virus severe acute respiratory syndrome of coronavirus 2 (SARS-CoV-2). Prognosis of SARS-CoV-2 infection predominantly occurs at the angiotensin-converting enzyme 2 receptor and transmembrane protease serine type 2 positive (ACE2 + TMPRSS2)+ epithelial cells of the mucosal surface like nasal, oral mucosae, and/or the conjunctival surface of the eye where it has interacted along with the immune system. The primary host response towards the pathogen starts from an immune microenvironment of nasopharynx-associated lymphoid tissue (NALT) and mucosa-associated lymphoid tissue (MALT). The presence of exhausted lymphocytes, lymphopenia, pneumonia and cytokine storm is the hallmark of COVID-19. The multifaceted nature of co-morbidity factors like obesity and type 2 diabetes and its effects on immunity can alter the pathogenesis of SARS-CoV-2 infection. Adipose tissue is a crucial endocrine organ that secretes a plethora of factors like adipokines, cytokines, and chemokines that have a profound impact on metabolism and augments the expression of mucosal pro-inflammatory cytokines, like tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), and the interleukin-12 (IL-12)/IL-23. Mucosal immunization could be a superior approach to activate mucosal and systemic immune responses against pathogenic invasion at mucosal surface entry ports. Mucosal vaccines are also able to generate strong systemic humoral immunity—required to neutralize any virus particle that dodges the primary immune response. To develop an efficient vaccine against mucosal pathogens, considering the designing of the delivery route, immunomodulatory features, and adjuvants are very important. In this article, we further provide evidence to understand the significant role of mucosal immunity, along with secretory and circulating immunoglobulin A (IgA) antibodies in generating a novel mucosal vaccine against COVID-19. Moreover, along with mucosal vaccines, we should look for combination treatment strategies with plant bioactive molecules. Glycan-binding lectins against viral proteins for targeted activation of mucosal immune response are one of such examples. This might play a promising role to halt this emerging virus.

[Names] => Swapan K. Chatterjee ... Maria Nilda M. Munoz [Doi] => 10.37349/ei.2021.00025 [Published] => December 31, 2021 [Viewed] => 2666 [Downloaded] => 94 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00025 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 47 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:374–397 [Recommend] => 0 [Keywords] => Cytokine storm, obesity, interferon-gamma, nasopharynx-associated lymphoid tissue, mucosal immunity, mucosal vaccine, immunoglobulin A, coronavirus disease 2019 [DetailTitle] => Vaccine-induced Immune Responses Against SARS-CoV-2 Infections [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/47 [Id] => 100325 [ris] => https://www.explorationpub.com/uploads/Article/A100325/86f2a17c0561a2417224572874900632.ris [bib] => https://www.explorationpub.com/uploads/Article/A100325/1eaa07b1a5cf6731bcad4052832354bc.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-26 [CitethisArticle] => Chatterjee SK, Saha S, Munoz MNM. Activation of mucosal immunity and novel prophylactic and therapeutic strategy in combating COVID-19. Explor Immunol. 2021;1:374-97. https://doi.org/10.37349/ei.2021.00025 [Jindex] => 0 [CName] => Swapan K.Chatterjee, [CEmail] => swapan1chatterjee@gmail.com, [Ris_Time] => 2021-12-31 06:24:10 [Bib_Time] => 2021-12-31 06:24:10 [KeysWordContens] => Activation of mucosal immunity and novel prophylactic and therapeutic strategy in combating COVID-19, Cytokine storm, obesity, interferon-gamma, nasopharynx-associated lymphoid tissue, mucosal immunity, mucosal vaccine, immunoglobulin A, coronavirus disease 2019, Coronavirus disease 2019 (COVID-19) emerges as an expeditiously growing pandemic, in the human population caused by the highly transmissible RNA virus severe acute respiratory syndrome of coronavirus 2 (SARS-CoV-2). Prognosis of SARS-CoV-2 infection predominantly occurs at the angiotensin-converting enzyme 2 receptor and transmembrane protease serine type 2 positive (ACE2 + TMPRSS2)+ epithelial cells of the mucosal surface like nasal, oral mucosae, and/or the conjunctival surface of the eye where it has interacted along with the immune system. The primary host response towards the pathogen starts from an immune microenvironment of nasopharynx-associated lymphoid tissue (NALT) and mucosa-associated lymphoid tissue (MALT). The presence of exhausted lymphocytes, lymphopenia, pneumonia and cytokine storm is the hallmark of COVID-19. The multifaceted nature of co-morbidity factors like obesity and type 2 diabetes and its effects on immunity can alter the pathogenesis of SARS-CoV-2 infection. Adipose tissue is a crucial endocrine organ that secretes a plethora of factors like adipokines, cytokines, and chemokines that have a profound impact on metabolism and augments the expression of mucosal pro-inflammatory cytokines, like tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), and the interleukin-12 (IL-12)/IL-23. Mucosal immunization could be a superior approach to activate mucosal and systemic immune responses against pathogenic invasion at mucosal surface entry ports. Mucosal vaccines are also able to generate strong systemic humoral immunity—required to neutralize any virus particle that dodges the primary immune response. To develop an efficient vaccine against mucosal pathogens, considering the designing of the delivery route, immunomodulatory features, and adjuvants are very important. In this article, we further provide evidence to understand the significant role of mucosal immunity, along with secretory and circulating immunoglobulin A (IgA) antibodies in generating a novel mucosal vaccine against COVID-19. Moreover, along with mucosal vaccines, we should look for combination treatment strategies with plant bioactive molecules. Glycan-binding lectins against viral proteins for targeted activation of mucosal immune response are one of such examples. This might play a promising role to halt this emerging virus. ,Swapan K. Chatterjee ... Maria Nilda M. Munoz [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [25] => Array ( [ArticleId] => 225 [Create_Time] => 2021-12-16 [zipUrl] => https://www.explorationpub.com/uploads/zip/202303/20230302023944.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100326/100326.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100326/100326.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100326/100326_cover.png [JournalsId] => 5 [Title] => A unique vaccine for birth control and treatment of advanced stage cancers secreting ectopically human chorionic gonadotropin [Abstract] => This article is a tribute and homage to Gerard Chaouat who invited me to contribute this article. My years in France have remained very memorable to me. Reviewed briefly is the vaccine that was made [AbstractComplete] =>

This article is a tribute and homage to Gerard Chaouat who invited me to contribute this article. My years in France have remained very memorable to me. Reviewed briefly is the vaccine that was made against human chorionic gonadotropin (hCG) to prevent unwanted pregnancy in sexually active women. It has now been developed as a genetically engineered recombinant vaccine and passed onto industry for its production under good manufacturing practices (GMP) conditions for confirmatory trials. The trials have received the approval of the Drugs Controller General of India. The trials have started but have been interrupted by the coronavirus disease 2019 (COVID-19) pandemic. This vaccine is likely to have another highly beneficial application in the treatment of cancers expressing ectopically hCG.

[Names] => Gursaran P. Talwar ... Krishna M. Ella [Doi] => 10.37349/ei.2021.00026 [Published] => December 31, 2021 [Viewed] => 2054 [Downloaded] => 36 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00026 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:398–405 [Recommend] => 0 [Keywords] => Prevention of pregnancy, recombinant vaccine, Mycobacterium indicus pranii adjuvant, monoclonal antibody, cancers [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100326 [ris] => https://www.explorationpub.com/uploads/Article/A100326/4335e995a68053fd03da532f03cf86f9.ris [bib] => https://www.explorationpub.com/uploads/Article/A100326/6fc4c8526bedde2177b83bc2cbb3a306.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Talwar GP, Gupta JC, Puruswani S, Vyas HK, Nand KN, Pal P, et al. A unique vaccine for birth control and treatment of advanced stage cancers secreting ectopically human chorionic gonadotropin. Explor Immunol. 2021;1:398-405. https://doi.org/10.37349/ei.2021.00026 [Jindex] => 0 [CName] => Gursaran P.Talwar, [CEmail] => gptalwar@gmail.com, [Ris_Time] => 2021-12-31 08:54:06 [Bib_Time] => 2021-12-31 08:54:06 [KeysWordContens] => A unique vaccine for birth control and treatment of advanced stage cancers secreting ectopically human chorionic gonadotropin, Prevention of pregnancy, recombinant vaccine, Mycobacterium indicus pranii adjuvant, monoclonal antibody, cancers, This article is a tribute and homage to Gerard Chaouat who invited me to contribute this article. My years in France have remained very memorable to me. Reviewed briefly is the vaccine that was made against human chorionic gonadotropin (hCG) to prevent unwanted pregnancy in sexually active women. It has now been developed as a genetically engineered recombinant vaccine and passed onto industry for its production under good manufacturing practices (GMP) conditions for confirmatory trials. The trials have received the approval of the Drugs Controller General of India. The trials have started but have been interrupted by the coronavirus disease 2019 (COVID-19) pandemic. This vaccine is likely to have another highly beneficial application in the treatment of cancers expressing ectopically hCG. ,Gursaran P. Talwar ... Krishna M. Ella [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [26] => Array ( [ArticleId] => 227 [Create_Time] => 2021-12-20 [zipUrl] => https://www.explorationpub.com/uploads/zip/202112/20211231064718.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100327/100327.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100327/100327.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100327/100327_cover.png [JournalsId] => 5 [Title] => Progesterone induced blocking factor in health and disease [Abstract] => The foetus expressing paternal antigens ought to be “rejected” by the maternal immune system. However, the immunological relationship of the mother and the foetus does not follow the rules of transplantation immunology. Maternal immune functions are re-adjusted during pregnancy, to create a tolerant environment for the developing foetus. Progesterone and its downstream mediator; the progesterone induced blocking factor (PIBF) are important in this process. The mRNA transcribed from the PIBF1 gene contains 18 exons, and codes for a 90 kDa protein. The 90 kDa form is associated with the centrosome and plays a role in cell cycle regulation, while smaller isoforms produced by alternative spicing are secreted, and bind to the glycosylphosphatidylinositol (GPI) anchored PIBF receptor. Upon ligation, the former forms a heterodimer with the alpha chain of the interleukin-4 (IL-4) receptor and activates the Janus kinase/signal transducers and activators of transcription (Jak/STAT) pathway, via which, PIBF induces increased production of T helper2 (Th2) cytokines. PIBF regulates natural killer (NK) cytotoxicity, by inhibiting perforin release from the cytoplasmic granules of NK cells. During normal human pregnancy, the serum concentrations of PIBF increase with gestational age, and lower than normal serum levels predict spontaneous pregnancy termination. Depletion of PIBF during the peri-implantation period in mice, results in lower implantation and increased resorption rates, together with increased decidual and peripheral NK activity, downregulation of the genes implicated in T cell activation in CD4+ cells, and Th1 differentiation of the T cells. PIBF is expressed in rapidly proliferating immature cells as well as several tumours, and regulates invasion. The PIBF gene has been identified in the chromosomal region 13q21-q22—which is a common site for somatic deletions in a variety of malignant tumours. These data suggest that PIBF might be involved in tumorigenesis [AbstractComplete] =>

The foetus expressing paternal antigens ought to be “rejected” by the maternal immune system. However, the immunological relationship of the mother and the foetus does not follow the rules of transplantation immunology. Maternal immune functions are re-adjusted during pregnancy, to create a tolerant environment for the developing foetus. Progesterone and its downstream mediator; the progesterone induced blocking factor (PIBF) are important in this process. The mRNA transcribed from the PIBF1 gene contains 18 exons, and codes for a 90 kDa protein. The 90 kDa form is associated with the centrosome and plays a role in cell cycle regulation, while smaller isoforms produced by alternative spicing are secreted, and bind to the glycosylphosphatidylinositol (GPI) anchored PIBF receptor. Upon ligation, the former forms a heterodimer with the alpha chain of the interleukin-4 (IL-4) receptor and activates the Janus kinase/signal transducers and activators of transcription (Jak/STAT) pathway, via which, PIBF induces increased production of T helper2 (Th2) cytokines. PIBF regulates natural killer (NK) cytotoxicity, by inhibiting perforin release from the cytoplasmic granules of NK cells. During normal human pregnancy, the serum concentrations of PIBF increase with gestational age, and lower than normal serum levels predict spontaneous pregnancy termination. Depletion of PIBF during the peri-implantation period in mice, results in lower implantation and increased resorption rates, together with increased decidual and peripheral NK activity, downregulation of the genes implicated in T cell activation in CD4+ cells, and Th1 differentiation of the T cells. PIBF is expressed in rapidly proliferating immature cells as well as several tumours, and regulates invasion. The PIBF gene has been identified in the chromosomal region 13q21-q22—which is a common site for somatic deletions in a variety of malignant tumours. These data suggest that PIBF might be involved in tumorigenesis.

[Names] => Julia Szekeres-Bartho [Doi] => 10.37349/ei.2021.00027 [Published] => December 31, 2021 [Viewed] => 1611 [Downloaded] => 60 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00027 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:406–417 [Recommend] => 0 [Keywords] => Progesterone, progesterone induced blocking factor, pregnancy, tumour, cytokines, invasion [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100327 [ris] => https://www.explorationpub.com/uploads/Article/A100327/2203812ce05ac73397d376c634884cdb.ris [bib] => https://www.explorationpub.com/uploads/Article/A100327/336c7a7a2834ae807d789d538c722929.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-25 [CitethisArticle] => Szekeres-Bartho J. Progesterone induced blocking factor in health and disease. Explor Immunol. 2021;1:406-17. https://doi.org/10.37349/ei.2021.00027 [Jindex] => 0 [CName] => JuliaSzekeres-Bartho, [CEmail] => Szekeres.julia@pte.hu, [Ris_Time] => 2021-12-31 10:05:39 [Bib_Time] => 2021-12-31 10:08:26 [KeysWordContens] => Progesterone induced blocking factor in health and disease, Progesterone, progesterone induced blocking factor, pregnancy, tumour, cytokines, invasion, The foetus expressing paternal antigens ought to be “rejected” by the maternal immune system. However, the immunological relationship of the mother and the foetus does not follow the rules of transplantation immunology. Maternal immune functions are re-adjusted during pregnancy, to create a tolerant environment for the developing foetus. Progesterone and its downstream mediator; the progesterone induced blocking factor (PIBF) are important in this process. The mRNA transcribed from the PIBF1 gene contains 18 exons, and codes for a 90 kDa protein. The 90 kDa form is associated with the centrosome and plays a role in cell cycle regulation, while smaller isoforms produced by alternative spicing are secreted, and bind to the glycosylphosphatidylinositol (GPI) anchored PIBF receptor. Upon ligation, the former forms a heterodimer with the alpha chain of the interleukin-4 (IL-4) receptor and activates the Janus kinase/signal transducers and activators of transcription (Jak/STAT) pathway, via which, PIBF induces increased production of T helper2 (Th2) cytokines. PIBF regulates natural killer (NK) cytotoxicity, by inhibiting perforin release from the cytoplasmic granules of NK cells. During normal human pregnancy, the serum concentrations of PIBF increase with gestational age, and lower than normal serum levels predict spontaneous pregnancy termination. Depletion of PIBF during the peri-implantation period in mice, results in lower implantation and increased resorption rates, together with increased decidual and peripheral NK activity, downregulation of the genes implicated in T cell activation in CD4+ cells, and Th1 differentiation of the T cells. PIBF is expressed in rapidly proliferating immature cells as well as several tumours, and regulates invasion. The PIBF gene has been identified in the chromosomal region 13q21-q22—which is a common site for somatic deletions in a variety of malignant tumours. These data suggest that PIBF might be involved in tumorigenesis. ,Julia Szekeres-Bartho [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [27] => Array ( [ArticleId] => 231 [Create_Time] => 2021-12-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202201/20220104012117.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100328/100328.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100328/100328.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100328/100328_cover.png [JournalsId] => 5 [Title] => Crosstalk between keratinocytes and immune cells in inflammatory skin diseases [Abstract] => Cutaneous homeostasis is maintained by dynamic cellular communications between different cell types in the skin through interactions with various mediators, including cytokines, chemokines and antim [AbstractComplete] =>

Cutaneous homeostasis is maintained by dynamic cellular communications between different cell types in the skin through interactions with various mediators, including cytokines, chemokines and antimicrobial peptides/proteins (AMPs). Keratinocytes, as the major cell type of the epidermis, not only form a passive physical barrier, but also actively participate in the pathogenesis of many, if not all, inflammatory skin diseases. Keratinocytes highly interact with immune cells to shape, amplify or regulate inflammatory responses, thus triggering and/or sustaining these inflammatory skin diseases. In this review, crosstalk between keratinocytes and immune cells is summarized, and its contributions to two major inflammatory skin disorders including psoriasis and atopic dermatitis are highlighted.

[Names] => Xinhui Ni, Yuping Lai [Doi] => 10.37349/ei.2021.00028 [Published] => December 31, 2021 [Viewed] => 2451 [Downloaded] => 150 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00028 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 42 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:418–431 [Recommend] => 0 [Keywords] => Crosstalk, keratinocytes, immune cells, inflammatory skin diseases [DetailTitle] => Cross Talk Among Skin Cells and Immune Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/42 [Id] => 100328 [ris] => https://www.explorationpub.com/uploads/Article/A100328/7aaf69ac5dee9de6162f9e3546fc9e6d.ris [bib] => https://www.explorationpub.com/uploads/Article/A100328/daac37c2a5bc45d21f7ecf04dfe4920f.bib [ens] => [Cited] => 8 [Cited_Time] => 2024-04-26 [CitethisArticle] => Ni X, Lai Y. Crosstalk between keratinocytes and immune cells in inflammatory skin diseases. Explor Immunol. 2021;1:418-31. https://doi.org/10.37349/ei.2021.00028 [Jindex] => 0 [CName] => YupingLai, [CEmail] => yplai@bio.ecnu.edu.cn, [Ris_Time] => 2021-12-30 10:37:22 [Bib_Time] => 2021-12-28 05:14:34 [KeysWordContens] => Crosstalk between keratinocytes and immune cells in inflammatory skin diseases, Crosstalk, keratinocytes, immune cells, inflammatory skin diseases, Cutaneous homeostasis is maintained by dynamic cellular communications between different cell types in the skin through interactions with various mediators, including cytokines, chemokines and antimicrobial peptides/proteins (AMPs). Keratinocytes, as the major cell type of the epidermis, not only form a passive physical barrier, but also actively participate in the pathogenesis of many, if not all, inflammatory skin diseases. Keratinocytes highly interact with immune cells to shape, amplify or regulate inflammatory responses, thus triggering and/or sustaining these inflammatory skin diseases. In this review, crosstalk between keratinocytes and immune cells is summarized, and its contributions to two major inflammatory skin disorders including psoriasis and atopic dermatitis are highlighted. ,Xinhui Ni, Yuping Lai [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [28] => Array ( [ArticleId] => 237 [Create_Time] => 2021-12-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202201/20220128075142.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100329/100329.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100329/100329.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100329/100329-cover.png [JournalsId] => 5 [Title] => New variants of SARS-CoV-2, vaccine immune response and the Brazilian reality [Abstract] => Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a highly pathogenic β-coronavirus, is the etiologic agent of coronavirus disease 2019 (COVID-19), which gave rise to a diffi [AbstractComplete] =>

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a highly pathogenic β-coronavirus, is the etiologic agent of coronavirus disease 2019 (COVID-19), which gave rise to a difficult to control pandemic, especially in Brazil. Approximately 4,000 mutations have been identified in SARS-CoV-2, with the majority being redundant without having any biological effect on the virus. The aim of the present study was to objectively understand how new SARS-CoV-2 variants can affect vaccine response, in addition to highlighting the current situation in Brazil in the face of the pandemic and considering epidemiological and immunological aspects of COVID-19. The main protective correlate investigated in most vaccines is the neutralizing antibody titer induced by immunizing agents, observed in the pre-clinical phase in animals, whose action is to block the binding of the spike protein to the angiotensin-converting enzyme 2 (ACE2) receptor, preventing infection. Up to the second half of 2021, the variants that are of greatest concern worldwide and require molecular surveillance are Alpha variant (or B.1.1.7 lineage), Beta (or B.1.351 lineage), Gamma (or P1 lineage) and Delta (or B.1.617.2 lineage). Brazil finds itself in a highly unfavorable scenario, with the circulation of variants of concern, mainly Gamma and Delta, with high fatality rates for COVID-19 and low vaccination rate. Given the still latent situation of the COVID-19 pandemic in Brazil, the lack of global planning for action strategies for non-pharmacological prevention measures, there is an imminent risk of the emergence of new variants due to the finding of susceptible hosts and the high proliferative rate of SARS-CoV-2. It is urgent to increase the genotyping of positive samples isolated from infected individuals, the speed of vaccination of the entire population and the unification of non-pharmacological preventive measures throughout the country.

[Names] => Marileia Chaves Andrade ... Hellen Oliveira Rosa [Doi] => 10.37349/ei.2021.00029 [Published] => December 31, 2021 [Viewed] => 1134 [Downloaded] => 40 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00029 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 47 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:432–439 [Recommend] => 0 [Keywords] => Severe acute respiratory syndrome coronavirus 2, coronavirus disease 2019, variants, vaccine, Brazil [DetailTitle] => Vaccine-induced Immune Responses Against SARS-CoV-2 Infections [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/47 [Id] => 100329 [ris] => https://www.explorationpub.com/uploads/Article/A100329/01aeb939a823716c3298546f9c5688b7.ris [bib] => https://www.explorationpub.com/uploads/Article/A100329/46cd4dc9bc68ca82e3303fb53d8df7a3.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Andrade MC, Gomes LG, Mendes VK, Rosa HO. New variants of SARS-CoV-2, vaccine immune response and the Brazilian reality. Explor Immunol. 2021;1:432-9. https://doi.org/10.37349/ei.2021.00029 [Jindex] => 0 [CName] => Marileia ChavesAndrade, [CEmail] => marileia.andrade@unimontes.br, [Ris_Time] => 2021-12-31 08:36:34 [Bib_Time] => 2021-12-31 08:36:34 [KeysWordContens] => New variants of SARS-CoV-2, vaccine immune response and the Brazilian reality, Severe acute respiratory syndrome coronavirus 2, coronavirus disease 2019, variants, vaccine, Brazil, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a highly pathogenic β-coronavirus, is the etiologic agent of coronavirus disease 2019 (COVID-19), which gave rise to a difficult to control pandemic, especially in Brazil. Approximately 4,000 mutations have been identified in SARS-CoV-2, with the majority being redundant without having any biological effect on the virus. The aim of the present study was to objectively understand how new SARS-CoV-2 variants can affect vaccine response, in addition to highlighting the current situation in Brazil in the face of the pandemic and considering epidemiological and immunological aspects of COVID-19. The main protective correlate investigated in most vaccines is the neutralizing antibody titer induced by immunizing agents, observed in the pre-clinical phase in animals, whose action is to block the binding of the spike protein to the angiotensin-converting enzyme 2 (ACE2) receptor, preventing infection. Up to the second half of 2021, the variants that are of greatest concern worldwide and require molecular surveillance are Alpha variant (or B.1.1.7 lineage), Beta (or B.1.351 lineage), Gamma (or P1 lineage) and Delta (or B.1.617.2 lineage). Brazil finds itself in a highly unfavorable scenario, with the circulation of variants of concern, mainly Gamma and Delta, with high fatality rates for COVID-19 and low vaccination rate. Given the still latent situation of the COVID-19 pandemic in Brazil, the lack of global planning for action strategies for non-pharmacological prevention measures, there is an imminent risk of the emergence of new variants due to the finding of susceptible hosts and the high proliferative rate of SARS-CoV-2. It is urgent to increase the genotyping of positive samples isolated from infected individuals, the speed of vaccination of the entire population and the unification of non-pharmacological preventive measures throughout the country. ,Marileia Chaves Andrade ... Hellen Oliveira Rosa [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [29] => Array ( [ArticleId] => 239 [Create_Time] => 2021-12-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202112/20211231165515.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100330/100330.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100330/100330.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100330/100330_cover.png [JournalsId] => 5 [Title] => State-of-the-art preclinical evaluation of COVID-19 vaccine candidates [Abstract] => The coronavirus disease 2019 (COVID-19) results from the infection of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and primarily affects the respiratory tissue. Since first reported [AbstractComplete] =>

The coronavirus disease 2019 (COVID-19) results from the infection of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and primarily affects the respiratory tissue. Since first reported from Wuhan, China in December 2019, the virus has resulted in an unprecedented pandemic. Vaccination against SARS-CoV-2 can control the further spread of the ongoing pandemic by making people immunised to SARS-CoV-2. Several vaccines have been approved for use in clinics, a lot many are in different stages of development. Diligent interpretations from the preclinical evaluation are crucial to identify the most effective and safest vaccine candidates. Multiple vaccine candidates/variants have been tested in small animal models with relative ease and further in non-human primate models before being taken into clinical development. Here, we review the state-of-the-art strategies employed for a thorough preclinical evaluation of COVID-19 vaccine candidates. We summarise the methods in place to identify indicators which make the vaccine candidate effective in controlling SARS-CoV-2 infection and/or COVID-19 and are safe for administration as inferred by their (1) biophysical/functional attributes (antigen expression, organization, functionality, and stability); (2) immunogenicity in animal models and protective correlates [SARS-CoV-2 specific binding/neutralising immunoglobulin titer, B/T-cell profiling, balanced T-helper type-1 (Th1) or type-2 (Th2) response (Th1:Th2), and anamnestic response]; (3) protective correlates as interpreted by controlled pathology of the respiratory tissue (pulmonary clinical and immunopathology); and finally, (4) strategies to monitor adverse effects of the vaccine candidates.

[Names] => Devlina Ghosh ... Abhishek Saxena [Doi] => 10.37349/ei.2021.00030 [Published] => December 31, 2021 [Viewed] => 1678 [Downloaded] => 77 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00030 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 47 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:440–460 [Recommend] => 0 [Keywords] => Coronavirus disease 2019, severe acute respiratory syndrome coronavirus-2, World Health Organization, vaccines, antibody, virus, immune response, animal models [DetailTitle] => Vaccine-induced Immune Responses Against SARS-CoV-2 Infections [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/47 [Id] => 100330 [ris] => https://www.explorationpub.com/uploads/Article/A100330/1ba0cd96e328f38383eb52e077935ee7.ris [bib] => https://www.explorationpub.com/uploads/Article/A100330/049e441374f5ec1c7b2692bfd86d8414.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Ghosh D, Bai B, Ji Q, Palliyil S, Yang G, Kumar A, et al. State-of-the-art preclinical evaluation of COVID-19 vaccine candidates. Explor Immunol. 2021;1:440-60. https://doi.org/10.37349/ei.2021.00030 [Jindex] => 0 [CName] => AlokKumar,AbhishekSaxena, [CEmail] => aloksgpgi@gmail.com,abhisheksaxena.abdn@gmail.com, [Ris_Time] => 2021-12-30 12:10:53 [Bib_Time] => 2021-12-30 12:10:53 [KeysWordContens] => State-of-the-art preclinical evaluation of COVID-19 vaccine candidates, Coronavirus disease 2019, severe acute respiratory syndrome coronavirus-2, World Health Organization, vaccines, antibody, virus, immune response, animal models, The coronavirus disease 2019 (COVID-19) results from the infection of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and primarily affects the respiratory tissue. Since first reported from Wuhan, China in December 2019, the virus has resulted in an unprecedented pandemic. Vaccination against SARS-CoV-2 can control the further spread of the ongoing pandemic by making people immunised to SARS-CoV-2. Several vaccines have been approved for use in clinics, a lot many are in different stages of development. Diligent interpretations from the preclinical evaluation are crucial to identify the most effective and safest vaccine candidates. Multiple vaccine candidates/variants have been tested in small animal models with relative ease and further in non-human primate models before being taken into clinical development. Here, we review the state-of-the-art strategies employed for a thorough preclinical evaluation of COVID-19 vaccine candidates. We summarise the methods in place to identify indicators which make the vaccine candidate effective in controlling SARS-CoV-2 infection and/or COVID-19 and are safe for administration as inferred by their (1) biophysical/functional attributes (antigen expression, organization, functionality, and stability); (2) immunogenicity in animal models and protective correlates [SARS-CoV-2 specific binding/neutralising immunoglobulin titer, B/T-cell profiling, balanced T-helper type-1 (Th1) or type-2 (Th2) response (Th1:Th2), and anamnestic response]; (3) protective correlates as interpreted by controlled pathology of the respiratory tissue (pulmonary clinical and immunopathology); and finally, (4) strategies to monitor adverse effects of the vaccine candidates. ,Devlina Ghosh ... Abhishek Saxena [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [30] => Array ( [ArticleId] => 240 [Create_Time] => 2021-12-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202204/20220408075817.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100331/100331.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100331/100331.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100331/100331_cover.png [JournalsId] => 5 [Title] => Pregnancy depends on a delicate balance of immune activation and regulation [Abstract] => It is well recognized that immune tolerance is important to prevent semiallografted fetuses from rejection by maternal immunocompetent cells; however, immune activation also plays an important role [AbstractComplete] =>

It is well recognized that immune tolerance is important to prevent semiallografted fetuses from rejection by maternal immunocompetent cells; however, immune activation also plays an important role in placental development and fetal growth. Basic and clinical studies have shown that an imbalance between immune activation and regulation can lead to implantation failure, miscarriage, and preeclampsia. Here, the balance between immunostimulation and immunoregulation in reproduction will be reviewed.

[Names] => Shigeru Saito ... Sayaka Tsuda [Doi] => 10.37349/ei.2021.00031 [Published] => December 31, 2021 [Viewed] => 1464 [Downloaded] => 44 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2021.00031 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2021;1:461–478 [Recommend] => 0 [Keywords] => Cytokine, immune activation, implantation failure, miscarriage, preeclampsia, tolerance [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100331 [ris] => https://www.explorationpub.com/uploads/Article/A100331/77b8e461e5c7bc72a92ca94210e8ca56.ris [bib] => https://www.explorationpub.com/uploads/Article/A100331/af3ed0a944271c607530c94dcd3e5ea2.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Saito S, Nakashima A, Shima T, Tsuda S. Pregnancy depends on a delicate balance of immune activation and regulation. Explor Immunol. 2021;1:461-78. https://doi.org/10.37349/ei.2021.00031 [Jindex] => 0 [CName] => ShigeruSaito, [CEmail] => s30saito@med.u-toyama.ac.jp, [Ris_Time] => 2021-12-31 04:46:45 [Bib_Time] => 2021-12-31 10:14:54 [KeysWordContens] => Pregnancy depends on a delicate balance of immune activation and regulation, Cytokine, immune activation, implantation failure, miscarriage, preeclampsia, tolerance, It is well recognized that immune tolerance is important to prevent semiallografted fetuses from rejection by maternal immunocompetent cells; however, immune activation also plays an important role in placental development and fetal growth. Basic and clinical studies have shown that an imbalance between immune activation and regulation can lead to implantation failure, miscarriage, and preeclampsia. Here, the balance between immunostimulation and immunoregulation in reproduction will be reviewed. ,Shigeru Saito ... Sayaka Tsuda [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [31] => Array ( [ArticleId] => 247 [Create_Time] => 2022-02-11 [zipUrl] => https://www.explorationpub.com/uploads/zip/202202/20220225081733.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100332/100332.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100332/100332.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100332/100332_cover.png [JournalsId] => 5 [Title] => Fertility and COVID-19 vaccination [Abstract] => One of the most troubling developments of 2021 has been the number of fertile-age women who have been led to believe that mRNA vaccines against severe acute respiratory syndrome coronavirus-2 [SARS-CoV-2, coronavirus disease 2019 (COVID-19)] can cause infertility via cross-reactivity of immune response. Specifically, cross-reactivity of developed antibodies to syncytin-1, a protein found in human cell fusion, placentation and recently identified in the envelope gene of a human endogenous defective retrovirus, HERV-W (see “Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis”. Nature.2000;403:785–9. doi: 10.1038/35001608). The mechanism, evidence, and evaluation of the claim is presented concluding in a rejection due to lack of evidence. [AbstractComplete] =>

One of the most troubling developments of 2021 has been the number of fertile-age women who have been led to believe that mRNA vaccines against severe acute respiratory syndrome coronavirus-2 [SARS-CoV-2, coronavirus disease 2019 (COVID-19)] can cause infertility via cross-reactivity of immune response. Specifically, cross-reactivity of developed antibodies to syncytin-1, a protein found in human cell fusion, placentation and recently identified in the envelope gene of a human endogenous defective retrovirus, HERV-W (see “Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis”. Nature. 2000;403:785–9. doi: 10.1038/35001608). The mechanism, evidence, and evaluation of the claim is presented concluding in a rejection due to lack of evidence.

[Names] => Iosif M. Gershteyn [Doi] => 10.37349/ei.2022.00032 [Published] => February 11, 2022 [Viewed] => 1390 [Downloaded] => 30 [Subject] => Perspective [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00032 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:1–8 [Recommend] => 0 [Keywords] => Fertility, messenger RNA, vaccine, coronavirus disease 2019, syncytin-1 [DetailTitle] => [DetailUrl] => [Id] => 100332 [ris] => https://www.explorationpub.com/uploads/Article/A100332/ed5b166eef4454d1b7b3717a1158c096.ris [bib] => https://www.explorationpub.com/uploads/Article/A100332/ee8a740fc7efaeddfab6a7cf3a30dadb.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Gershteyn IM. Fertility and COVID-19 vaccination. Explor Immunol. 2022;2:1-8. https://doi.org/10.37349/ei.2022.00032 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-01-24 05:04:37 [Bib_Time] => 2022-01-24 05:04:37 [KeysWordContens] => Fertility and COVID-19 vaccination, Fertility, messenger RNA, vaccine, coronavirus disease 2019, syncytin-1, One of the most troubling developments of 2021 has been the number of fertile-age women who have been led to believe that mRNA vaccines against severe acute respiratory syndrome coronavirus-2 [SARS-CoV-2, coronavirus disease 2019 (COVID-19)] can cause infertility via cross-reactivity of immune response. Specifically, cross-reactivity of developed antibodies to syncytin-1, a protein found in human cell fusion, placentation and recently identified in the envelope gene of a human endogenous defective retrovirus, HERV-W (see “Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis”. Nature. 2000;403:785–9. doi: 10.1038/35001608). The mechanism, evidence, and evaluation of the claim is presented concluding in a rejection due to lack of evidence. ,Iosif M. Gershteyn [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [32] => Array ( [ArticleId] => 249 [Create_Time] => 2022-02-11 [zipUrl] => https://www.explorationpub.com/uploads/zip/202305/20230520021006.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100333/100333.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100333/100333.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100333/100333_cover.png [JournalsId] => 5 [Title] => Immune titers of protection against severe acute respiratory syndrome coronavirus 2: are we there yet? [Abstract] => A few pieces of research exist about the protective titer against severe acute respiratory syndrome (SARS) coronavirus 2 (CoV-2; SARS-CoV-2) in monkeys and humans in which the protection could be sh [AbstractComplete] =>

A few pieces of research exist about the protective titer against severe acute respiratory syndrome (SARS) coronavirus 2 (CoV-2; SARS-CoV-2) in monkeys and humans in which the protection could be shown as dose-dependent. Early studies supposed that higher levels of pre-existing neutralizing antibodies (Nabs) against SARS-CoV-2 can potentially correlate with the protection to consequent infection. The data so far showed that cellular immunity is as essential as the humoral one. If needed, its presence can be beneficial if the titer of immunoglobulins is not optimal. It is also known that the immune response to the vaccine is similar to the one after natural infection with a production of very high naturalization titers antibodies. However, medical community is still unaware of the immunoglobulin titer needed for protection against the virus. The answers to the questions regarding correlates of protection are yet to be discovered. Still, no studies indicate a specific virus-Nab titer, so one can assume a patient is protected from being infected in the future. The evoked immunological response is indeed encouraging, but a future investigation is needed. Nonetheless, it remains a mystery how long the immunity lasts and whether it will be enough to shield the patients in the long run. Therefore, identifying immune protection correlations, including neutralization titer of antibodies and T cell immune response against SARS-CoV-2, could give a clue. Unfortunately, recent studies in the field have been more controversial than concise, and the data available is far from consensus.

[Names] => Yoanna Slabakova ... Tsvetelina Velikova [Doi] => 10.37349/ei.2022.00033 [Published] => February 11, 2022 [Viewed] => 1428 [Downloaded] => 26 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00033 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 47 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:9–24 [Recommend] => 0 [Keywords] => Severe acute respiratory syndrome coronavirus 2, coronavirus disease 2019, antibodies, correlates of protection, immunoglobulin titers, B cells, T cells [DetailTitle] => Vaccine-induced Immune Responses Against SARS-CoV-2 Infections [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/47 [Id] => 100333 [ris] => https://www.explorationpub.com/uploads/Article/A100333/2d54cd0ce234a57b08f2055feaa2a73d.ris [bib] => https://www.explorationpub.com/uploads/Article/A100333/78b15ac88eaef9f129c295f014fccb90.bib [ens] => [Cited] => 5 [Cited_Time] => 2024-04-25 [CitethisArticle] => Slabakova Y, Gerenska D, Ivanov N, Velikova T. Immune titers of protection against severe acute respiratory syndrome coronavirus 2: are we there yet? Explor Immunol. 2022;2:9–24. https://doi.org/10.37349/ei.2022.00033 [Jindex] => 0 [CName] => TsvetelinaVelikova, [CEmail] => tsvelikova@medfac.mu-sofia.bg, [Ris_Time] => 2022-02-10 01:37:27 [Bib_Time] => 2022-02-10 01:37:27 [KeysWordContens] => Immune titers of protection against severe acute respiratory syndrome coronavirus 2: are we there yet?, Severe acute respiratory syndrome coronavirus 2, coronavirus disease 2019, antibodies, correlates of protection, immunoglobulin titers, B cells, T cells, A few pieces of research exist about the protective titer against severe acute respiratory syndrome (SARS) coronavirus 2 (CoV-2; SARS-CoV-2) in monkeys and humans in which the protection could be shown as dose-dependent. Early studies supposed that higher levels of pre-existing neutralizing antibodies (Nabs) against SARS-CoV-2 can potentially correlate with the protection to consequent infection. The data so far showed that cellular immunity is as essential as the humoral one. If needed, its presence can be beneficial if the titer of immunoglobulins is not optimal. It is also known that the immune response to the vaccine is similar to the one after natural infection with a production of very high naturalization titers antibodies. However, medical community is still unaware of the immunoglobulin titer needed for protection against the virus. The answers to the questions regarding correlates of protection are yet to be discovered. Still, no studies indicate a specific virus-Nab titer, so one can assume a patient is protected from being infected in the future. The evoked immunological response is indeed encouraging, but a future investigation is needed. Nonetheless, it remains a mystery how long the immunity lasts and whether it will be enough to shield the patients in the long run. Therefore, identifying immune protection correlations, including neutralization titer of antibodies and T cell immune response against SARS-CoV-2, could give a clue. Unfortunately, recent studies in the field have been more controversial than concise, and the data available is far from consensus. ,Yoanna Slabakova ... Tsvetelina Velikova [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [33] => Array ( [ArticleId] => 251 [Create_Time] => 2022-02-17 [zipUrl] => https://www.explorationpub.com/uploads/zip/202202/20220217014941.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100334/100334.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100334/100334.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100334/100334_cover.png [JournalsId] => 5 [Title] => Endometriosis and autoimmunity [Abstract] => Endometriosis is an inflammatory oestrogen-dependent chronic disease and is mainly expressed by pain and increased infertility. Several studies showed an increased prevalence of autoimmune systemic [AbstractComplete] =>

Endometriosis is an inflammatory oestrogen-dependent chronic disease and is mainly expressed by pain and increased infertility. Several studies showed an increased prevalence of autoimmune systemic diseases and various autoantibodies in endometriosis. The association of these autoimmune markers and diseases could raise the fact that endometriosis is an authentic autoimmune or inflammatory disease and thus could argue for the use of immunomodulatory therapies. Usually, it is considered that the autoantibodies did not directly act in endometrium implants growth, and could be rather implicated in endometriosis-related infertility. The use of immunomodulatory strategies could be an important alternative or additional strategy to the use of hormones and surgery but need prospective well-designed trials.

[Names] => Noémie Abisror ... Arsene Mekinian [Doi] => 10.37349/ei.2022.00034 [Published] => February 16, 2022 [Viewed] => 1207 [Downloaded] => 27 [Subject] => Perspective [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00034 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:25–31 [Recommend] => 0 [Keywords] => Endometriosis, autoimmune diseases, immunomodulation [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100334 [ris] => https://www.explorationpub.com/uploads/Article/A100334/8e7bc28f8089cbcc6f40ed6e3faecaf7.ris [bib] => https://www.explorationpub.com/uploads/Article/A100334/1325bdaf35ca5dd217b01c83c5bececa.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Abisror N, Kolanska K, Cheloufi M, Selleret L, d’Argent E, Kayem G, et al. Endometriosis and autoimmunity. Explor Immunol. 2022;2:25–31. https://doi.org/10.37349/ei.2022.00034 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-02-24 06:23:26 [Bib_Time] => 2022-02-24 06:23:26 [KeysWordContens] => Endometriosis and autoimmunity, Endometriosis, autoimmune diseases, immunomodulation, Endometriosis is an inflammatory oestrogen-dependent chronic disease and is mainly expressed by pain and increased infertility. Several studies showed an increased prevalence of autoimmune systemic diseases and various autoantibodies in endometriosis. The association of these autoimmune markers and diseases could raise the fact that endometriosis is an authentic autoimmune or inflammatory disease and thus could argue for the use of immunomodulatory therapies. Usually, it is considered that the autoantibodies did not directly act in endometrium implants growth, and could be rather implicated in endometriosis-related infertility. The use of immunomodulatory strategies could be an important alternative or additional strategy to the use of hormones and surgery but need prospective well-designed trials. ,Noémie Abisror ... Arsene Mekinian [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [34] => Array ( [ArticleId] => 255 [Create_Time] => 2022-02-17 [zipUrl] => https://www.explorationpub.com/uploads/zip/202303/20230301073028.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100335/100335.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100335/100335.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100335/100335_cover.png [JournalsId] => 5 [Title] => γδT cells: alternative treasure in antitumor immunity [Abstract] => In recent decades, abundant methods for targeted tumor cell immunotherapy have been developed. It was recently discovered that excellent curative effects observed in hematological tumors cannot be achieved in solid tumors, as serious side effects will occur. [AbstractComplete] =>

In recent decades, abundant methods for targeted tumor cell immunotherapy have been developed. It was recently discovered that excellent curative effects observed in hematological tumors cannot be achieved in solid tumors, as serious side effects will occur. These are all derived from engineered adaptive immune cells, the use of which will bring limitations. γδT cells have a unique ability to respond to a variety of tumor cells while linking innate immunity and adaptive immunity, and thus, they are an ideal source of therapeutic allogeneic cells. This review introduces strategies that can optimize the clinical application of γδT cells to provide novel ideas for adoptive immunotherapy in the future.

[Names] => Xiangjin Zhang ... Wei He [Doi] => 10.37349/ei.2022.00035 [Published] => February 17, 2022 [Viewed] => 1222 [Downloaded] => 38 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00035 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 50 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:32–47 [Recommend] => 0 [Keywords] => Adoptive immunotherapy, γδT cells, antitumor capacity [DetailTitle] => Interplay of γδ T cells and Tumor Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/50 [Id] => 100335 [ris] => https://www.explorationpub.com/uploads/Article/A100335/c9ab6e15e303bf58ee7fb175662e91de.ris [bib] => https://www.explorationpub.com/uploads/Article/A100335/aeeb02bc80ed68c3e6f1708eb6c1231d.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Zhang X, Xu Y, Chen H, Zhang J, He W. γδT cells: alternative treasure in antitumor immunity. Explor Immunol. 2022;2:32–47. https://doi.org/10.37349/ei.2022.00035 [Jindex] => 0 [CName] => HuiChen,JianminZhang,WeiHe, [CEmail] => chenhui_1980@126.com,jzhang42@163.com,heweingd@126.com, [Ris_Time] => 2022-02-17 02:40:43 [Bib_Time] => 2022-02-17 02:40:43 [KeysWordContens] => γδT cells: alternative treasure in antitumor immunity, Adoptive immunotherapy, γδT cells, antitumor capacity, In recent decades, abundant methods for targeted tumor cell immunotherapy have been developed. It was recently discovered that excellent curative effects observed in hematological tumors cannot be achieved in solid tumors, as serious side effects will occur. These are all derived from engineered adaptive immune cells, the use of which will bring limitations. γδT cells have a unique ability to respond to a variety of tumor cells while linking innate immunity and adaptive immunity, and thus, they are an ideal source of therapeutic allogeneic cells. This review introduces strategies that can optimize the clinical application of γδT cells to provide novel ideas for adoptive immunotherapy in the future. ,Xiangjin Zhang ... Wei He [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [35] => Array ( [ArticleId] => 259 [Create_Time] => 2022-02-18 [zipUrl] => https://www.explorationpub.com/uploads/zip/202202/20220218053950.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100336/100336.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100336/100336.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100336/100336_cover.png [JournalsId] => 5 [Title] => The microbiota is a potential mediator of the crosstalk between γδ T cells and tumors [Abstract] => γδ T cells are one of the immune cell types that express antigen receptors. γδ T cells are able to recognize pathogens or cancer cells independently o [AbstractComplete] =>

γδ T cells are one of the immune cell types that express antigen receptors. γδ T cells are able to recognize pathogens or cancer cells independently of human leukocyte antigen restriction, which is an important feature of αβ T cells. Therefore, γδ T cells are considered the bridge between innate and adaptive immunity. These cells exhibit important roles in immune surveillance, exert immune defense against tumors and have become promising effector cells for cancer immunotherapy. However, in particular circumstances, the tumor microenvironment seems to render γδ T cells immunosuppressive and even tumor-promoting, emphasizing the importance of regulating γδ T functions in realizing their translation into practical cancer immunotherapy. In recent years, increasing evidence has demonstrated that the intratumoral and peritumoral microbiota can have complex effects on tumor immunology. Thus, understanding the role of microbiota in the crosstalk between γδ T cells and tumors will provide insights for developing adjuvant immunotherapy with precise regulation of tumor-related microbiota. In the present review, the effects of microbiota on γδ T cell receptor repertoire and the roles of microbiota in some common tumors will be discussed, with implications for future cancer therapy.

[Names] => Huidi Wang ... Jia Yin [Doi] => 10.37349/ei.2022.00036 [Published] => February 18, 2022 [Viewed] => 1272 [Downloaded] => 30 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00036 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 50 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:48–63 [Recommend] => 0 [Keywords] => γδcells, tumor, microbiota, tumor micromilieu [DetailTitle] => Interplay of γδ T cells and Tumor Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/50 [Id] => 100336 [ris] => https://www.explorationpub.com/uploads/Article/A100336/2eaf86a0a61707339011d0a2bc9e5251.ris [bib] => https://www.explorationpub.com/uploads/Article/A100336/6371fa69b54cb021b2a96878d9467c71.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-25 [CitethisArticle] => Wang H, Li J, He Y, Yin J. The microbiota is a potential mediator of the crosstalk between γδ T cells and tumors. Explor Immunol. 2022;2:48–63. https://doi.org/10.37349/ei.2022.00036 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-02-24 06:23:55 [Bib_Time] => 2022-02-24 06:23:55 [KeysWordContens] => The microbiota is a potential mediator of the crosstalk between γδ T cells and tumors, γδcells, tumor, microbiota, tumor micromilieu, γδ T cells are one of the immune cell types that express antigen receptors. γδ T cells are able to recognize pathogens or cancer cells independently of human leukocyte antigen restriction, which is an important feature of αβ T cells. Therefore, γδ T cells are considered the bridge between innate and adaptive immunity. These cells exhibit important roles in immune surveillance, exert immune defense against tumors and have become promising effector cells for cancer immunotherapy. However, in particular circumstances, the tumor microenvironment seems to render γδ T cells immunosuppressive and even tumor-promoting, emphasizing the importance of regulating γδ T functions in realizing their translation into practical cancer immunotherapy. In recent years, increasing evidence has demonstrated that the intratumoral and peritumoral microbiota can have complex effects on tumor immunology. Thus, understanding the role of microbiota in the crosstalk between γδ T cells and tumors will provide insights for developing adjuvant immunotherapy with precise regulation of tumor-related microbiota. In the present review, the effects of microbiota on γδ T cell receptor repertoire and the roles of microbiota in some common tumors will be discussed, with implications for future cancer therapy. ,Huidi Wang ... Jia Yin [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [36] => Array ( [ArticleId] => 260 [Create_Time] => 2022-02-23 [zipUrl] => https://www.explorationpub.com/uploads/zip/202303/20230301083414.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100337/100337.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100337/100337.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100337/100337_cover.png [JournalsId] => 5 [Title] => Tumor-associated protein ligands recognized by human γδ T cell receptor and their implications in cancer therapy [Abstract] => In recent years, immunologists have been working to utilize the functional mechanism of the immune system to research new tumor treatment methods and achieved a major breakthrough in 2013, which was [AbstractComplete] =>

In recent years, immunologists have been working to utilize the functional mechanism of the immune system to research new tumor treatment methods and achieved a major breakthrough in 2013, which was listed as one of the top 10 scientific breakthroughs of 2013 by Science magazine (see “Cancer immunotherapy”. Science. 2013;342:1417. doi: 10.1126/science.1249481). Currently, two main methods are used in clinical tumor immunotherapy: immune checkpoint inhibitors and chimeric antigen receptor (CAR) T cells. Clinical responses to checkpoint inhibitors rely on blockade of the target neoantigens expressed on the surfaces of tumor cells, which can inhibit T cell activity and prevent the T cell immune response; therefore, the therapeutic effect is limited by the tumor antigen expression level. While CAR-T cell therapy can partly enhance neoantigen recognition of T cells, problems remain in the current treatment for solid tumors, such as restricted transport of adoptively transferred cells to the tumor site and off-targets. Immunologists have therefore turned their attention to γδ T cells, which are not restricted by the major histocompatibility complex (MHC) for neoantigen recognition and are able to initiate a rapid immune response at an early stage. However, due to the lack of an understanding of the antigens that γδ T cells recognize, the role of γδ T cells in tumorigenesis and tumor development is not clearly understood. In the past few years, extensive data identifying antigen ligands recognized by γδ T cells have been obtained, mainly focusing on bisphosphonates and small-molecule polypeptides, but few studies have focused on protein ligands recognized by γδ T cells. In this paper, we reviewed and analyzed the tumor-associated protein ligands of γδ T cells that have been discovered thus far, hoping to provide new ideas for the comprehensive application of γδ T cells in tumor immunotherapy.

[Names] => Chang Liu ... Wei He [Doi] => 10.37349/ei.2022.00037 [Published] => February 22, 2022 [Viewed] => 1316 [Downloaded] => 44 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00037 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 50 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:64–78 [Recommend] => 0 [Keywords] => γδ T cells, tumor-associated protein ligands, immunotherapy [DetailTitle] => Interplay of γδ T cells and Tumor Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/50 [Id] => 100337 [ris] => https://www.explorationpub.com/uploads/Article/A100337/15747ce8509e0937aa0f412d2783f740.ris [bib] => https://www.explorationpub.com/uploads/Article/A100337/55d51a4c5634d398ba738fb16b8db91c.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Liu C, Xu Y, Chen H, Zhang J, He W. Tumor-associated protein ligands recognized by human γδ T cell receptor and their implications in cancer therapy. Explor Immunol. 2022;2:64–78. https://doi.org/10.37349/ei.2022.00037 [Jindex] => 0 [CName] => HuiChen,JianminZhang,WeiHe, [CEmail] => chenhui_1980@126.com,jzhang42@163.com,heweingd@126.com, [Ris_Time] => 2022-02-24 06:24:21 [Bib_Time] => 2022-02-24 06:24:21 [KeysWordContens] => Tumor-associated protein ligands recognized by human γδ T cell receptor and their implications in cancer therapy, γδ T cells, tumor-associated protein ligands, immunotherapy, In recent years, immunologists have been working to utilize the functional mechanism of the immune system to research new tumor treatment methods and achieved a major breakthrough in 2013, which was listed as one of the top 10 scientific breakthroughs of 2013 by Science magazine (see “Cancer immunotherapy”. Science. 2013;342:1417. doi: 10.1126/science.1249481). Currently, two main methods are used in clinical tumor immunotherapy: immune checkpoint inhibitors and chimeric antigen receptor (CAR) T cells. Clinical responses to checkpoint inhibitors rely on blockade of the target neoantigens expressed on the surfaces of tumor cells, which can inhibit T cell activity and prevent the T cell immune response; therefore, the therapeutic effect is limited by the tumor antigen expression level. While CAR-T cell therapy can partly enhance neoantigen recognition of T cells, problems remain in the current treatment for solid tumors, such as restricted transport of adoptively transferred cells to the tumor site and off-targets. Immunologists have therefore turned their attention to γδ T cells, which are not restricted by the major histocompatibility complex (MHC) for neoantigen recognition and are able to initiate a rapid immune response at an early stage. However, due to the lack of an understanding of the antigens that γδ T cells recognize, the role of γδ T cells in tumorigenesis and tumor development is not clearly understood. In the past few years, extensive data identifying antigen ligands recognized by γδ T cells have been obtained, mainly focusing on bisphosphonates and small-molecule polypeptides, but few studies have focused on protein ligands recognized by γδ T cells. In this paper, we reviewed and analyzed the tumor-associated protein ligands of γδ T cells that have been discovered thus far, hoping to provide new ideas for the comprehensive application of γδ T cells in tumor immunotherapy. ,Chang Liu ... Wei He [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [37] => Array ( [ArticleId] => 263 [Create_Time] => 2022-02-24 [zipUrl] => https://www.explorationpub.com/uploads/zip/202403/20240315080318.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100338/100338.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100338/100338.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100338/100338_cover.png [JournalsId] => 5 [Title] => γδ T cell costimulatory ligands in antitumor immunity [Abstract] => Antitumor immunity relies on the ability of T cells to recognize and kill tumor targets. γδ T cells are a specialized subset of T cells that predominantly localizes to non-ly [AbstractComplete] =>

Antitumor immunity relies on the ability of T cells to recognize and kill tumor targets. γδ T cells are a specialized subset of T cells that predominantly localizes to non-lymphoid tissue such as the skin, gut, and lung where they are actively involved in tumor immunosurveillance. γδ T cells respond to self-stress ligands that are increased on many tumor cells, and these interactions provide costimulatory signals that promote their activation and cytotoxicity. This review will cover costimulatory molecules that are known to be critical for the function of γδ T cells with a specific focus on mouse dendritic epidermal T cells (DETC). DETC are a prototypic tissue-resident γδ T cell population with known roles in antitumor immunity and are therefore useful for identifying mechanisms that may control activation of other γδ T cell subsets within non-lymphoid tissues. This review concludes with a brief discussion on how γδ T cell costimulatory molecules can be targeted for improved cancer immunotherapy.

[Names] => Joseph M. McGraw, Deborah A. Witherden [Doi] => 10.37349/ei.2022.00038 [Published] => February 24, 2022 [Viewed] => 2237 [Downloaded] => 74 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00038 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 50 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:79–97 [Recommend] => 1 [Keywords] => γδ T cell, costimulation, natural killer group 2D, junctional adhesion molecule-like protein, CD100, lymphocyte function-associated antigen 1, CD316 [DetailTitle] => Interplay of γδ T cells and Tumor Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/50 [Id] => 100338 [ris] => https://www.explorationpub.com/uploads/Article/A100338/430a5b414b2ffbeed3c443fd95df57be.ris [bib] => https://www.explorationpub.com/uploads/Article/A100338/7c9081a028d2d4869b9892d0b7485d64.bib [ens] => [Cited] => 2 [Cited_Time] => 2024-04-26 [CitethisArticle] => McGraw JM, Witherden DA. γδ T cell costimulatory ligands in antitumor immunity. Explor Immunol. 2022;2:79–97. https://doi.org/10.37349/ei.2022.00038 [Jindex] => 0 [CName] => Deborah A.Witherden, [CEmail] => deborahw@scripps.edu, [Ris_Time] => 2022-02-28 02:08:33 [Bib_Time] => 2022-02-28 02:08:33 [KeysWordContens] => γδ T cell costimulatory ligands in antitumor immunity, γδ T cell, costimulation, natural killer group 2D, junctional adhesion molecule-like protein, CD100, lymphocyte function-associated antigen 1, CD316, Antitumor immunity relies on the ability of T cells to recognize and kill tumor targets. γδ T cells are a specialized subset of T cells that predominantly localizes to non-lymphoid tissue such as the skin, gut, and lung where they are actively involved in tumor immunosurveillance. γδ T cells respond to self-stress ligands that are increased on many tumor cells, and these interactions provide costimulatory signals that promote their activation and cytotoxicity. This review will cover costimulatory molecules that are known to be critical for the function of γδ T cells with a specific focus on mouse dendritic epidermal T cells (DETC). DETC are a prototypic tissue-resident γδ T cell population with known roles in antitumor immunity and are therefore useful for identifying mechanisms that may control activation of other γδ T cell subsets within non-lymphoid tissues. This review concludes with a brief discussion on how γδ T cell costimulatory molecules can be targeted for improved cancer immunotherapy. ,Joseph M. McGraw, Deborah A. Witherden [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [38] => Array ( [ArticleId] => 264 [Create_Time] => 2022-02-25 [zipUrl] => https://www.explorationpub.com/uploads/zip/202303/20230301073911.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100339/100339.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100339/100339.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100339/100339_cover.png [JournalsId] => 5 [Title] => Novel insights based on the plasticity of γδ T cells in the tumor microenvironment [Abstract] => γδ T cells express unique T cell receptor (TCR) γ and TCR δ chains, with structural and functional heterogeneity. Taking advantage of the diverse γδ TCR repertoire or other ligand-receptor interactions, γδ T cells can recognize a broad spectrum of tumor-associated antigens (TAAs) in a major histocompatibility complex (MHC)-independent manner, [AbstractComplete] =>

γδ T cells express unique T cell receptor (TCR) γ and TCR δ chains, with structural and functional heterogeneity. Taking advantage of the diverse γδ TCR repertoire or other ligand-receptor interactions, γδ T cells can recognize a broad spectrum of tumor-associated antigens (TAAs) in a major histocompatibility complex (MHC)—independent manner, thereby activating downstream pleiotropic effects. γδ T cells recruited into the tumor microenvironment can act as effector cells to mediate cancer immune surveillance. Their advantage lies in the ability to perceive tumors with a low mutation load, thus establishing the first line of defense against pathogens. Activated γδ T cells exhibit strong cytotoxic activity and cytokine secretion functions and are effective antitumor lymphocytes with simple and direct recognition modes and rapid responses. However, the clinical application of tumor—infiltrating γδ T cells has certain limitations. First, γδ T cells exposed to complicated cytokine networks are potentially affected by multiple inhibitory mechanisms. Additionally, these cells show highly flexible and dynamic plasticity and are extremely easily polarized into regulatory phenotypes. This review further emphasizes the diversified cross-talk between γδ T cells and other immune cells. Effective immunity of the body is often manifested by counterbalance under mutual restriction. Therefore, an in-depth understanding of γδ T cells that play conflicting roles in the tumor microenvironment is necessary. These cells may be a key factor ultimately mediating the deviation of the antagonistic response between tumor inhibition and tumor promotion. Finally, it retrospectively analyze the activation strategies and clinical relevance of existing γδ T cell adoptive immunotherapies. According to current challenges, there is a need to explore innovative immunotherapies, maximize the tumor-killing efficacy of γδ T cells, and attenuate or eliminate tumor immunosuppression. It is hoped that the host immune status can be accurately predicted and gradually advance γδ T cell precise individualized medicine.

[Names] => Yue Wang ... Wei He [Doi] => 10.37349/ei.2022.00039 [Published] => February 24, 2022 [Viewed] => 2411 [Downloaded] => 87 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00039 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 50 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:98–132 [Recommend] => 1 [Keywords] => γδ T cells, tumor microenvironment, plasticity, cytokines, immunosuppression, cross-talk, precision immunotherapy [DetailTitle] => Interplay of γδ T cells and Tumor Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/50 [Id] => 100339 [ris] => https://www.explorationpub.com/uploads/Article/A100339/7a3b9e0d7e7df600f09df1f1a249c491.ris [bib] => https://www.explorationpub.com/uploads/Article/A100339/77b5fadda3c7cbcccf78774649287dd1.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-26 [CitethisArticle] => Wang Y, Xu Y, Chen H, Zhang J, He W. Novel insights based on the plasticity of γδ T cells in the tumor microenvironment. Explor Immunol. 2022;2:98–132. https://doi.org/10.37349/ei.2022.00039 [Jindex] => 0 [CName] => HuiChen,JianminZhang,WeiHe, [CEmail] => chenhui_1980@126.com,jzhang42@163.com,heweingd@126.com, [Ris_Time] => 2022-02-24 07:00:40 [Bib_Time] => 2022-02-24 07:00:40 [KeysWordContens] => Novel insights based on the plasticity of γδ T cells in the tumor microenvironment, γδ T cells, tumor microenvironment, plasticity, cytokines, immunosuppression, cross-talk, precision immunotherapy, γδ T cells express unique T cell receptor (TCR) γ and TCR δ chains, with structural and functional heterogeneity. Taking advantage of the diverse γδ TCR repertoire or other ligand-receptor interactions, γδ T cells can recognize a broad spectrum of tumor-associated antigens (TAAs) in a major histocompatibility complex (MHC)—independent manner, thereby activating downstream pleiotropic effects. γδ T cells recruited into the tumor microenvironment can act as effector cells to mediate cancer immune surveillance. Their advantage lies in the ability to perceive tumors with a low mutation load, thus establishing the first line of defense against pathogens. Activated γδ T cells exhibit strong cytotoxic activity and cytokine secretion functions and are effective antitumor lymphocytes with simple and direct recognition modes and rapid responses. However, the clinical application of tumor—infiltrating γδ T cells has certain limitations. First, γδ T cells exposed to complicated cytokine networks are potentially affected by multiple inhibitory mechanisms. Additionally, these cells show highly flexible and dynamic plasticity and are extremely easily polarized into regulatory phenotypes. This review further emphasizes the diversified cross-talk between γδ T cells and other immune cells. Effective immunity of the body is often manifested by counterbalance under mutual restriction. Therefore, an in-depth understanding of γδ T cells that play conflicting roles in the tumor microenvironment is necessary. These cells may be a key factor ultimately mediating the deviation of the antagonistic response between tumor inhibition and tumor promotion. Finally, it retrospectively analyze the activation strategies and clinical relevance of existing γδ T cell adoptive immunotherapies. According to current challenges, there is a need to explore innovative immunotherapies, maximize the tumor-killing efficacy of γδ T cells, and attenuate or eliminate tumor immunosuppression. It is hoped that the host immune status can be accurately predicted and gradually advance γδ T cell precise individualized medicine. ,Yue Wang ... Wei He [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [39] => Array ( [ArticleId] => 277 [Create_Time] => 2022-03-16 [zipUrl] => https://www.explorationpub.com/uploads/zip/202203/20220316091347.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100340/100340.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100340/100340.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100340/100340_cover.png [JournalsId] => 5 [Title] => High avidity of vaccine-induced immunoglobulin G against SARS-CoV-2: potential relevance for protective humoral immunity [Abstract] => Avidity of immunoglobulin G (IgG) is defined as its binding strength to its target antigen. As a consequence of affinity maturation of the IgG response, avidity is maturing as well. Therefore, acute [AbstractComplete] =>

Avidity of immunoglobulin G (IgG) is defined as its binding strength to its target antigen. As a consequence of affinity maturation of the IgG response, avidity is maturing as well. Therefore, acute infections are characterized by low-avidity IgG, whereas past infections are usually associated with high-avidity IgG. Avidity maturation is also observed as a consequence of optimal vaccination. Avidity has been shown to play a significant role in protective humoral immunity in many microbial systems. After severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, the situation is different compared to other viral infections, as the moderate degree of avidity reached in most cases of infection is similar to that reached after only one vaccination step. In contrast, two vaccination steps lead to a much higher avidity of IgG directed towards viral spike protein S1 (S1) in the majority of vaccinated individuals. Therefore, it seems that two vaccination steps allow for a more extended affinity/avidity maturation than natural infection. The degree of avidity maturation after two vaccination steps is heterogeneous. It can be further enhanced by a third vaccination step. Complete avidity maturation seems to depend on sustained availability of antigen during the maturation process. Variants of concern seem to increase the affinity of their receptor-binding domain (RBD) to angiotensin-converting enzyme-2 (ACE2) and/or to decrease the susceptibility for neutralizing antibodies. Classical neutralization tests do not necessarily reflect the avidity of neutralizing IgG, as they operationally dissect the binding reaction between S1 and IgG from the binding of the S1 to ACE2. This approach fades out critical competition reactions between IgG and ACE for RBD of the S1. Quantitative avidity determination might be an essential tool to define individuals that only possess suboptimal protective immunity after vaccination and therefore might benefit from an additional booster immunization.

[Names] => Georg Bauer [Doi] => 10.37349/ei.2022.00040 [Published] => March 16, 2022 [Viewed] => 2346 [Downloaded] => 66 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00040 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 47 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:133–156 [Recommend] => 0 [Keywords] => Humoral immune response, avidity, severe acute respiratory syndrome coronavirus 2, protective immunity [DetailTitle] => Vaccine-induced Immune Responses Against SARS-CoV-2 Infections [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/47 [Id] => 100340 [ris] => https://www.explorationpub.com/uploads/Article/A100340/02a1f10deaacac6352d0df63794c5e01.ris [bib] => https://www.explorationpub.com/uploads/Article/A100340/ef5c5ccde7d23e8b6b4041d05c39c514.bib [ens] => [Cited] => 7 [Cited_Time] => 2024-04-25 [CitethisArticle] => Bauer G. High avidity of vaccine-induced immunoglobulin G against SARS-CoV-2: potential relevance for protective humoral immunity. Explor Immunol. 2022;2:133–56. https://doi.org/10.37349/ei.2022.00040 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-03-14 03:04:09 [Bib_Time] => 2022-03-14 03:06:50 [KeysWordContens] => High avidity of vaccine-induced immunoglobulin G against SARS-CoV-2: potential relevance for protective humoral immunity, Humoral immune response, avidity, severe acute respiratory syndrome coronavirus 2, protective immunity, Avidity of immunoglobulin G (IgG) is defined as its binding strength to its target antigen. As a consequence of affinity maturation of the IgG response, avidity is maturing as well. Therefore, acute infections are characterized by low-avidity IgG, whereas past infections are usually associated with high-avidity IgG. Avidity maturation is also observed as a consequence of optimal vaccination. Avidity has been shown to play a significant role in protective humoral immunity in many microbial systems. After severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, the situation is different compared to other viral infections, as the moderate degree of avidity reached in most cases of infection is similar to that reached after only one vaccination step. In contrast, two vaccination steps lead to a much higher avidity of IgG directed towards viral spike protein S1 (S1) in the majority of vaccinated individuals. Therefore, it seems that two vaccination steps allow for a more extended affinity/avidity maturation than natural infection. The degree of avidity maturation after two vaccination steps is heterogeneous. It can be further enhanced by a third vaccination step. Complete avidity maturation seems to depend on sustained availability of antigen during the maturation process. Variants of concern seem to increase the affinity of their receptor-binding domain (RBD) to angiotensin-converting enzyme-2 (ACE2) and/or to decrease the susceptibility for neutralizing antibodies. Classical neutralization tests do not necessarily reflect the avidity of neutralizing IgG, as they operationally dissect the binding reaction between S1 and IgG from the binding of the S1 to ACE2. This approach fades out critical competition reactions between IgG and ACE for RBD of the S1. Quantitative avidity determination might be an essential tool to define individuals that only possess suboptimal protective immunity after vaccination and therefore might benefit from an additional booster immunization. ,Georg Bauer [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [40] => Array ( [ArticleId] => 280 [Create_Time] => 2022-03-16 [zipUrl] => https://www.explorationpub.com/uploads/zip/202303/20230301091430.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100341/100341.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100341/100341.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100341/100341_cover.png [JournalsId] => 5 [Title] => The role of γδ T cells in the context of allogeneic stem cell transplantation [Abstract] => Allogeneic stem cell transplantation is currently the only curative approach for a variety of malignant and non-malignant diseases. In the early transplant era, the intent of this treatment was to a [AbstractComplete] =>

Allogeneic stem cell transplantation is currently the only curative approach for a variety of malignant and non-malignant diseases. In the early transplant era, the intent of this treatment was to apply an intensive myeloablative regimen to eliminate residual malignant cells followed by the hematopoietic rescue of the patients with donor hematopoietic stem cells. However, the focus has shifted over time and allogeneic transplantation is nowadays seen as a cellular therapy in which the donor-derived immune system mounts an anti-infectious and especially an anti-tumor effect in the posttransplant phase. In order to further augment the anti-tumor effect, various approaches have been developed, including the manipulation of the donor-derived immune system in vivo or the adoptive transfer of ex vivo-expanded donor-derived effector cells. Based on their lack of alloreactivity, γδ+ T cells are shifting into the spotlight of research in the context of allogeneic transplantation. Their exploitation with regard to their anti-infectious and anti-tumor properties and their in vivo and ex vivo manipulation will lead to new therapeutic approaches to improve the outcome of patients after allogeneic stem cell transplantation. In this review, the important role of γδ+ T cells in allogeneic matched and mismatched transplantation is summarized and an outlook is discussed on how to best make use of this unique cell population.

[Names] => Rupert Handgretinger ... Manon Queudeville [Doi] => 10.37349/ei.2022.00041 [Published] => March 16, 2022 [Viewed] => 1088 [Downloaded] => 43 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00041 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 50 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:157–167 [Recommend] => 0 [Keywords] => Allogeneic stem cell transplantation, γδ T cells, immunotherapy, adoptive transfer, chimeric antigen receptor T cells [DetailTitle] => Interplay of γδ T cells and Tumor Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/50 [Id] => 100341 [ris] => https://www.explorationpub.com/uploads/Article/A100341/6acec143eeae5df4705ed9c4216777b2.ris [bib] => https://www.explorationpub.com/uploads/Article/A100341/6931c9a86bb92702f29b2ca3b938edd6.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-25 [CitethisArticle] => Handgretinger R, Lang P, Queudeville M. The role of γδ T cells in the context of allogeneic stem cell transplantation. Explor Immunol. 2022;2:157–67. https://doi.org/10.37349/ei.2022.00041 [Jindex] => 0 [CName] => RupertHandgretinger, [CEmail] => Rupert.Handgretinger@med.uni-tuebingen.de, [Ris_Time] => 2022-03-14 07:46:10 [Bib_Time] => 2022-03-14 07:46:10 [KeysWordContens] => The role of γδ T cells in the context of allogeneic stem cell transplantation, Allogeneic stem cell transplantation, γδ T cells, immunotherapy, adoptive transfer, chimeric antigen receptor T cells, Allogeneic stem cell transplantation is currently the only curative approach for a variety of malignant and non-malignant diseases. In the early transplant era, the intent of this treatment was to apply an intensive myeloablative regimen to eliminate residual malignant cells followed by the hematopoietic rescue of the patients with donor hematopoietic stem cells. However, the focus has shifted over time and allogeneic transplantation is nowadays seen as a cellular therapy in which the donor-derived immune system mounts an anti-infectious and especially an anti-tumor effect in the posttransplant phase. In order to further augment the anti-tumor effect, various approaches have been developed, including the manipulation of the donor-derived immune system in vivo or the adoptive transfer of ex vivo-expanded donor-derived effector cells. Based on their lack of alloreactivity, γδ+ T cells are shifting into the spotlight of research in the context of allogeneic transplantation. Their exploitation with regard to their anti-infectious and anti-tumor properties and their in vivo and ex vivo manipulation will lead to new therapeutic approaches to improve the outcome of patients after allogeneic stem cell transplantation. In this review, the important role of γδ+ T cells in allogeneic matched and mismatched transplantation is summarized and an outlook is discussed on how to best make use of this unique cell population. ,Rupert Handgretinger ... Manon Queudeville [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [41] => Array ( [ArticleId] => 282 [Create_Time] => 2022-03-17 [zipUrl] => https://www.explorationpub.com/uploads/zip/202203/20220317053558.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100342/100342.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100342/100342.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100342/100342_cover.png [JournalsId] => 5 [Title] => Augmenting human gamma delta lymphocytes for cancer therapy with chimeric antigen receptors [Abstract] => Gamma delta lymphocytes (γδ T) sit at the interface between innate and adaptive immunity. They have the capacity to recognize cancer cells by interaction of their surface receptors with an array of cancer cell surface target antigens. Interactions include the binding of γδ T cell receptors, the ligands for which are diverse and do not involve classical major histocompatibility complex (MHC) molecules. Moreover, a variety of natural killer-like and fragment crystallizable gamma (Fcγ) receptors confer additional cancer reactivity. Given this innate capacity to recognize and kill cancer cells, there appears less rationale for redirecting specific to cancer cell surface antigens through chimeric antigen receptor (CAR) expression. Several groups have however reported research findings that expression of CARs in γδ T cells can confer additional specificity or functionality. Though limited in number, these studies collectively identify the potential of CAR-T engineering to augment and fine tune anti-cancer responses. Together with the lack of graft versus host disease induced by allogeneic γδ T cells, these insights should encourage researchers to explore additional γδ T-CAR refinements for the development of off-the-shelf anti-cancer cell therapies. [AbstractComplete] =>

Gamma delta lymphocytes (γδ T) sit at the interface between innate and adaptive immunity. They have the capacity to recognize cancer cells by interaction of their surface receptors with an array of cancer cell surface target antigens. Interactions include the binding of γδ T cell receptors, the ligands for which are diverse and do not involve classical major histocompatibility complex (MHC) molecules. Moreover, a variety of natural killer-like and fragment crystallizable gamma (Fcγ) receptors confer additional cancer reactivity. Given this innate capacity to recognize and kill cancer cells, there appears less rationale for redirecting specific to cancer cell surface antigens through chimeric antigen receptor (CAR) expression. Several groups have however reported research findings that expression of CARs in γδ T cells can confer additional specificity or functionality. Though limited in number, these studies collectively identify the potential of CAR-T engineering to augment and fine tune anti-cancer responses. Together with the lack of graft versus host disease induced by allogeneic γδ T cells, these insights should encourage researchers to explore additional γδ T-CAR refinements for the development of off-the-shelf anti-cancer cell therapies.

[Names] => Gabrielle M. Ferry, John Anderson [Doi] => 10.37349/ei.2022.00042 [Published] => March 17, 2022 [Viewed] => 1337 [Downloaded] => 57 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00042 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 50 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:168–179 [Recommend] => 0 [Keywords] => Chimeric antigen receptor, gamma delta lymphocytes, adoptive cancer immunotherapy [DetailTitle] => Interplay of γδ T cells and Tumor Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/50 [Id] => 100342 [ris] => https://www.explorationpub.com/uploads/Article/A100342/207f524c98e7ce884bbb977b068b9d63.ris [bib] => https://www.explorationpub.com/uploads/Article/A100342/155ef2d79e8752c79a089ca23b455335.bib [ens] => [Cited] => 3 [Cited_Time] => 2024-04-25 [CitethisArticle] => Ferry GM, Anderson J. Augmenting human gamma delta lymphocytes for cancer therapy with chimeric antigen receptors. Explor Immunol. 2022;2:168–79. https://doi.org/10.37349/ei.2022.00042 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-03-18 00:43:09 [Bib_Time] => 2022-03-18 00:43:09 [KeysWordContens] => Augmenting human gamma delta lymphocytes for cancer therapy with chimeric antigen receptors, Chimeric antigen receptor, gamma delta lymphocytes, adoptive cancer immunotherapy, Gamma delta lymphocytes (γδ T) sit at the interface between innate and adaptive immunity. They have the capacity to recognize cancer cells by interaction of their surface receptors with an array of cancer cell surface target antigens. Interactions include the binding of γδ T cell receptors, the ligands for which are diverse and do not involve classical major histocompatibility complex (MHC) molecules. Moreover, a variety of natural killer-like and fragment crystallizable gamma (Fcγ) receptors confer additional cancer reactivity. Given this innate capacity to recognize and kill cancer cells, there appears less rationale for redirecting specific to cancer cell surface antigens through chimeric antigen receptor (CAR) expression. Several groups have however reported research findings that expression of CARs in γδ T cells can confer additional specificity or functionality. Though limited in number, these studies collectively identify the potential of CAR-T engineering to augment and fine tune anti-cancer responses. Together with the lack of graft versus host disease induced by allogeneic γδ T cells, these insights should encourage researchers to explore additional γδ T-CAR refinements for the development of off-the-shelf anti-cancer cell therapies. ,Gabrielle M. Ferry, John Anderson [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [42] => Array ( [ArticleId] => 283 [Create_Time] => 2022-03-18 [zipUrl] => https://www.explorationpub.com/uploads/zip/202203/20220316082739.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100343/100343.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100343/100343.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100343/100343_cover.png [JournalsId] => 5 [Title] => Paradigms in HIV vaccine research [Abstract] => Although a large number of preventative human immunodeficiency virus (HIV) vaccine trials have been carried out during the last 30 years, it is remarkable that an effective HIV vaccine has not yet b [AbstractComplete] =>

Although a large number of preventative human immunodeficiency virus (HIV) vaccine trials have been carried out during the last 30 years, it is remarkable that an effective HIV vaccine has not yet been developed. Research paradigms correspond to theoretical assumptions and particular strategies that scientists use when they try to solve a particular problem. Many paradigms used successfully in vaccinology were ineffective with HIV. For instance: 1) The structure-based reverse vaccinology approach failed because investigators tried to generate a vaccine starting with the antigenic structure of HIV-envelope (Env) epitopes bound to neutralizing monoclonal antibodies (mAbs) derived from HIV-infected individuals. They assumed that this antigenic structure would also possess the immunogenic capacity of inducing in vaccinees a polyclonal antibody (Ab) response with the same neutralizing capacity as the mAb. 2) The structures observed in epitope-paratope crystallographic complexes result from mutually induced fit between the two partners and do not correspond to the structures present in the free molecules before they had interacted. 3) The affinity-matured neutralizing mAbs obtained from chronically infected individuals did not recognize the germline predecessors of these Abs present in vaccinees. 4) The HIV p17 matrix protein that lines the inner surface of the viral membrane is one of the most disordered proteins identified on our planet and this prevents the induced Abs from binding to the glycosylated HIV gp120 protein. 5) Vaccinologists need to solve so-called inverse problems, for instance, guessing what are the multiple causes that produced an earlier wanted beneficial effect such as the absence of deleterious HIV infection in elite controllers. Since the immune system consists of numerous subsystems that have not yet been elucidated, it is impossible to solve the inverse problems posed by each subsystem. 6) Vaccinology is an empirical science that only sometimes succeeds because we do not understand the complex mechanisms that lead to protective immune responses.

[Names] => Marc H.V. Van Regenmortel [Doi] => 10.37349/ei.2022.00043 [Published] => March 17, 2022 [Viewed] => 1112 [Downloaded] => 36 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00043 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 63 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:180–184 [Recommend] => 0 [Keywords] => Causality, direct problem, inverse problem, explanation, paradoxes, immunogenicity [DetailTitle] => Old and New Paradigms in Viral Vaccinology [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/63 [Id] => 100343 [ris] => https://www.explorationpub.com/uploads/Article/A100343/194efe4027117b86ed3bb442a0fc1826.ris [bib] => https://www.explorationpub.com/uploads/Article/A100343/d77e30f18a0a373d5c1dccdb1a4a0f72.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Van Regenmortel MHV. Paradigms in HIV vaccine research. Explor Immunol. 2022;2:180–4. https://doi.org/10.37349/ei.2022.00043 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-03-16 07:48:48 [Bib_Time] => 2022-03-16 07:48:48 [KeysWordContens] => Paradigms in HIV vaccine research, Causality, direct problem, inverse problem, explanation, paradoxes, immunogenicity, Although a large number of preventative human immunodeficiency virus (HIV) vaccine trials have been carried out during the last 30 years, it is remarkable that an effective HIV vaccine has not yet been developed. Research paradigms correspond to theoretical assumptions and particular strategies that scientists use when they try to solve a particular problem. Many paradigms used successfully in vaccinology were ineffective with HIV. For instance: 1) The structure-based reverse vaccinology approach failed because investigators tried to generate a vaccine starting with the antigenic structure of HIV-envelope (Env) epitopes bound to neutralizing monoclonal antibodies (mAbs) derived from HIV-infected individuals. They assumed that this antigenic structure would also possess the immunogenic capacity of inducing in vaccinees a polyclonal antibody (Ab) response with the same neutralizing capacity as the mAb. 2) The structures observed in epitope-paratope crystallographic complexes result from mutually induced fit between the two partners and do not correspond to the structures present in the free molecules before they had interacted. 3) The affinity-matured neutralizing mAbs obtained from chronically infected individuals did not recognize the germline predecessors of these Abs present in vaccinees. 4) The HIV p17 matrix protein that lines the inner surface of the viral membrane is one of the most disordered proteins identified on our planet and this prevents the induced Abs from binding to the glycosylated HIV gp120 protein. 5) Vaccinologists need to solve so-called inverse problems, for instance, guessing what are the multiple causes that produced an earlier wanted beneficial effect such as the absence of deleterious HIV infection in elite controllers. Since the immune system consists of numerous subsystems that have not yet been elucidated, it is impossible to solve the inverse problems posed by each subsystem. 6) Vaccinology is an empirical science that only sometimes succeeds because we do not understand the complex mechanisms that lead to protective immune responses. ,Marc H.V. Van Regenmortel [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [43] => Array ( [ArticleId] => 290 [Create_Time] => 2022-04-15 [zipUrl] => https://www.explorationpub.com/uploads/zip/202204/20220420062020.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100344/100344.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100344/100344.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100344/100344_cover.png [JournalsId] => 5 [Title] => Single-cell differentiation trajectories define early stages of a human cutaneous T-cell lymphoma [Abstract] => Aim: The aim of this article is to characterize in detail the γδ T lymphocytes from an adult patient with primary cutaneous T-cell lymphoma of γδ s [AbstractComplete] =>

Aim:

The aim of this article is to characterize in detail the γδ T lymphocytes from an adult patient with primary cutaneous T-cell lymphoma of γδ subtype (γδ CTCL).

Methods:

Here this article reports trajectory mapping on high-resolution differentiation trajectories of γδ T lymphocytes digitally extracted from a scRNAseq dataset.

Results:

In the patch-to-plaque progression of CTCL, the TCRVγnon9 subset of γδ T cells differentiated from naive T cells (Tn) and central memory T cells (Tcm) to abundant effector memory T cells (Tem) while other cutaneous γδ T and CD8 T cells remained unchanged.

Conclusions:

This transcriptomic switch underlies the emergence of a CTCL-like progression of the TCRVγnon9 γδ T subtype and suggests new routes for treating these diseases.

[Names] => Juan-Pablo Cerapio ... Jean-Jacques Fournie [Doi] => 10.37349/ei.2022.00044 [Published] => April 15, 2022 [Viewed] => 1570 [Downloaded] => 35 [Subject] => Original Article [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00044 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 50 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:185–199 [Recommend] => 0 [Keywords] => Gamma delta lymphoma, scRNAseq, differentiation, trajectory [DetailTitle] => Interplay of γδ T cells and Tumor Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/50 [Id] => 100344 [ris] => https://www.explorationpub.com/uploads/Article/A100344/4b0af8f634423bd28bf3368d57691096.ris [bib] => https://www.explorationpub.com/uploads/Article/A100344/e0e2f2025f706043dc7d1f0a88f68391.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Cerapio JP, Perrier M, Pont F, Laurent C, Bertani S, Fournie JJ. Single‐cell differentiation trajectories define early stages of a human cutaneous T-cell lymphoma. Explor Immunol. 2022;2:185–99. https://doi.org/10.37349/ei.2022.00044 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-04-15 03:28:37 [Bib_Time] => 2022-04-15 03:28:37 [KeysWordContens] => Single-cell differentiation trajectories define early stages of a human cutaneous T-cell lymphoma, Gamma delta lymphoma, scRNAseq, differentiation, trajectory, Aim: The aim of this article is to characterize in detail the γδ T lymphocytes from an adult patient with primary cutaneous T-cell lymphoma of γδ subtype (γδ CTCL). Methods: Here this article reports trajectory mapping on high-resolution differentiation trajectories of γδ T lymphocytes digitally extracted from a scRNAseq dataset. Results: In the patch-to-plaque progression of CTCL, the TCRVγnon9 subset of γδ T cells differentiated from naive T cells (Tn) and central memory T cells (Tcm) to abundant effector memory T cells (Tem) while other cutaneous γδ T and CD8 T cells remained unchanged. Conclusions: This transcriptomic switch underlies the emergence of a CTCL-like progression of the TCRVγnon9 γδ T subtype and suggests new routes for treating these diseases. ,Juan-Pablo Cerapio ... Jean-Jacques Fournie [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [44] => Array ( [ArticleId] => 293 [Create_Time] => 2022-04-22 [zipUrl] => https://www.explorationpub.com/uploads/zip/202204/20220422064110.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100345/100345.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100345/100345.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100345/100345_cover.png [JournalsId] => 5 [Title] => Thymosin alpha 1 therapy alleviates organ dysfunction of sepsis patients: a retrospective cohort study [Abstract] => Aim: Thymosin alpha 1 (Tα1) is a promising treatment for the improvement of sepsis patients. Until now, its function in reducing acute organ damage of sepsis patients is still unclear. The aim of this study was to determine whether Tα1 can alleviate organ dysfunction in sepsis patients. [AbstractComplete] =>

Aim:

Thymosin alpha 1 (Tα1) is a promising treatment for the improvement of sepsis patients. Until now, its function in reducing acute organ damage of sepsis patients is still unclear. The aim of this study was to determine whether Tα1 can alleviate organ dysfunction in sepsis patients.

Methods:

This study retrospectively enrolled sepsis patients from a multicenter randomized controlled trial [efficacy of Tα1 for severe sepsis (ETASS)]. The sequential organ failure assessment (SOFA) score on day 0 (initial), day 3, and day 7 was collected. Absolute SOFAday07 was defined as initial SOFA score minus SOFA score on day 7 (initial SOFA–SOFA day7). Delta SOFA score (ΔSOFAday07) was provided by the formula: (initial SOFA–SOFA day7) × 100/initial SOFA, and it was expressed as a percentage. After propensity score matching (1:1 ratio), baseline characteristics were well-balanced between the Tα1 group and placebo group. The primary outcome was evaluated with a comparison of ΔSOFAday07 decline between patients treated with or without Tα1 therapy.

Results:

Among 288 enrolled patients, 149 patients received both Tα1 and standard therapy (Tα1 group), and 139 patients received both placebo and standard therapy (placebo group). Compared with the placebo group, the Tα1 group had significantly lower Absolute SOFAday07 [95% confidence interval (CI) 0.8 (0–1.7), P = 0.049]. Among 111 pairs of patients matched by propensity score, the Tα1 group still had lower Absolute SOFAday07 [95% CI 1.0 (0.1–1.9), P = 0.029]. Meanwhile, Tα1 treatment could significantly improve ΔSOFAday07. When the amplitude of ΔSOFAday07 was graded, one third of patients in the Tα1 group had an increase of more than 60%, compared with 22% in the placebo group. Subgroup analysis found that the ΔSOFAday07 improved significantly after Tα1 therapy in sepsis patients with no immunoparalysis at baseline, no complications, and early intervention.

Conclusions:

For sepsis patients, Tα1 treatment can alleviate organ dysfunction, and ΔSOFAday07 can be used as an indicator of its therapeutic effect (ClinicalTrials.gov identifier: NCT00711620).

[Names] => Fei Pei ... on behalf of the China Critical Care Immunotherapy Research Group [Doi] => 10.37349/ei.2022.00045 [Published] => April 22, 2022 [Viewed] => 1350 [Downloaded] => 55 [Subject] => Original Article [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00045 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 53 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:200–210 [Recommend] => 0 [Keywords] => Immunoparalysis, immunotherapy, thymosin alpha 1, sepsis, sequential organ failure assessment score [DetailTitle] => The‌ ‌Sepsis‌ ‌induced‌ ‌Immune‌ ‌Conundrum [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/53 [Id] => 100345 [ris] => https://www.explorationpub.com/uploads/Article/A100345/9f5c1667acc267a937ad404395a3766e.ris [bib] => https://www.explorationpub.com/uploads/Article/A100345/bcc7c9c5a334e6afd21762bafbf242cb.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-25 [CitethisArticle] => Pei F, Liu Y, Zuo L, Gu B, Liang L, Wang L, et al. Thymosin alpha 1 therapy alleviates organ dysfunction of sepsis patients: a retrospective cohort study. Explor Immunol. 2022;2:200–10. https://doi.org/10.37349/ei.2022.00045 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-04-21 09:42:00 [Bib_Time] => 2022-04-21 09:42:00 [KeysWordContens] => Thymosin alpha 1 therapy alleviates organ dysfunction of sepsis patients: a retrospective cohort study, Immunoparalysis, immunotherapy, thymosin alpha 1, sepsis, sequential organ failure assessment score, Aim: Thymosin alpha 1 (Tα1) is a promising treatment for the improvement of sepsis patients. Until now, its function in reducing acute organ damage of sepsis patients is still unclear. The aim of this study was to determine whether Tα1 can alleviate organ dysfunction in sepsis patients. Methods: This study retrospectively enrolled sepsis patients from a multicenter randomized controlled trial [efficacy of Tα1 for severe sepsis (ETASS)]. The sequential organ failure assessment (SOFA) score on day 0 (initial), day 3, and day 7 was collected. Absolute SOFAday07 was defined as initial SOFA score minus SOFA score on day 7 (initial SOFA–SOFA day7). Delta SOFA score (ΔSOFAday07) was provided by the formula: (initial SOFA–SOFA day7) × 100/initial SOFA, and it was expressed as a percentage. After propensity score matching (1:1 ratio), baseline characteristics were well-balanced between the Tα1 group and placebo group. The primary outcome was evaluated with a comparison of ΔSOFAday07 decline between patients treated with or without Tα1 therapy. Results: Among 288 enrolled patients, 149 patients received both Tα1 and standard therapy (Tα1 group), and 139 patients received both placebo and standard therapy (placebo group). Compared with the placebo group, the Tα1 group had significantly lower Absolute SOFAday07 [95% confidence interval (CI) 0.8 (0–1.7), P = 0.049]. Among 111 pairs of patients matched by propensity score, the Tα1 group still had lower Absolute SOFAday07 [95% CI 1.0 (0.1–1.9), P = 0.029]. Meanwhile, Tα1 treatment could significantly improve ΔSOFAday07. When the amplitude of ΔSOFAday07 was graded, one third of patients in the Tα1 group had an increase of more than 60%, compared with 22% in the placebo group. Subgroup analysis found that the ΔSOFAday07 improved significantly after Tα1 therapy in sepsis patients with no immunoparalysis at baseline, no complications, and early intervention. Conclusions: For sepsis patients, Tα1 treatment can alleviate organ dysfunction, and ΔSOFAday07 can be used as an indicator of its therapeutic effect (ClinicalTrials.gov identifier: NCT00711620). ,Fei Pei ... [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [45] => Array ( [ArticleId] => 296 [Create_Time] => 2022-04-24 [zipUrl] => https://www.explorationpub.com/uploads/zip/202204/20220424014738.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100346/100346.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100346/100346.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100346/100346_cover.png [JournalsId] => 5 [Title] => A proposed new paradigm for an anti-AIDS tolerogenic vaccine [Abstract] => Until now, despite 30 years of intensive work, the RV144 human immunodeficiency virus (HIV) vaccine trial initiated in 2003 remains so far the most protective vaccine prototype of all those tested ( [AbstractComplete] =>

Until now, despite 30 years of intensive work, the RV144 human immunodeficiency virus (HIV) vaccine trial initiated in 2003 remains so far the most protective vaccine prototype of all those tested (32% reduction in the infection rate three years after the vaccination) and the HIV epidemic is still spreading worldwide. In addition, antiretroviral therapy (ART) for people living with HIV is given for life as no other pharmacological intervention has allowed to maintain an undetectable viral load after ART withdrawal. Pr Andrieu and colleagues discovered tolerogenic CD8+T-cells that suppress simian immunodeficiency virus (SIV) specific activation, ensuing SIV reverse transcription suppression and viral replication-defective in Chinese macaques vaccinated by intragastric route with inactivated SIV particles + Lactobacillus rhamnosus. Moreover, in HIV-infected elite controllers with specific genetic features (HLA-1-Bw4-80i and KIR3DL1 genes), Pr Andrieu found out that similar tolerogenic CD8+T-cells suppress in the same manner HIV-specific activation, HIV reverse transcription, and HIV replication. These data justify the development of a tolerogenic vaccine composed of inactivated HIV particles + Lactobacillus rhamnosus that could be used as a preventive or therapeutic vaccine.

[Names] => Christine Jacomet [Doi] => 10.37349/ei.2022.00046 [Published] => April 24, 2022 [Viewed] => 1147 [Downloaded] => 22 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00046 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 63 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:211–219 [Recommend] => 0 [Keywords] => HIV, vaccine, CD8+T-cells [DetailTitle] => Old and New Paradigms in Viral Vaccinology [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/63 [Id] => 100346 [ris] => https://www.explorationpub.com/uploads/Article/A100346/d3f567cd1e54f42f7c8b4a1fcaa19aa1.ris [bib] => https://www.explorationpub.com/uploads/Article/A100346/b44b7a07d65621ced56ffdaa4e0795c4.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Jacomet C. A proposed new paradigm for an anti-AIDS tolerogenic vaccine. Explor Immunol. 2022;2:211–9. https://doi.org/10.37349/ei.2022.00046 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-04-21 06:06:43 [Bib_Time] => 2022-04-21 06:06:43 [KeysWordContens] => A proposed new paradigm for an anti-AIDS tolerogenic vaccine, HIV, vaccine, CD8+T-cells, Until now, despite 30 years of intensive work, the RV144 human immunodeficiency virus (HIV) vaccine trial initiated in 2003 remains so far the most protective vaccine prototype of all those tested (32% reduction in the infection rate three years after the vaccination) and the HIV epidemic is still spreading worldwide. In addition, antiretroviral therapy (ART) for people living with HIV is given for life as no other pharmacological intervention has allowed to maintain an undetectable viral load after ART withdrawal. Pr Andrieu and colleagues discovered tolerogenic CD8+T-cells that suppress simian immunodeficiency virus (SIV) specific activation, ensuing SIV reverse transcription suppression and viral replication-defective in Chinese macaques vaccinated by intragastric route with inactivated SIV particles + Lactobacillus rhamnosus. Moreover, in HIV-infected elite controllers with specific genetic features (HLA-1-Bw4-80i and KIR3DL1 genes), Pr Andrieu found out that similar tolerogenic CD8+T-cells suppress in the same manner HIV-specific activation, HIV reverse transcription, and HIV replication. These data justify the development of a tolerogenic vaccine composed of inactivated HIV particles + Lactobacillus rhamnosus that could be used as a preventive or therapeutic vaccine. ,Christine Jacomet [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [46] => Array ( [ArticleId] => 306 [Create_Time] => 2022-04-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202204/20220428040734.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100347/100347.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100347/100347.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100347/100347_cover.png [JournalsId] => 5 [Title] => Anti-cancer γδ T lymphocytes: contradictory past and promising future [Abstract] => Recent anti-cancer strategies are based on the stimulation of anti-tumor immune reaction, exploiting distinct lymphocyte subsets. Among them, γδ T cells represent optimal anti-cancer candidates, especially in those tissues where they are highly localized, such as the respiratory or gastrointestinal tract. One important challenge has been the identification of stimulating drugs able to induce and maintain γδ T cell-mediated anti-cancer immune response. Amino-bisphosphonates (N-BPs) have been largely employed in anti-cancer clinical trials due to their ability to upregulate the accumulation of pyrophosphates that promote the activation of Vγ9Vδ2 T cells. This activation depends on the butyrophilin A family, which is crucial in contributing to Vγ9Vδ2 T cells stimulation but is not equally expressed in all cancer tissues. Thus, the clinical outcome of such treatments is still a challenge. In this viewpoint, a critical picture of γδ T cells as effective anti-cancer effectors is designed, with a specific focus on the best immune-stimulating therapeutic schemes involving this lymphocyte subset and the tools available to measure their efficacy and presence in tumor tissues. Some pre-clinical models, useful to measure γδ T cell anti-cancer potential and their response to stimulating drugs, therapeutic monoclonal antibodies, or bispecific antibodies are described. Computerized imaging and digital pathology are also proposed as a help in the identification of co-stimulatory molecules and localization of γδ T cell effectors. Finally, two types of novel drug preparation are proposed: nanoparticles loaded with N-BPs and pro-drug formulations that enhance the effectiveness of γδ T lymphocyte stimulation. [AbstractComplete] =>

Recent anti-cancer strategies are based on the stimulation of anti-tumor immune reaction, exploiting distinct lymphocyte subsets. Among them, γδ T cells represent optimal anti-cancer candidates, especially in those tissues where they are highly localized, such as the respiratory or gastrointestinal tract. One important challenge has been the identification of stimulating drugs able to induce and maintain γδ T cell-mediated anti-cancer immune response. Amino-bisphosphonates (N-BPs) have been largely employed in anti-cancer clinical trials due to their ability to upregulate the accumulation of pyrophosphates that promote the activation of Vγ9Vδ2 T cells. This activation depends on the butyrophilin A family, which is crucial in contributing to Vγ9Vδ2 T cells stimulation but is not equally expressed in all cancer tissues. Thus, the clinical outcome of such treatments is still a challenge. In this viewpoint, a critical picture of γδ T cells as effective anti-cancer effectors is designed, with a specific focus on the best immune-stimulating therapeutic schemes involving this lymphocyte subset and the tools available to measure their efficacy and presence in tumor tissues. Some pre-clinical models, useful to measure γδ T cell anti-cancer potential and their response to stimulating drugs, therapeutic monoclonal antibodies, or bispecific antibodies are described. Computerized imaging and digital pathology are also proposed as a help in the identification of co-stimulatory molecules and localization of γδ T cell effectors. Finally, two types of novel drug preparation are proposed: nanoparticles loaded with N-BPs and pro-drug formulations that enhance the effectiveness of γδ T lymphocyte stimulation.

[Names] => Alessandro Poggi, Maria Raffaella Zocchi [Doi] => 10.37349/ei.2022.00047 [Published] => April 28, 2022 [Viewed] => 1112 [Downloaded] => 34 [Subject] => Perspective [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00047 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 50 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:220–228 [Recommend] => 0 [Keywords] => Butyrophilins, zoledronic acid, amino-bisphosphonates, 3D models [DetailTitle] => Interplay of γδ T cells and Tumor Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/50 [Id] => 100347 [ris] => https://www.explorationpub.com/uploads/Article/A100347/7c9542b119d206650af9060bd8616832.ris [bib] => https://www.explorationpub.com/uploads/Article/A100347/fc077779a13e438cecdf7a21be288970.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Poggi A, Zocchi MR. Anti-cancer γδ T lymphocytes: contradictory past and promising future. Explor Immunol. 2022;2:220–8. https://doi.org/10.37349/ei.2022.00047 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-04-27 08:27:45 [Bib_Time] => 2022-04-27 08:27:45 [KeysWordContens] => Anti-cancer γδ T lymphocytes: contradictory past and promising future, Butyrophilins, zoledronic acid, amino-bisphosphonates, 3D models, Recent anti-cancer strategies are based on the stimulation of anti-tumor immune reaction, exploiting distinct lymphocyte subsets. Among them, γδ T cells represent optimal anti-cancer candidates, especially in those tissues where they are highly localized, such as the respiratory or gastrointestinal tract. One important challenge has been the identification of stimulating drugs able to induce and maintain γδ T cell-mediated anti-cancer immune response. Amino-bisphosphonates (N-BPs) have been largely employed in anti-cancer clinical trials due to their ability to upregulate the accumulation of pyrophosphates that promote the activation of Vγ9Vδ2 T cells. This activation depends on the butyrophilin A family, which is crucial in contributing to Vγ9Vδ2 T cells stimulation but is not equally expressed in all cancer tissues. Thus, the clinical outcome of such treatments is still a challenge. In this viewpoint, a critical picture of γδ T cells as effective anti-cancer effectors is designed, with a specific focus on the best immune-stimulating therapeutic schemes involving this lymphocyte subset and the tools available to measure their efficacy and presence in tumor tissues. Some pre-clinical models, useful to measure γδ T cell anti-cancer potential and their response to stimulating drugs, therapeutic monoclonal antibodies, or bispecific antibodies are described. Computerized imaging and digital pathology are also proposed as a help in the identification of co-stimulatory molecules and localization of γδ T cell effectors. Finally, two types of novel drug preparation are proposed: nanoparticles loaded with N-BPs and pro-drug formulations that enhance the effectiveness of γδ T lymphocyte stimulation. ,Alessandro Poggi, Maria Raffaella Zocchi [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [47] => Array ( [ArticleId] => 308 [Create_Time] => 2022-05-07 [zipUrl] => https://www.explorationpub.com/uploads/zip/202205/20220507081959.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100348/100348.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100348/100348.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100348/100348_cover.png [JournalsId] => 5 [Title] => Mechanism of NLRP3 inflammasome activation and its role in Alzheimer’s disease [Abstract] => Alzheimer’s disease (AD) is a common neurological disease in the elderly, and the major manifestations are cognitive dysfunction, neuronal loss, and neuropathic lesions in the brain. In [AbstractComplete] =>

Alzheimer’s disease (AD) is a common neurological disease in the elderly, and the major manifestations are cognitive dysfunction, neuronal loss, and neuropathic lesions in the brain. In the process of AD pathogenesis, the inflammatory response plays an indispensable role. The nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome containing NOD, leucine-rich repeat (LRR), and pyran domains is a multi-molecular complex that can detect dangerous signals related to neurological diseases. The assembly of NLRP3 inflammasome promotes the maturation of interleukin-1beta (IL-1β) and IL-18 mediated by caspase-1 in microglia, which leads to neuroinflammation and finally contributes to the occurrence and development of AD. This review aimed to clarify the structure and activating mechanism of NLRP3 inflammasome and its key role in the pathogenesis of AD, summarize the latest findings on the suppression of NLRP3 inflammasome activation for the treatment of AD, as well as indicate that targeting regulation of NLRP3 inflammasome assembly may be a potential strategy for the treatment of AD, providing a theoretical basis for the research of AD.

[Names] => Xiaohan Gao ... Xueling Dai [Doi] => 10.37349/ei.2022.00048 [Published] => May 07, 2022 [Viewed] => 2453 [Downloaded] => 72 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00048 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:229–244 [Recommend] => 1 [Keywords] => Alzheimer’s disease, NOD-like receptor family pyrin domain containing 3 inflammasome, apoptosis-associated speck-like protein containing a caspase-1 recruitment domain, caspase-1, β-amyloid [DetailTitle] => [DetailUrl] => [Id] => 100348 [ris] => https://www.explorationpub.com/uploads/Article/A100348/9f529d7e3fbdfd849665bfb7b91d9d12.ris [bib] => https://www.explorationpub.com/uploads/Article/A100348/d9ad405651e4b1875f9ea59037867d70.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-26 [CitethisArticle] => Gao X, Zhang X, Sun Y, Dai X. Mechanism of NLRP3 inflammasome activation and its role in Alzheimer’s disease. Explor Immunol. 2022;2:229–44. https://doi.org/10.37349/ei.2022.00048 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-05-07 08:26:17 [Bib_Time] => 2022-05-07 08:29:41 [KeysWordContens] => Mechanism of NLRP3 inflammasome activation and its role in Alzheimer’s disease, Alzheimer’s disease, NOD-like receptor family pyrin domain containing 3 inflammasome, apoptosis-associated speck-like protein containing a caspase-1 recruitment domain, caspase-1, β-amyloid, Alzheimer’s disease (AD) is a common neurological disease in the elderly, and the major manifestations are cognitive dysfunction, neuronal loss, and neuropathic lesions in the brain. In the process of AD pathogenesis, the inflammatory response plays an indispensable role. The nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome containing NOD, leucine-rich repeat (LRR), and pyran domains is a multi-molecular complex that can detect dangerous signals related to neurological diseases. The assembly of NLRP3 inflammasome promotes the maturation of interleukin-1beta (IL-1β) and IL-18 mediated by caspase-1 in microglia, which leads to neuroinflammation and finally contributes to the occurrence and development of AD. This review aimed to clarify the structure and activating mechanism of NLRP3 inflammasome and its key role in the pathogenesis of AD, summarize the latest findings on the suppression of NLRP3 inflammasome activation for the treatment of AD, as well as indicate that targeting regulation of NLRP3 inflammasome assembly may be a potential strategy for the treatment of AD, providing a theoretical basis for the research of AD. ,Xiaohan Gao ... Xueling Dai [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [48] => Array ( [ArticleId] => 309 [Create_Time] => 2022-05-17 [zipUrl] => https://www.explorationpub.com/uploads/zip/202207/20220706065738.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100349/100349.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100349/100349.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100349/100349_cover.png [JournalsId] => 5 [Title] => SARS-CoV-2: overview of immune response, insights into vaccine platforms and their challenges [Abstract] => The crown-like shaped viruses known as coronaviruses which were first reported in the 1960’s have caused three epidemics in the past two decades namely, coronavirus disease-19 (COVID-19), severe acute respiratory syndrome (SARS), and Middle East respiratory syndrome (MERS). SARS coronavirus 2 (SARS-CoV-2) was first reported in the latter half of December in Wuhan, a city of China, with people affected by deadly pneumonia with unknown etiology. Since then, the world has experienced two phases of virus spread with different symptoms and disease severity. This review embarks on the journey to investigate candidate molecules of this virus which can and are being investigated for various vaccine formulations and to discuss immunity developed against this virus. [AbstractComplete] =>

The crown-like shaped viruses known as coronaviruses which were first reported in the 1960’s have caused three epidemics in the past two decades namely, coronavirus disease-19 (COVID-19), severe acute respiratory syndrome (SARS), and Middle East respiratory syndrome (MERS). SARS coronavirus 2 (SARS-CoV-2) was first reported in the latter half of December in Wuhan, a city of China, with people affected by deadly pneumonia with unknown etiology. Since then, the world has experienced two phases of virus spread with different symptoms and disease severity. This review embarks on the journey to investigate candidate molecules of this virus which can and are being investigated for various vaccine formulations and to discuss immunity developed against this virus.

[Names] => Balram Ji Omar ... Manju O. Pai [Doi] => 10.37349/ei.2022.00049 [Published] => May 16, 2022 [Viewed] => 1266 [Downloaded] => 25 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00049 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 47 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:245–263 [Recommend] => 0 [Keywords] => Severe acute respiratory syndrome coronavirus 2, Wuhan, vaccine, immunity, challenges [DetailTitle] => Vaccine-induced Immune Responses Against SARS-CoV-2 Infections [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/47 [Id] => 100349 [ris] => https://www.explorationpub.com/uploads/Article/A100349/61f69670555c719f51b7e6a7b64f0a2d.ris [bib] => https://www.explorationpub.com/uploads/Article/A100349/20013f1e6c43234f60fb205d54ef525b.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Omar BJ, Singh A, Singh V, Kothari A, Pai MO. SARS-CoV-2: overview of immune response, insights into vaccine platforms and their challenges. Explor Immunol. 2022;2:245–63. https://doi.org/10.37349/ei.2022.00049 [Jindex] => 0 [CName] => Manju O.Pai, [CEmail] => manjuohripai@gmail.com, [Ris_Time] => 2022-05-17 01:05:26 [Bib_Time] => 2022-05-17 01:05:26 [KeysWordContens] => SARS-CoV-2: overview of immune response, insights into vaccine platforms and their challenges, Severe acute respiratory syndrome coronavirus 2, Wuhan, vaccine, immunity, challenges, The crown-like shaped viruses known as coronaviruses which were first reported in the 1960’s have caused three epidemics in the past two decades namely, coronavirus disease-19 (COVID-19), severe acute respiratory syndrome (SARS), and Middle East respiratory syndrome (MERS). SARS coronavirus 2 (SARS-CoV-2) was first reported in the latter half of December in Wuhan, a city of China, with people affected by deadly pneumonia with unknown etiology. Since then, the world has experienced two phases of virus spread with different symptoms and disease severity. This review embarks on the journey to investigate candidate molecules of this virus which can and are being investigated for various vaccine formulations and to discuss immunity developed against this virus. ,Balram Ji Omar ... Manju O. Pai [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [49] => Array ( [ArticleId] => 310 [Create_Time] => 2022-05-19 [zipUrl] => https://www.explorationpub.com/uploads/zip/202303/20230301091739.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100350/100350.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100350/100350.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100350/100350_cover.png [JournalsId] => 5 [Title] => Therapeutic and prophylactic applications of self-replicating RNA viruses [Abstract] => Self-replicating RNA viruses have been commonly used for preventive and therapeutic interventions in the fields of infectious diseases and cancers. Both RNA viruses with single-stranded RNA genomes [AbstractComplete] =>

Self-replicating RNA viruses have been commonly used for preventive and therapeutic interventions in the fields of infectious diseases and cancers. Both RNA viruses with single-stranded RNA genomes of positive and negative polarity have been utilized. Expression of viral surface proteins from self-replicating RNA virus vectors has elicited strong immune responses and provided protection against challenges with lethal doses of pathogens in various animal models using recombinant viral particles, RNA replicons, or plasmid-based replicon vectors. Similarly, immunization with self-replicating RNA virus vectors expressing tumor antigens has induced tumor-specific antibody (Ab) responses, inhibited tumor growth, eradicated tumors, and protected immunized animals against tumor challenges. Clinical trials have demonstrated good safety and tolerance of self-replicating RNA viruses. Although the number of clinical trials is low, robust immune responses and protection against challenges with pathogens and tumor cells have been achieved. The Ervebo vaccine against Ebola virus disease has been approved by both the European Medicines Agency (EMA) and the US Food and Drug Administration (FDA).

[Names] => Kenneth Lundstrom [Doi] => 10.37349/ei.2022.00050 [Published] => May 18, 2022 [Viewed] => 1569 [Downloaded] => 42 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00050 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 63 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:264–292 [Recommend] => 0 [Keywords] => Self-amplification, recombinant particles, RNA replicons, DNA replicons, vaccines, infectious diseases, cancer [DetailTitle] => Old and New Paradigms in Viral Vaccinology [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/63 [Id] => 100350 [ris] => https://www.explorationpub.com/uploads/Article/A100350/44506e2cbe81c99950cc1ecce550b8f4.ris [bib] => https://www.explorationpub.com/uploads/Article/A100350/a40a701fcbdd5c2b95d9c2e84298f34e.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-25 [CitethisArticle] => Lundstrom K. Therapeutic and prophylactic applications of self-replicating RNA viruses. Explor Immunol. 2022;2:264–92. https://doi.org/10.37349/ei.2022.00050 [Jindex] => 0 [CName] => KennethLundstrom, [CEmail] => lundstromkenneth@gmail.com, [Ris_Time] => 2022-05-19 00:58:01 [Bib_Time] => 2022-05-19 00:58:01 [KeysWordContens] => Therapeutic and prophylactic applications of self-replicating RNA viruses, Self-amplification, recombinant particles, RNA replicons, DNA replicons, vaccines, infectious diseases, cancer, Self-replicating RNA viruses have been commonly used for preventive and therapeutic interventions in the fields of infectious diseases and cancers. Both RNA viruses with single-stranded RNA genomes of positive and negative polarity have been utilized. Expression of viral surface proteins from self-replicating RNA virus vectors has elicited strong immune responses and provided protection against challenges with lethal doses of pathogens in various animal models using recombinant viral particles, RNA replicons, or plasmid-based replicon vectors. Similarly, immunization with self-replicating RNA virus vectors expressing tumor antigens has induced tumor-specific antibody (Ab) responses, inhibited tumor growth, eradicated tumors, and protected immunized animals against tumor challenges. Clinical trials have demonstrated good safety and tolerance of self-replicating RNA viruses. Although the number of clinical trials is low, robust immune responses and protection against challenges with pathogens and tumor cells have been achieved. The Ervebo vaccine against Ebola virus disease has been approved by both the European Medicines Agency (EMA) and the US Food and Drug Administration (FDA). ,Kenneth Lundstrom [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [50] => Array ( [ArticleId] => 312 [Create_Time] => 2022-05-25 [zipUrl] => https://www.explorationpub.com/uploads/zip/202205/20220524064326.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100351/100351.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100351/100351.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100351/100351_cover.png [JournalsId] => 5 [Title] => Janus face of sepsis: a viewpoint [Abstract] => Treatment of sepsis currently relies on eliminating the causal pathogen and supportive care, whereas almost no approaches to interfere with the defining event of a “dysregulated host response” are available. This review points to the striking correlation of two phenotypes of sepsis etiopathology with the concept of bipartite response patterns of higher organisms to microbial attacks. According to this concept, the phenotypes of sepsis can be interpreted as either resistance or tolerance responses to infection that got out of hand. This concept might allow focusing sepsis research and related patient studies on key conundrums of current sepsis research: how do resistance responses result in immunopathology and how can tolerance lead to systemic immunosuppression or even immunoparalysis? The heuristic vigor of these questions might inspire experimental efforts and clinical studies and ultimately advance the therapeutic armamentarium for sepsis care. [AbstractComplete] =>

Treatment of sepsis currently relies on eliminating the causal pathogen and supportive care, whereas almost no approaches to interfere with the defining event of a “dysregulated host response” are available. This review points to the striking correlation of two phenotypes of sepsis etiopathology with the concept of bipartite response patterns of higher organisms to microbial attacks. According to this concept, the phenotypes of sepsis can be interpreted as either resistance or tolerance responses to infection that got out of hand. This concept might allow focusing sepsis research and related patient studies on key conundrums of current sepsis research: how do resistance responses result in immunopathology and how can tolerance lead to systemic immunosuppression or even immunoparalysis? The heuristic vigor of these questions might inspire experimental efforts and clinical studies and ultimately advance the therapeutic armamentarium for sepsis care.

[Names] => Michael Bauer, Reinhard Wetzker [Doi] => 10.37349/ei.2022.00051 [Published] => May 24, 2022 [Viewed] => 986 [Downloaded] => 29 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00051 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 53 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:293–302 [Recommend] => 0 [Keywords] => Sepsis, immunopathology, immunosuppression, resistance, tolerance [DetailTitle] => The‌ ‌Sepsis‌ ‌induced‌ ‌Immune‌ ‌Conundrum [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/53 [Id] => 100351 [ris] => https://www.explorationpub.com/uploads/Article/A100351/671abedcff83ea2a5c24fd4e77279196.ris [bib] => https://www.explorationpub.com/uploads/Article/A100351/d890de6d836a4e2b4e062c171b4c6580.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Bauer M, Wetzker R. Janus face of sepsis: a viewpoint. Explor Immunol. 2022;2:293–302. https://doi.org/10.37349/ei.2022.00051 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-05-25 00:47:13 [Bib_Time] => 2022-05-25 00:47:13 [KeysWordContens] => Janus face of sepsis: a viewpoint, Sepsis, immunopathology, immunosuppression, resistance, tolerance, Treatment of sepsis currently relies on eliminating the causal pathogen and supportive care, whereas almost no approaches to interfere with the defining event of a “dysregulated host response” are available. This review points to the striking correlation of two phenotypes of sepsis etiopathology with the concept of bipartite response patterns of higher organisms to microbial attacks. According to this concept, the phenotypes of sepsis can be interpreted as either resistance or tolerance responses to infection that got out of hand. This concept might allow focusing sepsis research and related patient studies on key conundrums of current sepsis research: how do resistance responses result in immunopathology and how can tolerance lead to systemic immunosuppression or even immunoparalysis? The heuristic vigor of these questions might inspire experimental efforts and clinical studies and ultimately advance the therapeutic armamentarium for sepsis care. ,Michael Bauer, Reinhard Wetzker [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [51] => Array ( [ArticleId] => 313 [Create_Time] => 2022-05-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202205/20220531081637.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100352/100352.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100352/100352.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100352/100352_cover.png [JournalsId] => 5 [Title] => Sensing of viral lung infections by cGAS-STING [Abstract] => Lower respiratory tract infections caused over 4 million deaths per year worldwide, especially in low-income countries. Viral respiratory infections often occur as rapidly spreading seasonal endemic [AbstractComplete] =>

Lower respiratory tract infections caused over 4 million deaths per year worldwide, especially in low-income countries. Viral respiratory infections often occur as rapidly spreading seasonal endemic or epidemic, and sometimes due to new respiratory viruses including corona viruses. The first level of host defense against viral infection is based on the innate immune system and intracellular killing mechanisms. The latter is activated by the release of viral DNA or RNA into the cytosol of the infected cells during the initial phase of virus replication. Viral DNA and RNA are recognized by the cyclic guanosine monophosphate (cGMP)-adenosine monophosphate (AMP) synthase (cGAS)–stimulator of interferon (IFN) genes (STING) sensing pathway, leading to the activation of type-I and -III IFN synthesis, with the aim to limit viral replication. However, the efficacy of the cGAS-STING sensing mechanism seems to vary with different viruses, and therefore, so is the efficacy of the host defense mechanism. Viral DNA can be sensed by different proteins including DNA-dependent activator of IFN regulating factor (DAI), cGAS, and toll-like receptor-9 (TLR-9). Viral RNA is recognized by retinoid acid-inducible gene 1 (RIG-1), TLR-7 and TLR-8. The question if cGAS also recognizes viral RNA remains unclear. The activation of IFN synthesis by cGAS is initiated by the recognition of purines and pyrimidines and their enzymatic conversion into cGMP and cyclic AMP (cAMP), followed by the activation of STING. In addition, it is indicated that several viruses can evade the cGAS-STING signaling and escape the host defense. This review aims to summarize the role of cGAS-STING as a host defense mechanism against viral respiratory tract infections.

[Names] => Lei Fang, Michael Roth [Doi] => 10.37349/ei.2022.00052 [Published] => May 30, 2022 [Viewed] => 1194 [Downloaded] => 37 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00052 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 65 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:303–319 [Recommend] => 0 [Keywords] => Asthma, cGAS-STING, chronic obstructive pulmonary disease, respiratory tract infection, viral host defense [DetailTitle] => DNA Sensing in Lung Inflammation [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/65 [Id] => 100352 [ris] => https://www.explorationpub.com/uploads/Article/A100352/54ac43c9cf5bc28151a3b879deb7d6f6.ris [bib] => https://www.explorationpub.com/uploads/Article/A100352/8400917269fc9b69fdd13d21dbba9a72.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-25 [CitethisArticle] => Fang L, Roth M. Sensing of viral lung infections by cGAS-STING. Explor Immunol. 2022;2:303–19. https://doi.org/10.37349/ei.2022.00052 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-05-31 08:19:17 [Bib_Time] => 2022-05-31 08:19:17 [KeysWordContens] => Sensing of viral lung infections by cGAS-STING, Asthma, cGAS-STING, chronic obstructive pulmonary disease, respiratory tract infection, viral host defense, Lower respiratory tract infections caused over 4 million deaths per year worldwide, especially in low-income countries. Viral respiratory infections often occur as rapidly spreading seasonal endemic or epidemic, and sometimes due to new respiratory viruses including corona viruses. The first level of host defense against viral infection is based on the innate immune system and intracellular killing mechanisms. The latter is activated by the release of viral DNA or RNA into the cytosol of the infected cells during the initial phase of virus replication. Viral DNA and RNA are recognized by the cyclic guanosine monophosphate (cGMP)-adenosine monophosphate (AMP) synthase (cGAS)–stimulator of interferon (IFN) genes (STING) sensing pathway, leading to the activation of type-I and -III IFN synthesis, with the aim to limit viral replication. However, the efficacy of the cGAS-STING sensing mechanism seems to vary with different viruses, and therefore, so is the efficacy of the host defense mechanism. Viral DNA can be sensed by different proteins including DNA-dependent activator of IFN regulating factor (DAI), cGAS, and toll-like receptor-9 (TLR-9). Viral RNA is recognized by retinoid acid-inducible gene 1 (RIG-1), TLR-7 and TLR-8. The question if cGAS also recognizes viral RNA remains unclear. The activation of IFN synthesis by cGAS is initiated by the recognition of purines and pyrimidines and their enzymatic conversion into cGMP and cyclic AMP (cAMP), followed by the activation of STING. In addition, it is indicated that several viruses can evade the cGAS-STING signaling and escape the host defense. This review aims to summarize the role of cGAS-STING as a host defense mechanism against viral respiratory tract infections. ,Lei Fang, Michael Roth [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [52] => Array ( [ArticleId] => 316 [Create_Time] => 2022-05-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202303/20230301092006.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100353/100353.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100353/100353.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100353/100353_cover.png [JournalsId] => 5 [Title] => Obesity and cancer: the gammadelta T cell link [Abstract] => Obesity has become a worldwide scourge, affecting more than 10% of adults worldwide. While widely recognized to be associated with increased incidence of medical conditions such as diabe [AbstractComplete] =>

Obesity has become a worldwide scourge, affecting more than 10% of adults worldwide. While widely recognized to be associated with increased incidence of medical conditions such as diabetes mellitus and atherosclerosis, obesity also accounts for 9% of the cancer burden in some populations. This is due in part to perturbation of protective immune mechanisms involving natural killer cells, macrophages, and neutrophils. Recent studies indicate that γδ T cells play a prominent protective role against cancer, but in some circumstances are detrimental and pro tumorogenic. In this review, the current scientific literature was explored to determine whether and how obesity affects the anti- and pro-tumoral functions of γδ T cells. Considerable perturbations of γδ T cells by obesity were revealed, suggesting that the “obesity-γδ T cell axis” may profoundly impact the increased incidence of cancer in obese individuals and is worthy of further study.

[Names] => Ilan Bank [Doi] => 10.37349/ei.2022.00053 [Published] => May 31, 2022 [Viewed] => 1173 [Downloaded] => 40 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00053 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 50 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:320–333 [Recommend] => 0 [Keywords] => Gammadelta T cells, obesity, interleukin-17, cancer [DetailTitle] => Interplay of γδ T cells and Tumor Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/50 [Id] => 100353 [ris] => https://www.explorationpub.com/uploads/Article/A100353/bba5ddc2debc9b8a56c25ebd832812ba.ris [bib] => https://www.explorationpub.com/uploads/Article/A100353/a69bd51ceb5ba152b95411f67dc9cfdb.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-25 [CitethisArticle] => Bank I. Obesity and cancer: the gammadelta T cell link. Explor Immunol. 2022;2:320–33. https://doi.org/10.37349/ei.2022.00053 [Jindex] => 0 [CName] => IlanBank, [CEmail] => ibank@tauex.tau.ac.il, [Ris_Time] => 2022-05-31 06:39:32 [Bib_Time] => 2022-05-31 06:39:32 [KeysWordContens] => Obesity and cancer: the gammadelta T cell link, Gammadelta T cells, obesity, interleukin-17, cancer, Obesity has become a worldwide scourge, affecting more than 10% of adults worldwide. While widely recognized to be associated with increased incidence of medical conditions such as diabetes mellitus and atherosclerosis, obesity also accounts for 9% of the cancer burden in some populations. This is due in part to perturbation of protective immune mechanisms involving natural killer cells, macrophages, and neutrophils. Recent studies indicate that γδ T cells play a prominent protective role against cancer, but in some circumstances are detrimental and pro tumorogenic. In this review, the current scientific literature was explored to determine whether and how obesity affects the anti- and pro-tumoral functions of γδ T cells. Considerable perturbations of γδ T cells by obesity were revealed, suggesting that the “obesity-γδ T cell axis” may profoundly impact the increased incidence of cancer in obese individuals and is worthy of further study. ,Ilan Bank [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [53] => Array ( [ArticleId] => 318 [Create_Time] => 2022-06-08 [zipUrl] => https://www.explorationpub.com/uploads/zip/202206/20220607110552.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100354/100354.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100354/100354.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100354/100354_cover.png [JournalsId] => 5 [Title] => Allogeneic gamma delta T cells as adoptive cellular therapy for hematologic malignancies [Abstract] => Cancer immunotherapy, especially T-cell driven targeting, has significantly evolved and improved over the past decade, paving the way to treat previously refractory cancers. Hematologic malignancies [AbstractComplete] =>

Cancer immunotherapy, especially T-cell driven targeting, has significantly evolved and improved over the past decade, paving the way to treat previously refractory cancers. Hematologic malignancies, given their direct tumor accessibility and less immunosuppressive microenvironment compared to solid tumors, are better suited to be targeted by cellular immunotherapies. Gamma delta (γδ) T cells, with their unique attributes spanning the entirety of the immune system, make a tantalizing therapeutic platform for cancer immunotherapy. Their inherent anti-tumor properties, ability to act like antigen-presenting cells, and the advantage of having no major histocompatibility complex (MHC) restrictions, allow for greater flexibility in their utility to target tumors, compared to their αβ T cell counterpart. Their MHC-independent anti-tumor activity, coupled with their ability to be easily expanded from peripheral blood, enhance their potential to be used as an allogeneic product. In this review, the potential of utilizing γδ T cells to target hematologic malignancies is described, with a specific focus on their applicability as an allogeneic adoptive cellular therapy product.

[Names] => Navdeep Jhita, Sunil S. Raikar [Doi] => 10.37349/ei.2022.00054 [Published] => June 07, 2022 [Viewed] => 2770 [Downloaded] => 103 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00054 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 50 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:334–350 [Recommend] => 0 [Keywords] => Gamma delta T cells, allogeneic, immunotherapy, leukemia, chimeric antigen receptor [DetailTitle] => Interplay of γδ T cells and Tumor Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/50 [Id] => 100354 [ris] => https://www.explorationpub.com/uploads/Article/A100354/3260d9d44afb171ec1fa8570b23516b2.ris [bib] => https://www.explorationpub.com/uploads/Article/A100354/9c262dffe9fb8474637af6499a02b5e1.bib [ens] => [Cited] => 11 [Cited_Time] => 2024-04-26 [CitethisArticle] => Jhita N, Raikar SS. Allogeneic gamma delta T cells as adoptive cellular therapy for hematologic malignancies. Explor Immunol. 2022;2:334–50. https://doi.org/10.37349/ei.2022.00054 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-06-02 05:40:47 [Bib_Time] => 2022-06-02 05:40:47 [KeysWordContens] => Allogeneic gamma delta T cells as adoptive cellular therapy for hematologic malignancies, Gamma delta T cells, allogeneic, immunotherapy, leukemia, chimeric antigen receptor, Cancer immunotherapy, especially T-cell driven targeting, has significantly evolved and improved over the past decade, paving the way to treat previously refractory cancers. Hematologic malignancies, given their direct tumor accessibility and less immunosuppressive microenvironment compared to solid tumors, are better suited to be targeted by cellular immunotherapies. Gamma delta (γδ) T cells, with their unique attributes spanning the entirety of the immune system, make a tantalizing therapeutic platform for cancer immunotherapy. Their inherent anti-tumor properties, ability to act like antigen-presenting cells, and the advantage of having no major histocompatibility complex (MHC) restrictions, allow for greater flexibility in their utility to target tumors, compared to their αβ T cell counterpart. Their MHC-independent anti-tumor activity, coupled with their ability to be easily expanded from peripheral blood, enhance their potential to be used as an allogeneic product. In this review, the potential of utilizing γδ T cells to target hematologic malignancies is described, with a specific focus on their applicability as an allogeneic adoptive cellular therapy product. ,Navdeep Jhita, Sunil S. Raikar [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [54] => Array ( [ArticleId] => 319 [Create_Time] => 2022-06-08 [zipUrl] => https://www.explorationpub.com/uploads/zip/202303/20230301092328.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100355/100355.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100355/100355.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100355/100355_cover.png [JournalsId] => 5 [Title] => The influence of reproductive hormones on systemic lupus erythematosus [Abstract] => Humans are afflicted by a wide spectrum of autoimmune disorders, ranging from those affecting just one or a few organs to those associated with more systemic effects. In most instances, the etiology [AbstractComplete] =>

Humans are afflicted by a wide spectrum of autoimmune disorders, ranging from those affecting just one or a few organs to those associated with more systemic effects. In most instances, the etiology of such disorders remains unknown; a consequence of this lack of knowledge is a lack of specific treatment options. Systemic lupus erythematosus (SLE) is the prototypic systemic autoimmune disorder; pathology is believed to be antibody-mediated, and multiple organs are targeted. Periods of disease “flares” are often followed by long periods of remission. The fact that SLE is more commonly observed in females, and also that it more particularly manifests in females in the reproductive age group, has quite naturally drawn attention to the potential roles that hormones play in disease onset and progression. This review attempts to shed light on the influences that key hormones might have on disease indicators and pathology. Databases (Google Scholar, PubMed) were searched for the following keywords (sometimes in certain combinations), in conjunction with the term “lupus” or “SLE”: autoantibodies, recurrent abortion, polycystic ovarian syndrome (PCOS), preeclampsia, pre-term delivery, estrogens, progesterone, androgens, prolactin, leptin, human chorionic gonadotropin (hCG). Cited publications included both research articles and reviews.

[Names] => Ruchi Sachdeva, Rahul Pal [Doi] => 10.37349/ei.2022.00055 [Published] => June 07, 2022 [Viewed] => 2452 [Downloaded] => 40 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00055 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:351–362 [Recommend] => 0 [Keywords] => Autoimmune diseases, systemic lupus erythematosus, sex steroids, prolactin, leptin, human chorionic gonadotropin, reproductive dysfunction [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100355 [ris] => https://www.explorationpub.com/uploads/Article/A100355/8a45a1abd0a6fbef9d546695c5a677d9.ris [bib] => https://www.explorationpub.com/uploads/Article/A100355/7b7b426a827b2f5a0610f2a02a115ea3.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Sachdeva R, Pal R. The influence of reproductive hormones on systemic lupus erythematosus. Explor Immunol. 2022;2:351–62. https://doi.org/10.37349/ei.2022.00055 [Jindex] => 0 [CName] => RahulPal, [CEmail] => rahul@nii.ac.in, [Ris_Time] => 2022-06-02 07:14:30 [Bib_Time] => 2022-06-02 07:14:30 [KeysWordContens] => The influence of reproductive hormones on systemic lupus erythematosus, Autoimmune diseases, systemic lupus erythematosus, sex steroids, prolactin, leptin, human chorionic gonadotropin, reproductive dysfunction, Humans are afflicted by a wide spectrum of autoimmune disorders, ranging from those affecting just one or a few organs to those associated with more systemic effects. In most instances, the etiology of such disorders remains unknown; a consequence of this lack of knowledge is a lack of specific treatment options. Systemic lupus erythematosus (SLE) is the prototypic systemic autoimmune disorder; pathology is believed to be antibody-mediated, and multiple organs are targeted. Periods of disease “flares” are often followed by long periods of remission. The fact that SLE is more commonly observed in females, and also that it more particularly manifests in females in the reproductive age group, has quite naturally drawn attention to the potential roles that hormones play in disease onset and progression. This review attempts to shed light on the influences that key hormones might have on disease indicators and pathology. Databases (Google Scholar, PubMed) were searched for the following keywords (sometimes in certain combinations), in conjunction with the term “lupus” or “SLE”: autoantibodies, recurrent abortion, polycystic ovarian syndrome (PCOS), preeclampsia, pre-term delivery, estrogens, progesterone, androgens, prolactin, leptin, human chorionic gonadotropin (hCG). Cited publications included both research articles and reviews. ,Ruchi Sachdeva, Rahul Pal [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [55] => Array ( [ArticleId] => 322 [Create_Time] => 2022-06-14 [zipUrl] => https://www.explorationpub.com/uploads/zip/202206/20220614004214.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100356/100356.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100356/100356.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100356/100356_cover.png [JournalsId] => 5 [Title] => Inviting regulatory T cells to pregnant endometrium: friends or foes in adverse pregnancy outcomes? [Abstract] => Among decidual immune cells, regulatory T cells (Tregs) have been unanimously recognized as central contributors to tolerance and maintenance of healthy pregnancy. Numerical and functional downregul [AbstractComplete] =>

Among decidual immune cells, regulatory T cells (Tregs) have been unanimously recognized as central contributors to tolerance and maintenance of healthy pregnancy. Numerical and functional downregulation of Tregs or disturbed interaction of Tregs with trophoblasts and other immune cells have been linked to early pregnancy loss such as idiopathic infertility and miscarriage and later-onset adverse pregnancy outcomes including preeclampsia. This review focuses on the mechanisms for regulating the generation, expansion, and function of Tregs, the roles of Tregs in maintaining maternal immune tolerance through crosstalk with trophoblasts and other decidual regulatory immune cells, and how Tregs may play foes to pregnancy and contribute to the programming of pregnancy-related complications. Therapeutic options for implantation failure and adverse pregnancy outcomes are now part of the emerging significance of Tregs in pregnancy tolerance and maintenance.

[Names] => Shibin Cheng ... Surendra Sharma [Doi] => 10.37349/ei.2022.00056 [Published] => June 13, 2022 [Viewed] => 1080 [Downloaded] => 24 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00056 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:363–382 [Recommend] => 0 [Keywords] => Regulatory T cells, immune tolerance, pregnancy, trophoblast, natural killer cell [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100356 [ris] => https://www.explorationpub.com/uploads/Article/A100356/89de21aaf60ccae57bd52145eaa18d62.ris [bib] => https://www.explorationpub.com/uploads/Article/A100356/4472ec7fb046de7892fd5ae8f00bb0f2.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Cheng S, Wang Z, Sharma S. Inviting regulatory T cells to pregnant endometrium: friends or foes in adverse pregnancy outcomes? Explor Immunol. 2022;2:363–82. https://doi.org/10.37349/ei.2022.00056 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-06-14 00:45:31 [Bib_Time] => 2022-06-14 00:45:31 [KeysWordContens] => Inviting regulatory T cells to pregnant endometrium: friends or foes in adverse pregnancy outcomes?, Regulatory T cells, immune tolerance, pregnancy, trophoblast, natural killer cell, Among decidual immune cells, regulatory T cells (Tregs) have been unanimously recognized as central contributors to tolerance and maintenance of healthy pregnancy. Numerical and functional downregulation of Tregs or disturbed interaction of Tregs with trophoblasts and other immune cells have been linked to early pregnancy loss such as idiopathic infertility and miscarriage and later-onset adverse pregnancy outcomes including preeclampsia. This review focuses on the mechanisms for regulating the generation, expansion, and function of Tregs, the roles of Tregs in maintaining maternal immune tolerance through crosstalk with trophoblasts and other decidual regulatory immune cells, and how Tregs may play foes to pregnancy and contribute to the programming of pregnancy-related complications. Therapeutic options for implantation failure and adverse pregnancy outcomes are now part of the emerging significance of Tregs in pregnancy tolerance and maintenance. ,Shibin Cheng ... Surendra Sharma [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [56] => Array ( [ArticleId] => 324 [Create_Time] => 2022-06-17 [zipUrl] => https://www.explorationpub.com/uploads/zip/202206/20220616055701.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100357/100357.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100357/100357.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100357/100357_cover.png [JournalsId] => 5 [Title] => A multispectral immunohistochemistry panel to investigate γδ T cells and butyrophilin molecules in the tumour microenvironment [Abstract] => Conventional immunohistochemistry methods though once fundamental for the individual staining of cell markers, have now been superseded by multispectral immunohistochemistry (mIHC). mIHC enables sim [AbstractComplete] =>

Conventional immunohistochemistry methods though once fundamental for the individual staining of cell markers, have now been superseded by multispectral immunohistochemistry (mIHC). mIHC enables simultaneous detection of multiple cell markers in situ using single formalin-fixed paraffin-embedded (FFPE) tissue sections. In addition to conserving patient tissue specimens, the ability to visualise more than one marker on individual cells allows for further refining of cell phenotypes, and provides insight into cell-to-cell interactions and spatial arrangements across single tissue sections. Here, a comprehensive protocol is described for the in situ interrogation of γδ T cells and phosphoantigen-presenting butyrophilin (BTN) molecules (BTN2A1 and BTN3A1) in human FFPE tissue using Opal™ tyramide signal amplification (TSA)-based mIHC. It is demonstrated that an effectively optimised Opal™-TSA 7-marker [CD3, Pan-γδ T cell receptor (TCR), granzyme B, BTN2A1, BTN3A1, tumour marker, 4’,6-diamidino-2-phenylindole (DAPI)] mIHC panel can be used to define the presence, localisation, and activation status of γδ T cells and the BTN2A1 and BTN3A1 ligands.

[Names] => Jessica Da Gama Duarte ... Andreas Behren [Doi] => 10.37349/ei.2022.00057 [Published] => June 16, 2022 [Viewed] => 1558 [Downloaded] => 53 [Subject] => Protocol [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00057 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 50 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:383–392 [Recommend] => 0 [Keywords] => γδT cells, multispectral immunohistochemistry, butyrophilin [DetailTitle] => Interplay of γδ T cells and Tumor Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/50 [Id] => 100357 [ris] => https://www.explorationpub.com/uploads/Article/A100357/7d619fb7c8a2611c25300b06dd2371f2.ris [bib] => https://www.explorationpub.com/uploads/Article/A100357/e057336cc034927c8f5af00d7936aa2f.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-26 [CitethisArticle] => Da Gama Duarte J, Quigley LT, Tavancheh E, Ostrouska S, Behren A. A multispectral immunohistochemistry panel to investigate γδ T cells and butyrophilin molecules in the tumour microenvironment. Explor Immunol. 2022;2:383–92. https://doi.org/10.37349/ei.2022.00057 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-06-15 03:47:19 [Bib_Time] => 2022-06-15 03:47:19 [KeysWordContens] => A multispectral immunohistochemistry panel to investigate γδ T cells and butyrophilin molecules in the tumour microenvironment, γδT cells, multispectral immunohistochemistry, butyrophilin, Conventional immunohistochemistry methods though once fundamental for the individual staining of cell markers, have now been superseded by multispectral immunohistochemistry (mIHC). mIHC enables simultaneous detection of multiple cell markers in situ using single formalin-fixed paraffin-embedded (FFPE) tissue sections. In addition to conserving patient tissue specimens, the ability to visualise more than one marker on individual cells allows for further refining of cell phenotypes, and provides insight into cell-to-cell interactions and spatial arrangements across single tissue sections. Here, a comprehensive protocol is described for the in situ interrogation of γδ T cells and phosphoantigen-presenting butyrophilin (BTN) molecules (BTN2A1 and BTN3A1) in human FFPE tissue using Opal™ tyramide signal amplification (TSA)-based mIHC. It is demonstrated that an effectively optimised Opal™-TSA 7-marker [CD3, Pan-γδ T cell receptor (TCR), granzyme B, BTN2A1, BTN3A1, tumour marker, 4’,6-diamidino-2-phenylindole (DAPI)] mIHC panel can be used to define the presence, localisation, and activation status of γδ T cells and the BTN2A1 and BTN3A1 ligands. ,Jessica Da Gama Duarte ... Andreas Behren [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [57] => Array ( [ArticleId] => 327 [Create_Time] => 2022-06-27 [zipUrl] => https://www.explorationpub.com/uploads/zip/202206/20220628063003.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100358/100358.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100358/100358.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100358/100358_cover.png [JournalsId] => 5 [Title] => Polycystic ovary syndrome and immune deregulation: what do hormones want to say? [Abstract] => Polycystic ovary syndrome (PCOS) is one of the most frequently observed endocrinopathies among women of reproductive age that redound to subfertility. The specific etiology of this heterogenic syndr [AbstractComplete] =>

Polycystic ovary syndrome (PCOS) is one of the most frequently observed endocrinopathies among women of reproductive age that redound to subfertility. The specific etiology of this heterogenic syndrome remains ambiguous. Metabolic complications, hormonal imbalance, deregulation in the immune system and their interrelationship make PCOS more complex. Hyperandrogenism and chronic low-grade inflammation modulate each other and enhance the self-perpetuation of PCOS. Even though there are many literature studies on PCOS and immune deregulation, this review focuses on the endocrine-immune nexus and how the altered endocrine system is embroiled in the immunopathology of PCOS.

[Names] => Betcy Susan Johnson, Malini Laloraya [Doi] => 10.37349/ei.2022.00058 [Published] => June 27, 2022 [Viewed] => 1847 [Downloaded] => 56 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00058 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:393–413 [Recommend] => 0 [Keywords] => Polycystic ovary syndrome, hyperandrogenism, immune deregulation, inflammation, autoimmunity [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100358 [ris] => https://www.explorationpub.com/uploads/Article/A100358/173f74914aa4258cb22d84befe927168.ris [bib] => https://www.explorationpub.com/uploads/Article/A100358/9d9c5f792390a9f1a0f008787c7e9076.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Johnson BS, Laloraya M. Polycystic ovary syndrome and immune deregulation: what do hormones want to say? Explor Immunol. 2022;2:393–413. https://doi.org/10.37349/ei.2022.00058 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-06-17 06:44:02 [Bib_Time] => 2022-06-17 06:44:02 [KeysWordContens] => Polycystic ovary syndrome and immune deregulation: what do hormones want to say?, Polycystic ovary syndrome, hyperandrogenism, immune deregulation, inflammation, autoimmunity, Polycystic ovary syndrome (PCOS) is one of the most frequently observed endocrinopathies among women of reproductive age that redound to subfertility. The specific etiology of this heterogenic syndrome remains ambiguous. Metabolic complications, hormonal imbalance, deregulation in the immune system and their interrelationship make PCOS more complex. Hyperandrogenism and chronic low-grade inflammation modulate each other and enhance the self-perpetuation of PCOS. Even though there are many literature studies on PCOS and immune deregulation, this review focuses on the endocrine-immune nexus and how the altered endocrine system is embroiled in the immunopathology of PCOS. ,Betcy Susan Johnson, Malini Laloraya [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [58] => Array ( [ArticleId] => 333 [Create_Time] => 2022-06-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202303/20230301093617.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100359/100359.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100359/100359.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100359/100359_cover.png [JournalsId] => 5 [Title] => Cytokines and pregnancy complications: modulation for prevention and treatment [Abstract] => “There is many a slip twist the cup and the lip” is a proverb that dates back to the 3rd century. This proverb comes to mind while writing a review on pregnancy loss; so many complications can occur between fertilization and development of the embryo through the long period of gestation until successful delivery of the baby. These include failure of implantation of the embryo, spontaneous miscarriage in the first trimester, pre-eclampsia in the second trimester, premature rupture of fetal membranes, pre-term labour, and pre-term delivery. The maternal immune system which does a phenomenal job of protecting the host from a daunting variety of infections, sometimes also mounts adverse reactions that complicate pregnancy and endanger the fetus. Maternal immune reactions that can adversely affect pregnancy have been shown to be mediated by lymphocytes, macrophages and natural killer cells, and by cytokines secreted by these cellular effectors. This review summarizes the deleterious effects of cytokines leading to recurrent spontaneous miscarriage, pre-eclampsia and pre-term delivery, which are the major complications of pregnancy. It then goes on to discuss the potential use of progesterone and dydrogesterone, an orally-administered progestogen, as immunomodulatory molecules that can be considered for the prevention and/or treatment of these complications. [AbstractComplete] =>

“There is many a slip twist the cup and the lip” is a proverb that dates back to the 3rd century. This proverb comes to mind while writing a review on pregnancy loss; so many complications can occur between fertilization and development of the embryo through the long period of gestation until successful delivery of the baby. These include failure of implantation of the embryo, spontaneous miscarriage in the first trimester, pre-eclampsia in the second trimester, premature rupture of fetal membranes, pre-term labour, and pre-term delivery. The maternal immune system which does a phenomenal job of protecting the host from a daunting variety of infections, sometimes also mounts adverse reactions that complicate pregnancy and endanger the fetus. Maternal immune reactions that can adversely affect pregnancy have been shown to be mediated by lymphocytes, macrophages and natural killer cells, and by cytokines secreted by these cellular effectors. This review summarizes the deleterious effects of cytokines leading to recurrent spontaneous miscarriage, pre-eclampsia and pre-term delivery, which are the major complications of pregnancy. It then goes on to discuss the potential use of progesterone and dydrogesterone, an orally-administered progestogen, as immunomodulatory molecules that can be considered for the prevention and/or treatment of these complications.

[Names] => Raj Raghupathy [Doi] => 10.37349/ei.2022.00059 [Published] => June 27, 2022 [Viewed] => 1504 [Downloaded] => 61 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00059 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:414–427 [Recommend] => 0 [Keywords] => Cytokines, recurrent miscarriage, pre-eclampsia, pre-term labour, progesterone, dydrogesterone [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100359 [ris] => https://www.explorationpub.com/uploads/Article/A100359/0a1983dc899ebc22aad96e7f28d39e98.ris [bib] => https://www.explorationpub.com/uploads/Article/A100359/e23dc0adf12a94d003bdbccf498073d7.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Raghupathy R. Cytokines and pregnancy complications: modulation for prevention and treatment. Explor Immunol. 2022;2:414–27. https://doi.org/10.37349/ei.2022.00059 [Jindex] => 0 [CName] => RajRaghupathy, [CEmail] => raj.raghupathy@ku.edu.kw, [Ris_Time] => 2022-06-23 07:43:27 [Bib_Time] => 2022-06-23 07:43:27 [KeysWordContens] => Cytokines and pregnancy complications: modulation for prevention and treatment, Cytokines, recurrent miscarriage, pre-eclampsia, pre-term labour, progesterone, dydrogesterone, “There is many a slip twist the cup and the lip” is a proverb that dates back to the 3rd century. This proverb comes to mind while writing a review on pregnancy loss; so many complications can occur between fertilization and development of the embryo through the long period of gestation until successful delivery of the baby. These include failure of implantation of the embryo, spontaneous miscarriage in the first trimester, pre-eclampsia in the second trimester, premature rupture of fetal membranes, pre-term labour, and pre-term delivery. The maternal immune system which does a phenomenal job of protecting the host from a daunting variety of infections, sometimes also mounts adverse reactions that complicate pregnancy and endanger the fetus. Maternal immune reactions that can adversely affect pregnancy have been shown to be mediated by lymphocytes, macrophages and natural killer cells, and by cytokines secreted by these cellular effectors. This review summarizes the deleterious effects of cytokines leading to recurrent spontaneous miscarriage, pre-eclampsia and pre-term delivery, which are the major complications of pregnancy. It then goes on to discuss the potential use of progesterone and dydrogesterone, an orally-administered progestogen, as immunomodulatory molecules that can be considered for the prevention and/or treatment of these complications. ,Raj Raghupathy [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [59] => Array ( [ArticleId] => 335 [Create_Time] => 2022-06-29 [zipUrl] => https://www.explorationpub.com/uploads/zip/202206/20220629005315.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100360/100360.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100360/100360.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100360/100360_cover.png [JournalsId] => 5 [Title] => Advances in innate immune memory of macrophages [Abstract] => Immunity is usually classified into two categories: innate immunity and adaptive immunity, distinguished by the process and characteristics of the immunological impact. It was widely assumed that on [AbstractComplete] =>

Immunity is usually classified into two categories: innate immunity and adaptive immunity, distinguished by the process and characteristics of the immunological impact. It was widely assumed that only adaptive immunity possessed memory features; however, current research has revealed that innate immunity, like adaptive immunity, possesses memory properties as well. “Trained immunity”, also known as “innate immune memory”, is a phenomenon that occurs when the immune system’s innate cells are stimulated and then undergo epigenetic reprogramming and metabolic alterations. When it comes to innate immunity, macrophages are essential since they have immunological memory capabilities and play a significant role in the body’s immunity. The concept of innate immune memory expands the definition of immunological memory and offers a broader view of immune response research. This article reviews the properties, mechanism, and significance of macrophage innate immune memory in disease.

[Names] => Safir Ullah Khan, Munir Ullah Khan [Doi] => 10.37349/ei.2022.00060 [Published] => June 28, 2022 [Viewed] => 1804 [Downloaded] => 83 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00060 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:428–441 [Recommend] => 0 [Keywords] => Macrophage, innate immune memory, epigenetic reprogramming, trained immunity [DetailTitle] => [DetailUrl] => [Id] => 100360 [ris] => https://www.explorationpub.com/uploads/Article/A100360/8a4fa57b0a617115b994d2f3972c430d.ris [bib] => https://www.explorationpub.com/uploads/Article/A100360/796d5aca3b621d429e2205ccab24a4db.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Khan SU, Khan MU. Advances in innate immune memory of macrophages. Explor Immunol. 2022;2:428–41. https://doi.org/10.37349/ei.2022.00060 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-06-27 03:39:19 [Bib_Time] => 2022-06-27 03:39:19 [KeysWordContens] => Advances in innate immune memory of macrophages, Macrophage, innate immune memory, epigenetic reprogramming, trained immunity, Immunity is usually classified into two categories: innate immunity and adaptive immunity, distinguished by the process and characteristics of the immunological impact. It was widely assumed that only adaptive immunity possessed memory features; however, current research has revealed that innate immunity, like adaptive immunity, possesses memory properties as well. “Trained immunity”, also known as “innate immune memory”, is a phenomenon that occurs when the immune system’s innate cells are stimulated and then undergo epigenetic reprogramming and metabolic alterations. When it comes to innate immunity, macrophages are essential since they have immunological memory capabilities and play a significant role in the body’s immunity. The concept of innate immune memory expands the definition of immunological memory and offers a broader view of immune response research. This article reviews the properties, mechanism, and significance of macrophage innate immune memory in disease. ,Safir Ullah Khan, Munir Ullah Khan [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [60] => Array ( [ArticleId] => 345 [Create_Time] => 2022-07-18 [zipUrl] => https://www.explorationpub.com/uploads/zip/202207/20220715082725.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100361/100361.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100361/100361.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100361/100361_cover.png [JournalsId] => 5 [Title] => In COVID-19, antigen size lower or larger than 70 kDa modulates the sepsis and memory B cells [Abstract] => This review pretends to shed light on the immune processes occurring in the coronavirus disease 2019 (COVID-19) from a perspective based on the antigens size, lower or larger than 70 kDa. This cutof [AbstractComplete] =>

This review pretends to shed light on the immune processes occurring in the coronavirus disease 2019 (COVID-19) from a perspective based on the antigens size, lower or larger than 70 kDa. This cutoff size point explains the host type of immune response against the antigenic proteins of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which may lead to the development of the memory B cells or, conversely, the immune suppression, apoptosis, viral escape, and sepsis. Here, based on previous experimental work and the review of related literature, the following is proposed: antigens < 70 kDa can access the germinal center through the follicular conduits, where the activated B cells can present the processed antigen to specific naive CD4+ T cells that, in interaction with the major histocompatibility complex class II (MHC-II), trigger the immune response T helper type 2 (Th2). Conversely, antigens > 70 kDa cannot circulate through the narrow follicular conduits network and might be captured within the subcapsular sinus by the macrophages and dendritic follicular cells. Then, these cognate antigens are presented, via complement receptors, to the B cells that acquire and present them through the MHC-II to the specific naive CD4+ T cells, triggering the immune response Th1. The sustained infected cells lysis can overfeed high levels of unassembled viral proteins < 70 kDa, which can lead to a strong and persistent B cell receptor (BCR) activation, enhancing the Th2 immune response, releasing interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β) that may lead to the immune paralysis, apoptosis, sepsis, and death. Finally, it is suggested that the polymerization of the viral antigens < 70 kDa into an antigenic polymer > 70 kDa could shift the immune response type from Th2 to Th1, developing the memory B cells and immunoglobulin G2 (IgG2) production, and avoiding the sepsis.

[Names] => Francisco Javier Martín Oncina [Doi] => 10.37349/ei.2022.00061 [Published] => July 17, 2022 [Viewed] => 1195 [Downloaded] => 33 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00061 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 53 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:442–453 [Recommend] => 0 [Keywords] => Coronavirus disease 2019, severe acute respiratory syndrome coronavirus 2, 70 kDa, antigen size, T helper type 1, T helper type 2, sepsis, immune memory [DetailTitle] => The‌ ‌Sepsis‌ ‌induced‌ ‌Immune‌ ‌Conundrum [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/53 [Id] => 100361 [ris] => https://www.explorationpub.com/uploads/Article/A100361/6d87deee2c91b62db3b2e163593ba89a.ris [bib] => https://www.explorationpub.com/uploads/Article/A100361/1b22e46864361464b35e3390012b3894.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Martín Oncina FJ. In COVID-19, antigen size lower or larger than 70 kDa modulates the sepsis and memory B cells. Explor Immunol. 2022;2:442–53. https://doi.org/10.37349/ei.2022.00061 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-07-15 02:48:12 [Bib_Time] => 2022-07-15 02:48:12 [KeysWordContens] => In COVID-19, antigen size lower or larger than 70 kDa modulates the sepsis and memory B cells, Coronavirus disease 2019, severe acute respiratory syndrome coronavirus 2, 70 kDa, antigen size, T helper type 1, T helper type 2, sepsis, immune memory, This review pretends to shed light on the immune processes occurring in the coronavirus disease 2019 (COVID-19) from a perspective based on the antigens size, lower or larger than 70 kDa. This cutoff size point explains the host type of immune response against the antigenic proteins of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which may lead to the development of the memory B cells or, conversely, the immune suppression, apoptosis, viral escape, and sepsis. Here, based on previous experimental work and the review of related literature, the following is proposed: antigens < 70 kDa can access the germinal center through the follicular conduits, where the activated B cells can present the processed antigen to specific naive CD4+ T cells that, in interaction with the major histocompatibility complex class II (MHC-II), trigger the immune response T helper type 2 (Th2). Conversely, antigens > 70 kDa cannot circulate through the narrow follicular conduits network and might be captured within the subcapsular sinus by the macrophages and dendritic follicular cells. Then, these cognate antigens are presented, via complement receptors, to the B cells that acquire and present them through the MHC-II to the specific naive CD4+ T cells, triggering the immune response Th1. The sustained infected cells lysis can overfeed high levels of unassembled viral proteins < 70 kDa, which can lead to a strong and persistent B cell receptor (BCR) activation, enhancing the Th2 immune response, releasing interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β) that may lead to the immune paralysis, apoptosis, sepsis, and death. Finally, it is suggested that the polymerization of the viral antigens < 70 kDa into an antigenic polymer > 70 kDa could shift the immune response type from Th2 to Th1, developing the memory B cells and immunoglobulin G2 (IgG2) production, and avoiding the sepsis. ,Francisco Javier Martín Oncina [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [61] => Array ( [ArticleId] => 347 [Create_Time] => 2022-07-27 [zipUrl] => https://www.explorationpub.com/uploads/zip/202207/20220727003603.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100362/100362.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100362/100362.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100362/100362_cover.png [JournalsId] => 5 [Title] => Endometriosis through an immunological lens: a pathophysiology based in immune dysregulation [Abstract] => Endometriosis (EMS) is an inflammatory, gynaecologic disease characterized by the growth of endometrial tissues outside the uterus. With no satisfactory therapies or non-invasive diagnostics availab [AbstractComplete] =>

Endometriosis (EMS) is an inflammatory, gynaecologic disease characterized by the growth of endometrial tissues outside the uterus. With no satisfactory therapies or non-invasive diagnostics available, a shift in perspectives on EMS pathophysiology is overdue. The implication of immune dysregulation in EMS pathogenesis and disease progression has been an evolving area of research, with numerous immune and inflammatory pathways identified. Traditional theories regarding the establishment of endometriotic lesions have lacked mechanistic explanations for their proliferation and survival until recent research unearthed the involvement of mesenchymal stem cell (MSC) and myeloid-derived suppressor cells (MDSCs) in a complex network of immune-endocrine signaling. The unique immunology of EMS is likely owing to estrogen dominance, as endocrine imbalance reliably cultivates immune dysregulation. Many of the phenomena observed in EMS parallel immune biology seen in various cancers, including accelerated somatic mutations in endometrial epithelial cells. Here, the high mutational load leads to EMS neoantigen development which potentially contributes to the lesion immune microenvironment. As well, EMS manifests comorbidity with several chronic inflammatory diseases that share common dysregulation of the interleukin-23 (IL-23)/IL-17 pathway (as seen in inflammatory bowel disease, psoriasis, and rheumatoid arthritis). EMS is especially relevant to the study of chronic pelvic pain (CPP) as 60% of EMS patients experience this symptom and chronic inflammation is believed to be central to the process of pain sensitization. Since the onset of the disease usually occurs in adolescence, and diagnosis only occurs years later once moderate to severe symptoms have developed, it is vital to innovate non-invasive diagnostic tools for earlier detection. Several potential biomarkers are being studied, including some cytokines, gene signatures, and extracellular vesicle (EV) signatures. By incorporating the immune perspectives of EMS into our research, approaches to diagnosis, and treatment solutions, the field has more promising avenues to clearly define EMS and offer patients relief.

[Names] => Alison McCallion ... Chandrakant Tayade [Doi] => 10.37349/ei.2022.00062 [Published] => July 26, 2022 [Viewed] => 1399 [Downloaded] => 62 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00062 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:454–483 [Recommend] => 0 [Keywords] => Endometriosis, immune dysregulation, mesenchymal stem cells, somatic mutation, estrogen dominance, chronic inflammation, cytokine pathways, extracellular vesicles [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100362 [ris] => https://www.explorationpub.com/uploads/Article/A100362/e82dbb0a71f043f6de34792e6bb1d879.ris [bib] => https://www.explorationpub.com/uploads/Article/A100362/0a694475a327af72571f75be25bcc016.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => McCallion A, Sisnett DJ, Zutautas KB, Hayati D, Spiess KG, Aleksieva S, et al. Endometriosis through an immunological lens: a pathophysiology based in immune dysregulation. Explor Immunol. 2022;2:454–83. https://doi.org/10.37349/ei.2022.00062 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-07-21 10:15:41 [Bib_Time] => 2022-07-21 10:15:41 [KeysWordContens] => Endometriosis through an immunological lens: a pathophysiology based in immune dysregulation, Endometriosis, immune dysregulation, mesenchymal stem cells, somatic mutation, estrogen dominance, chronic inflammation, cytokine pathways, extracellular vesicles, Endometriosis (EMS) is an inflammatory, gynaecologic disease characterized by the growth of endometrial tissues outside the uterus. With no satisfactory therapies or non-invasive diagnostics available, a shift in perspectives on EMS pathophysiology is overdue. The implication of immune dysregulation in EMS pathogenesis and disease progression has been an evolving area of research, with numerous immune and inflammatory pathways identified. Traditional theories regarding the establishment of endometriotic lesions have lacked mechanistic explanations for their proliferation and survival until recent research unearthed the involvement of mesenchymal stem cell (MSC) and myeloid-derived suppressor cells (MDSCs) in a complex network of immune-endocrine signaling. The unique immunology of EMS is likely owing to estrogen dominance, as endocrine imbalance reliably cultivates immune dysregulation. Many of the phenomena observed in EMS parallel immune biology seen in various cancers, including accelerated somatic mutations in endometrial epithelial cells. Here, the high mutational load leads to EMS neoantigen development which potentially contributes to the lesion immune microenvironment. As well, EMS manifests comorbidity with several chronic inflammatory diseases that share common dysregulation of the interleukin-23 (IL-23)/IL-17 pathway (as seen in inflammatory bowel disease, psoriasis, and rheumatoid arthritis). EMS is especially relevant to the study of chronic pelvic pain (CPP) as 60% of EMS patients experience this symptom and chronic inflammation is believed to be central to the process of pain sensitization. Since the onset of the disease usually occurs in adolescence, and diagnosis only occurs years later once moderate to severe symptoms have developed, it is vital to innovate non-invasive diagnostic tools for earlier detection. Several potential biomarkers are being studied, including some cytokines, gene signatures, and extracellular vesicle (EV) signatures. By incorporating the immune perspectives of EMS into our research, approaches to diagnosis, and treatment solutions, the field has more promising avenues to clearly define EMS and offer patients relief. ,Alison McCallion ... Chandrakant Tayade [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [62] => Array ( [ArticleId] => 348 [Create_Time] => 2022-08-11 [zipUrl] => https://www.explorationpub.com/uploads/zip/202208/20220810065600.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100363/100363.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100363/100363.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100363/100363_cover.png [JournalsId] => 5 [Title] => Small molecules targeting endolysosomal acidification and signaling in sepsis and severe SARS-CoV-2 infection/COVID-19 [Abstract] => Sepsis and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and its severe form coronavirus disease 2019 (COVID-19), represent the major medical challenges of the modern era. [AbstractComplete] =>

Sepsis and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and its severe form coronavirus disease 2019 (COVID-19), represent the major medical challenges of the modern era. Therapeutic options are limited, mostly symptomatic, partially relying on antibodies and corticosteroids and, in the case of SARS-CoV-2 infection, supplemented by the antiviral drug remdesivir, and more recently by molnupiravir, nirmatrelvir/ritonavir, and the Janus kinase (JAK) inhibitors tofacitinib and baricitinib. Sepsis and severe SARS-CoV-2 infection/COVID-19 share many features at the level of pathophysiology and pro-inflammatory mediators, thus enabling a common disease management strategy. New ideas in successfully targeting the prognostic severity and mortality marker pentraxin 3 (PTX3) in sepsis and severe SARS-CoV-2 infection/COVID-19; the complement (C3/C3a/C3aR and C5/C5a/C5aR axis); tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 expression; IL-6-triggered expression of C5aR receptor in vascular endothelial cells; and release of anti-inflammatory IL-10 are still missing. Small molecules with lysosomotropic characteristics such as the approved drugs amitriptyline, desloratadine, fluvoxamine, azelastine, and ambroxol have demonstrated their clinical benefits in rodent models of sepsis or clinical trials in COVID-19; however, their exact mode of action remains to be fully elucidated. Addressing disease-relevant targets such as viral infection of host cells, shedding of toll-like receptors (TLRs), expression of pro-inflammatory mediators such as TNF-α, IL-1β, IL-6, PTX3, and the complement receptor C5aR, highlight the advantages of this multi-target approach in comparison to current standards. Rational drug repurposing of approved drugs or screening for active compounds with virtually exclusively lysosomotropic pharmacologic effects is a major opportunity to improve prophylaxis and treatment of sepsis and/or SARS-CoV-2 infection, and its severe form COVID-19.

[Names] => Markus Blaess ... Hans-Peter Deigner [Doi] => 10.37349/ei.2022.00063 [Published] => August 11, 2022 [Viewed] => 1188 [Downloaded] => 35 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00063 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 53 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:484–509 [Recommend] => 0 [Keywords] => Sepsis, COVID-19, small molecules, lysosomotropism, drug repurposing, antibodies, lysosome, metabolites [DetailTitle] => The‌ ‌Sepsis‌ ‌induced‌ ‌Immune‌ ‌Conundrum [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/53 [Id] => 100363 [ris] => https://www.explorationpub.com/uploads/Article/A100363/237340ccde3c07cb0b0cdcf1ccbee957.ris [bib] => https://www.explorationpub.com/uploads/Article/A100363/be22ed4a9d24260212fe5d0619cd3f20.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Blaess M, Sommerfeld O, Csuk R, Deigner HP. Small molecules targeting endolysosomal acidification and signaling in sepsis and severe SARS-CoV-2 infection/COVID-19. 2022;2:484–509. https://doi.org/10.37349/ei.2022.00063 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-08-08 06:07:48 [Bib_Time] => 2022-08-08 06:07:48 [KeysWordContens] => Small molecules targeting endolysosomal acidification and signaling in sepsis and severe SARS-CoV-2 infection/COVID-19, Sepsis, COVID-19, small molecules, lysosomotropism, drug repurposing, antibodies, lysosome, metabolites, Sepsis and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and its severe form coronavirus disease 2019 (COVID-19), represent the major medical challenges of the modern era. Therapeutic options are limited, mostly symptomatic, partially relying on antibodies and corticosteroids and, in the case of SARS-CoV-2 infection, supplemented by the antiviral drug remdesivir, and more recently by molnupiravir, nirmatrelvir/ritonavir, and the Janus kinase (JAK) inhibitors tofacitinib and baricitinib. Sepsis and severe SARS-CoV-2 infection/COVID-19 share many features at the level of pathophysiology and pro-inflammatory mediators, thus enabling a common disease management strategy. New ideas in successfully targeting the prognostic severity and mortality marker pentraxin 3 (PTX3) in sepsis and severe SARS-CoV-2 infection/COVID-19; the complement (C3/C3a/C3aR and C5/C5a/C5aR axis); tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 expression; IL-6-triggered expression of C5aR receptor in vascular endothelial cells; and release of anti-inflammatory IL-10 are still missing. Small molecules with lysosomotropic characteristics such as the approved drugs amitriptyline, desloratadine, fluvoxamine, azelastine, and ambroxol have demonstrated their clinical benefits in rodent models of sepsis or clinical trials in COVID-19; however, their exact mode of action remains to be fully elucidated. Addressing disease-relevant targets such as viral infection of host cells, shedding of toll-like receptors (TLRs), expression of pro-inflammatory mediators such as TNF-α, IL-1β, IL-6, PTX3, and the complement receptor C5aR, highlight the advantages of this multi-target approach in comparison to current standards. Rational drug repurposing of approved drugs or screening for active compounds with virtually exclusively lysosomotropic pharmacologic effects is a major opportunity to improve prophylaxis and treatment of sepsis and/or SARS-CoV-2 infection, and its severe form COVID-19. ,Markus Blaess ... Hans-Peter Deigner [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [63] => Array ( [ArticleId] => 355 [Create_Time] => 2022-08-19 [zipUrl] => https://www.explorationpub.com/uploads/zip/202303/20230301094739.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100364/100364.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100364/100364.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100364/100364_cover.png [JournalsId] => 5 [Title] => Pathogenesis of the obstetric antiphospholipid syndrome: the key role of beta 2 glycoprotein I [Abstract] => Antiphospholipid syndrome (APS) is defined by recurrent pregnancy morbidity and/or vascular thrombosis associated with the persistent presence of antibodies against anionic phospholipid-binding prot [AbstractComplete] =>

Antiphospholipid syndrome (APS) is defined by recurrent pregnancy morbidity and/or vascular thrombosis associated with the persistent presence of antibodies against anionic phospholipid-binding proteins. Beta 2 glycoprotein I (β2GPI) and prothrombin (PT) are the major antigens for antiphospholipid antibodies (aPL) detectable by functional coagulation [lupus anticoagulant (LA)] or solid-phase assays [anti-β2GPI-dependent cardiolipin (aCL) and anti-β2GPI]. β2GPI-dependent aPL are responsible for the positivity of the three classification laboratory criteria. While medium/high titers of antibodies against β2GPI are risk factors for both the vascular and the obstetric manifestations of APS, persistent low titers are also associated with pregnancy complications. There is evidence from animal models of aPL-dependent fetal loss and from in vitro systems that β2GPI-dependent aPL can be pathogenic. β2GPI is physiologically found in large quantities at the placental level being available for the specific antibodies circulating in the maternal blood. Once bound to the protein, the antibodies trigger a local inflammation via the activation of the complement cascade and affect trophoblast and decidual function. The final result is represented by defective placentation, while thrombotic events are apparently less important. β2GPI is a pleiotropic molecule with scavenging properties towards several molecules including apoptotic material and displays anti-oxidant activity. These functions may explain the β2GPI placental localization in an area of intensive tissue remodeling and low oxygen tension. Since β2GPI interacts also with the complement and the coagulation cascade, its binding with specific antibodies may affect the physiology of placentation in several ways.

[Names] => Pier Luigi Meroni ... Francesco Tedesco [Doi] => 10.37349/ei.2022.00064 [Published] => August 19, 2022 [Viewed] => 761 [Downloaded] => 25 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00064 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:510–517 [Recommend] => 0 [Keywords] => Antiphospholipid syndrome, beta 2 glycoprotein I, miscarriages, placenta [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100364 [ris] => https://www.explorationpub.com/uploads/Article/A100364/e1502a8a97ad5eb19f3de384ba659df2.ris [bib] => https://www.explorationpub.com/uploads/Article/A100364/49b5f0f26ed35020c5edf00a85f2762b.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Meroni PL, Grossi C, Tedesco F. Pathogenesis of the obstetric antiphospholipid syndrome: the key role of beta 2 glycoprotein I. Explor Immunol. 2022;2:510–7. https://doi.org/10.37349/ei.2022.00064 [Jindex] => 0 [CName] => Pier LuigiMeroni, [CEmail] => pierluigi.meroni@unimi.it, [Ris_Time] => 2022-08-19 02:54:25 [Bib_Time] => 2022-08-19 02:54:25 [KeysWordContens] => Pathogenesis of the obstetric antiphospholipid syndrome: the key role of beta 2 glycoprotein I, Antiphospholipid syndrome, beta 2 glycoprotein I, miscarriages, placenta, Antiphospholipid syndrome (APS) is defined by recurrent pregnancy morbidity and/or vascular thrombosis associated with the persistent presence of antibodies against anionic phospholipid-binding proteins. Beta 2 glycoprotein I (β2GPI) and prothrombin (PT) are the major antigens for antiphospholipid antibodies (aPL) detectable by functional coagulation [lupus anticoagulant (LA)] or solid-phase assays [anti-β2GPI-dependent cardiolipin (aCL) and anti-β2GPI]. β2GPI-dependent aPL are responsible for the positivity of the three classification laboratory criteria. While medium/high titers of antibodies against β2GPI are risk factors for both the vascular and the obstetric manifestations of APS, persistent low titers are also associated with pregnancy complications. There is evidence from animal models of aPL-dependent fetal loss and from in vitro systems that β2GPI-dependent aPL can be pathogenic. β2GPI is physiologically found in large quantities at the placental level being available for the specific antibodies circulating in the maternal blood. Once bound to the protein, the antibodies trigger a local inflammation via the activation of the complement cascade and affect trophoblast and decidual function. The final result is represented by defective placentation, while thrombotic events are apparently less important. β2GPI is a pleiotropic molecule with scavenging properties towards several molecules including apoptotic material and displays anti-oxidant activity. These functions may explain the β2GPI placental localization in an area of intensive tissue remodeling and low oxygen tension. Since β2GPI interacts also with the complement and the coagulation cascade, its binding with specific antibodies may affect the physiology of placentation in several ways. ,Pier Luigi Meroni ... Francesco Tedesco [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [64] => Array ( [ArticleId] => 358 [Create_Time] => 2022-08-26 [zipUrl] => https://www.explorationpub.com/uploads/zip/202208/20220826011541.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100365/100365.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100365/100365.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100365/100365_cover.png [JournalsId] => 5 [Title] => Uterine natural killer cells and successful pregnancy: from mouse experiments to human physiology [Abstract] => Uterine natural killer (uNK) cells, a specific type of natural killer (NK) cells, are important cells at the foeto-maternal interface in humans as well as in mice. uNK cells are part of the innate l [AbstractComplete] =>

Uterine natural killer (uNK) cells, a specific type of natural killer (NK) cells, are important cells at the foeto-maternal interface in humans as well as in mice. uNK cells are part of the innate lymphoid cells group 1. Especially in the mouse, but also in the rat, many in vivo studies have been performed to evaluate the role of uNK cells in placental development. These studies have shown that uNK cells are not indispensable to pregnancy, but that they play an important role in optimal decidual angiogenesis in early pregnancy, trophoblast invasion and spiral artery remodelling in the mouse placenta. Based on the mouse studies, various in vitro studies, as well as immunohistological studies of the human placenta from elective abortions, have shown that uNK cells have similar functions in the human placenta. In the present narrative review, the role of the uNK cells in the development of the mouse and rat placenta will be discussed first. Thereafter, studies on the role of human uNK cells in the human placenta will be reviewed and these studies will be discussed in the light of the knowledge on mouse uNK cells.

[Names] => Marijke M. Faas [Doi] => 10.37349/ei.2022.00065 [Published] => August 25, 2022 [Viewed] => 1594 [Downloaded] => 30 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00065 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:518–539 [Recommend] => 1 [Keywords] => Uterine natural killer cells, human, mouse, pregnancy, decidua, placenta [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100365 [ris] => https://www.explorationpub.com/uploads/Article/A100365/ce7a940fce4697ccd57e3f8d118cf19b.ris [bib] => https://www.explorationpub.com/uploads/Article/A100365/eb0b17fd0404a4dc48acc85ac209cd13.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-26 [CitethisArticle] => Faas MM. Uterine natural killer cells and successful pregnancy: from mouse experiments to human physiology. Explor Immunol. 2022;2:518–39. https://doi.org/10.37349/ei.2022.00065 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-08-23 05:20:25 [Bib_Time] => 2022-08-23 05:20:25 [KeysWordContens] => Uterine natural killer cells and successful pregnancy: from mouse experiments to human physiology, Uterine natural killer cells, human, mouse, pregnancy, decidua, placenta, Uterine natural killer (uNK) cells, a specific type of natural killer (NK) cells, are important cells at the foeto-maternal interface in humans as well as in mice. uNK cells are part of the innate lymphoid cells group 1. Especially in the mouse, but also in the rat, many in vivo studies have been performed to evaluate the role of uNK cells in placental development. These studies have shown that uNK cells are not indispensable to pregnancy, but that they play an important role in optimal decidual angiogenesis in early pregnancy, trophoblast invasion and spiral artery remodelling in the mouse placenta. Based on the mouse studies, various in vitro studies, as well as immunohistological studies of the human placenta from elective abortions, have shown that uNK cells have similar functions in the human placenta. In the present narrative review, the role of the uNK cells in the development of the mouse and rat placenta will be discussed first. Thereafter, studies on the role of human uNK cells in the human placenta will be reviewed and these studies will be discussed in the light of the knowledge on mouse uNK cells. ,Marijke M. Faas [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [65] => Array ( [ArticleId] => 359 [Create_Time] => 2022-08-26 [zipUrl] => https://www.explorationpub.com/uploads/zip/202208/20220826014658.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100366/100366.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100366/100366.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100366/100366_cover.png [JournalsId] => 5 [Title] => γδ T cells: a sparkling star for clinical immunotherapy [Abstract] => Human γδ T cells are unconventional lymphocytes that function in innate and adaptive immune responses and immunosurveillance. These cells show potent cytotoxicity against tumor cells in a major histocompatibility complex unrestricted manner and have recently gained considerable attention as a sparkling star for clinical immunotherapy. Clinical immunotherapy trials with activated γδ T cells are tolerated well. However, clinical benefits are still unsatisfactory. Therefore, anti-tumor effects need to further increase the cytotoxicity of γδ T cells via several mechanisms, including the novel nitrogen-containing bisphosphonate products, adjuvant use with a bispecific antibody and chimeric antigen receptor, co-immunotherapy with γδ T cells plus immune checkpoint inhibitors, and adoptive immunotherapy with Vδ1 T cells and T cells engineered to express a defined γδ T cell receptor. Here, this article describes the crucial role of γδ T cells in anti-tumor immunity, concludes transduction strategies and summarizes the different development of novel approaches for clinical applications and cancer immunotherapy, which may be effective in overcoming current therapeutic limitations. [AbstractComplete] =>

Human γδ T cells are unconventional lymphocytes that function in innate and adaptive immune responses and immunosurveillance. These cells show potent cytotoxicity against tumor cells in a major histocompatibility complex unrestricted manner and have recently gained considerable attention as a sparkling star for clinical immunotherapy. Clinical immunotherapy trials with activated γδ T cells are tolerated well. However, clinical benefits are still unsatisfactory. Therefore, anti-tumor effects need to further increase the cytotoxicity of γδ T cells via several mechanisms, including the novel nitrogen-containing bisphosphonate products, adjuvant use with a bispecific antibody and chimeric antigen receptor, co-immunotherapy with γδ T cells plus immune checkpoint inhibitors, and adoptive immunotherapy with Vδ1 T cells and T cells engineered to express a defined γδ T cell receptor. Here, this article describes the crucial role of γδ T cells in anti-tumor immunity, concludes transduction strategies and summarizes the different development of novel approaches for clinical applications and cancer immunotherapy, which may be effective in overcoming current therapeutic limitations.

[Names] => Jiamian Zheng ... Zhenyi Jin [Doi] => 10.37349/ei.2022.00066 [Published] => August 26, 2022 [Viewed] => 979 [Downloaded] => 30 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00066 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:540–557 [Recommend] => 0 [Keywords] => γδT cell, immunotherapy, adoptive cell therapy [DetailTitle] => [DetailUrl] => [Id] => 100366 [ris] => https://www.explorationpub.com/uploads/Article/A100366/677a55bcc0dada11979c53c2e1a54c52.ris [bib] => https://www.explorationpub.com/uploads/Article/A100366/71a1394540b8f9d446e4e156f5c47cd8.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-25 [CitethisArticle] => Zheng J, Jiang X, Zhao H, Wang W, Wu X, Jin Z. γδ T cells: a sparkling star for clinical immunotherapy. Explor Immunol. 2022;2:540–57. https://doi.org/10.37349/ei.2022.00066 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-08-25 08:22:01 [Bib_Time] => 2022-08-25 08:22:01 [KeysWordContens] => γδ T cells: a sparkling star for clinical immunotherapy, γδT cell, immunotherapy, adoptive cell therapy, Human γδ T cells are unconventional lymphocytes that function in innate and adaptive immune responses and immunosurveillance. These cells show potent cytotoxicity against tumor cells in a major histocompatibility complex unrestricted manner and have recently gained considerable attention as a sparkling star for clinical immunotherapy. Clinical immunotherapy trials with activated γδ T cells are tolerated well. However, clinical benefits are still unsatisfactory. Therefore, anti-tumor effects need to further increase the cytotoxicity of γδ T cells via several mechanisms, including the novel nitrogen-containing bisphosphonate products, adjuvant use with a bispecific antibody and chimeric antigen receptor, co-immunotherapy with γδ T cells plus immune checkpoint inhibitors, and adoptive immunotherapy with Vδ1 T cells and T cells engineered to express a defined γδ T cell receptor. Here, this article describes the crucial role of γδ T cells in anti-tumor immunity, concludes transduction strategies and summarizes the different development of novel approaches for clinical applications and cancer immunotherapy, which may be effective in overcoming current therapeutic limitations. ,Jiamian Zheng ... Zhenyi Jin [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [66] => Array ( [ArticleId] => 360 [Create_Time] => 2022-08-26 [zipUrl] => https://www.explorationpub.com/uploads/zip/202208/20220826061826.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100367/100367.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100367/100367.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100367/100367_cover.png [JournalsId] => 5 [Title] => Contribution of immunology to build precision medicine in reproduction: present and future [Abstract] => Infertility affects millions of people of reproductive age. The failure of a blastocyst to implant is a leading cause of psychological distress. It became increasingly evident that an effective immu [AbstractComplete] =>

Infertility affects millions of people of reproductive age. The failure of a blastocyst to implant is a leading cause of psychological distress. It became increasingly evident that an effective immune dialogue occurs at each step in the fluids surrounding the oocyte, the spermatozoa, the embryo, or the endometrium. Exploring and deciphering this dialogue could potentially help understand why 50% of healthy euploid blastocysts fail to implant. Introducing immunology into reproductive medicine requires a change of mindset to bring immune hypothesis to clinical applications. Implantation of an embryo requires a prepared uterus in order to dialogue with the embryo, which is able to express and repair itself. Exploring the uterine immune profile of patients with previous implantation failures (IF) or recurrent miscarriages (RM) has already been developed and is under evaluation as a precision tool to equilibrate the uterine environment before implantation to increase the subsequent live birth rate after the embryo transfer. Immunology may also be fundamental in the future to identify through non-invasive procedure the competence of oocytes or embryos through reliable immune biomarkers quantified in follicular fluids or embryo supernatants during the in vitro fertilization (IVF) process. Non-invasive biomarkers would allow physicians to identify competent oocytes or embryos based on their ability to communicate with the mother and their energetic potential for all the self-repair processes that should occur during the preimplantation and the implantation period. This area of research is only beginning.

[Names] => Alaa Kazhalawi ... Nathalie Lédée [Doi] => 10.37349/ei.2022.00067 [Published] => August 26, 2022 [Viewed] => 1073 [Downloaded] => 24 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00067 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:558–571 [Recommend] => 0 [Keywords] => Infertility, immunology, embryo implantation, oocyte quality, reproduction [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100367 [ris] => https://www.explorationpub.com/uploads/Article/A100367/f6050b942d3e24d61f3502fc359efb00.ris [bib] => https://www.explorationpub.com/uploads/Article/A100367/bcffae4857601fb3d5d05c7b36c88b9a.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Kazhalawi A, Petitbarat M, Rahmati M, Lédée N. Contribution of immunology to build precision medicine in reproduction: present and future. Explor Immunol. 2022;2:558–71. https://doi.org/10.37349/ei.2022.00067 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-08-30 00:52:22 [Bib_Time] => 2022-08-30 00:52:22 [KeysWordContens] => Contribution of immunology to build precision medicine in reproduction: present and future, Infertility, immunology, embryo implantation, oocyte quality, reproduction, Infertility affects millions of people of reproductive age. The failure of a blastocyst to implant is a leading cause of psychological distress. It became increasingly evident that an effective immune dialogue occurs at each step in the fluids surrounding the oocyte, the spermatozoa, the embryo, or the endometrium. Exploring and deciphering this dialogue could potentially help understand why 50% of healthy euploid blastocysts fail to implant. Introducing immunology into reproductive medicine requires a change of mindset to bring immune hypothesis to clinical applications. Implantation of an embryo requires a prepared uterus in order to dialogue with the embryo, which is able to express and repair itself. Exploring the uterine immune profile of patients with previous implantation failures (IF) or recurrent miscarriages (RM) has already been developed and is under evaluation as a precision tool to equilibrate the uterine environment before implantation to increase the subsequent live birth rate after the embryo transfer. Immunology may also be fundamental in the future to identify through non-invasive procedure the competence of oocytes or embryos through reliable immune biomarkers quantified in follicular fluids or embryo supernatants during the in vitro fertilization (IVF) process. Non-invasive biomarkers would allow physicians to identify competent oocytes or embryos based on their ability to communicate with the mother and their energetic potential for all the self-repair processes that should occur during the preimplantation and the implantation period. This area of research is only beginning. ,Alaa Kazhalawi ... Nathalie Lédée [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [67] => Array ( [ArticleId] => 361 [Create_Time] => 2022-08-26 [zipUrl] => https://www.explorationpub.com/uploads/zip/202208/20220826103230.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100368/100368.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100368/100368.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100368/100368_cover.png [JournalsId] => 5 [Title] => Immune network operations in COVID-19 [Abstract] => The immune system, whose nature lies in being a complex network of interactions, lends itself well to being represented and studied using graph theory. However, it should be noted that although the [AbstractComplete] =>

The immune system, whose nature lies in being a complex network of interactions, lends itself well to being represented and studied using graph theory. However, it should be noted that although the formalization of models of the immune system is relatively recent, the medical use of its signaling network structure has been carried out empirically for centuries in vaccinology, immunopathology, and clinical immunology, as evidenced by the development of effective vaccines, the management of transplant rejection, the management of allergies, and the treatment of certain types of cancer and autoimmune diseases. A network optimization analogy is proposed through the employment of the system dynamic formalism of causal loop diagrams (CLDs), where current network operations (also known as NetOps) in information technology (IT), are interpreted as immune NetOps in coronavirus disease 2019 (COVID-19) treatment. Traffic shaping corresponds to signaling pathway modulation by immunosuppressors. Data caching corresponds to the activation of innate immunity by application of Bacillus Calmette-Guerin (BCG) and other vaccines. Data compression corresponds with the activation of adaptative immune response by vaccination with the actual approved COVID-19 vaccines. Buffer tuning corresponds with concurrent activation of innate and adaptative or specialized immune cells and antibodies that attack and destroy foreign invaders by trained immunity-based vaccines to develop. The present study delineates some experimental extensions and future developments. Given the complex communication architecture of signal transduction in the immune system, it is apparent that multiple parallel pathways influencing and regulating each other are not the exception but the norm. Thus, the transition from empirical immune NetOps to analytical immune NetOps is a goal for the near future in biomedicine.

[Names] => Javier Burgos-Salcedo [Doi] => 10.37349/ei.2022.00068 [Published] => August 26, 2022 [Viewed] => 782 [Downloaded] => 10 [Subject] => Perspective [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00068 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:572–580 [Recommend] => 0 [Keywords] => Systems immunology, immune networks, network operations, cell signaling pathways, COVID-19 [DetailTitle] => [DetailUrl] => [Id] => 100368 [ris] => https://www.explorationpub.com/uploads/Article/A100368/b62dc224d39e6b3def56017ea3c26a07.ris [bib] => https://www.explorationpub.com/uploads/Article/A100368/abc066b2b7b502abdf43425350b2c737.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Burgos-Salcedo J. Immune network operations in COVID-19. Explor Immunol. 2022;2:572–80. https://doi.org/10.37349/ei.2022.00068 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-08-24 05:53:48 [Bib_Time] => 2022-08-24 05:53:48 [KeysWordContens] => Immune network operations in COVID-19, Systems immunology, immune networks, network operations, cell signaling pathways, COVID-19, The immune system, whose nature lies in being a complex network of interactions, lends itself well to being represented and studied using graph theory. However, it should be noted that although the formalization of models of the immune system is relatively recent, the medical use of its signaling network structure has been carried out empirically for centuries in vaccinology, immunopathology, and clinical immunology, as evidenced by the development of effective vaccines, the management of transplant rejection, the management of allergies, and the treatment of certain types of cancer and autoimmune diseases. A network optimization analogy is proposed through the employment of the system dynamic formalism of causal loop diagrams (CLDs), where current network operations (also known as NetOps) in information technology (IT), are interpreted as immune NetOps in coronavirus disease 2019 (COVID-19) treatment. Traffic shaping corresponds to signaling pathway modulation by immunosuppressors. Data caching corresponds to the activation of innate immunity by application of Bacillus Calmette-Guerin (BCG) and other vaccines. Data compression corresponds with the activation of adaptative immune response by vaccination with the actual approved COVID-19 vaccines. Buffer tuning corresponds with concurrent activation of innate and adaptative or specialized immune cells and antibodies that attack and destroy foreign invaders by trained immunity-based vaccines to develop. The present study delineates some experimental extensions and future developments. Given the complex communication architecture of signal transduction in the immune system, it is apparent that multiple parallel pathways influencing and regulating each other are not the exception but the norm. Thus, the transition from empirical immune NetOps to analytical immune NetOps is a goal for the near future in biomedicine. ,Javier Burgos-Salcedo [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [68] => Array ( [ArticleId] => 363 [Create_Time] => 2022-08-29 [zipUrl] => https://www.explorationpub.com/uploads/zip/202208/20220829022854.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100369/100369.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100369/100369.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100369/100369_cover.png [JournalsId] => 5 [Title] => The human microbiome and the tumor microenvironment [Abstract] => The human microbiome has emerged as an intriguing field of scientific research. Its role in human physiology impacts both health and disease, contributing to the enhancement or impairment of metabol [AbstractComplete] =>

The human microbiome has emerged as an intriguing field of scientific research. Its role in human physiology impacts both health and disease, contributing to the enhancement or impairment of metabolic and immune functions. Sometimes referred to as our body’s “second genome”, the alteration of the microbiome’s bacterial ecology (dysbiosis), is linked to increasing numbers of illnesses, including cancer. The tumor microenvironment (TME) is the environment in which tumors grow and modulate the tumorigenic process depending on a myriad of distinct factors, including cell types, vascular system, and cytokines. Given the emerging relationship between the microbiome and the TME, this perspective aims to distill some of the key factors regulating the crosstalk between the microbiome and the TME. It also outlines why manipulating the microbiome may be a feasible strategy for anti-cancer therapy.

[Names] => Joseph F. Murphy [Doi] => 10.37349/ei.2022.00069 [Published] => August 29, 2022 [Viewed] => 1172 [Downloaded] => 49 [Subject] => Perspective [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00069 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 59 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:581–588 [Recommend] => 0 [Keywords] => Microbiome, microbiota, tumor microenvironment, immunotherapy [DetailTitle] => New insights in cancer immunology: the role of microbiota from immunosurveillance to immunotherapy [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/59 [Id] => 100369 [ris] => https://www.explorationpub.com/uploads/Article/A100369/4e5aa5e9ccae0008ec335318c2d7dc9b.ris [bib] => https://www.explorationpub.com/uploads/Article/A100369/63f1404d92e1e0bbe5897ab03fb80db9.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Murphy JF. The human microbiome and the tumor microenvironment. Explor Immunol. 2022;2:581–8. https://doi.org/10.37349/ei.2022.00069 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-08-29 02:42:39 [Bib_Time] => 2022-08-29 02:42:39 [KeysWordContens] => The human microbiome and the tumor microenvironment, Microbiome, microbiota, tumor microenvironment, immunotherapy, The human microbiome has emerged as an intriguing field of scientific research. Its role in human physiology impacts both health and disease, contributing to the enhancement or impairment of metabolic and immune functions. Sometimes referred to as our body’s “second genome”, the alteration of the microbiome’s bacterial ecology (dysbiosis), is linked to increasing numbers of illnesses, including cancer. The tumor microenvironment (TME) is the environment in which tumors grow and modulate the tumorigenic process depending on a myriad of distinct factors, including cell types, vascular system, and cytokines. Given the emerging relationship between the microbiome and the TME, this perspective aims to distill some of the key factors regulating the crosstalk between the microbiome and the TME. It also outlines why manipulating the microbiome may be a feasible strategy for anti-cancer therapy. ,Joseph F. Murphy [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [69] => Array ( [ArticleId] => 364 [Create_Time] => 2022-08-29 [zipUrl] => https://www.explorationpub.com/uploads/zip/202208/20220828020625.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100370/100370.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100370/100370.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100370/100370_cover.png [JournalsId] => 5 [Title] => Understanding sepsis-induced immunosuppression and organ dysfunctions: from immunosuppression to immunotherapy [Abstract] => Sepsis is a life-threatening condition caused by dysregulated host immune response to infection, leading to persistent inflammation followed by immunosuppression. Sepsis represents a substantial glo [AbstractComplete] =>

Sepsis is a life-threatening condition caused by dysregulated host immune response to infection, leading to persistent inflammation followed by immunosuppression. Sepsis represents a substantial global health problem owing to protracted inflammation, immune suppression, and susceptibility to nosocomial infections. Despite continuing progress in the development of antibiotics, fluid resuscitation, and other supportive care therapies, no specific immunomodulatory drugs or immunotherapeutic adjuncts for the treatment of sepsis are available to date. The advances in tertiary care facilities and patient care have improved the survival of sepsis patients in the initial hyper-inflammatory phase of sepsis. However, the majority of sepsis patients succumb later due to prolong immunosuppression. The sepsis-induced immune dysregulation and its long-term effects on mortality are under meticulous investigations that are still poorly defined. Sepsis leads to the impaired functions of the innate and adaptive immune systems. The exhaustion of T cells, reduced expression of human leukocytes antigen (HLA)-DR on monocytes, and induced uncontrolled apoptosis of immune cells have been reported as hallmark features of sepsis. Sepsis-induced immune cell apoptosis of immune cells is a primary contributing factor to the immunosuppression in sepsis. Preclinical studies have identified several new therapeutic targets for therapy in sepsis, including monoclonal antibodies (Abs) and anti-apoptotic agents to reduce T cells exhaustion, immune cells apoptosis, and restoring immune cells functions. Recent studies have centered on immune-modulatory therapy. The review article will focus solely on sepsis’ effects on innate and adaptive cells functions that contribute to immunosuppression. Finally, it is discussed how immune cells responsible for immunosuppression might be directly targeted to provide potential therapeutic benefits in treating sepsis and improving long-term survival.

[Names] => Dablu Lal Gupta ... D. N. Rao [Doi] => 10.37349/ei.2022.00070 [Published] => August 29, 2022 [Viewed] => 1120 [Downloaded] => 45 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00070 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 53 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:589–603 [Recommend] => 0 [Keywords] => Sepsis, immunosuppression, innate and adaptive immunity, multiple organ failure [DetailTitle] => The‌ ‌Sepsis‌ ‌induced‌ ‌Immune‌ ‌Conundrum [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/53 [Id] => 100370 [ris] => https://www.explorationpub.com/uploads/Article/A100370/2f38a595a3a5dc6e6b01ee0ff093e136.ris [bib] => https://www.explorationpub.com/uploads/Article/A100370/67b5fd4cebe3ab9830c41be122333106.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Gupta DL, Sinha T, Pathak R, Bhoi S, Rao DN. Understanding sepsis-induced immunosuppression and organ dysfunction’s: from immunosuppression to immunotherapy. Explor Immunol. 2022;2:589–603. https://doi.org/10.37349/ei.2022.00070 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-08-26 07:29:27 [Bib_Time] => 2022-08-26 07:29:27 [KeysWordContens] => Understanding sepsis-induced immunosuppression and organ dysfunctions: from immunosuppression to immunotherapy, Sepsis, immunosuppression, innate and adaptive immunity, multiple organ failure, Sepsis is a life-threatening condition caused by dysregulated host immune response to infection, leading to persistent inflammation followed by immunosuppression. Sepsis represents a substantial global health problem owing to protracted inflammation, immune suppression, and susceptibility to nosocomial infections. Despite continuing progress in the development of antibiotics, fluid resuscitation, and other supportive care therapies, no specific immunomodulatory drugs or immunotherapeutic adjuncts for the treatment of sepsis are available to date. The advances in tertiary care facilities and patient care have improved the survival of sepsis patients in the initial hyper-inflammatory phase of sepsis. However, the majority of sepsis patients succumb later due to prolong immunosuppression. The sepsis-induced immune dysregulation and its long-term effects on mortality are under meticulous investigations that are still poorly defined. Sepsis leads to the impaired functions of the innate and adaptive immune systems. The exhaustion of T cells, reduced expression of human leukocytes antigen (HLA)-DR on monocytes, and induced uncontrolled apoptosis of immune cells have been reported as hallmark features of sepsis. Sepsis-induced immune cell apoptosis of immune cells is a primary contributing factor to the immunosuppression in sepsis. Preclinical studies have identified several new therapeutic targets for therapy in sepsis, including monoclonal antibodies (Abs) and anti-apoptotic agents to reduce T cells exhaustion, immune cells apoptosis, and restoring immune cells functions. Recent studies have centered on immune-modulatory therapy. The review article will focus solely on sepsis’ effects on innate and adaptive cells functions that contribute to immunosuppression. Finally, it is discussed how immune cells responsible for immunosuppression might be directly targeted to provide potential therapeutic benefits in treating sepsis and improving long-term survival. ,Dablu Lal Gupta ... D. N. Rao [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [70] => Array ( [ArticleId] => 384 [Create_Time] => 2022-08-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202305/20230531024656.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100371/100371.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100371/100371.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100371/100371_cover.png [JournalsId] => 5 [Title] => Vaccine induced thrombotic thrombocytopenia: development and reactivity of anti-platelet factor 4 antibodies and immune pathogenic mechanisms [Abstract] => In ultrarare cases, patients vaccinated with DNA adenovirus vector vaccine against severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), develop a vaccine-induced immune thrombotic thrombocy [AbstractComplete] =>

In ultrarare cases, patients vaccinated with DNA adenovirus vector vaccine against severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), develop a vaccine-induced immune thrombotic thrombocytopenia (VITT), with a high incidence of fatal cases. The causative agent is the development of platelet factor 4 (PF4)-dependent antibodies that resemble heparin-induced thrombocytopenia (HIT) complication, although many differences can be noticed in clinical presentation, antibody reactivity, involved epitopes on the PF4 protein, and pathological mechanisms. From the literature review, and the experience of HIT and testing a few plasmas from patients with VITT, this review analyzes the possible mechanisms, which show the strong immunoglobulin G (IgG) antibody reactivity to PF4 alone, in the absence of heparin, and to a lesser extend to stoichiometric complexes of PF4 and heparin (H-PF4). In addition, much lower heparin concentrations are required for inhibiting antibody binding to PF4. These concentrations are much lower than those required for disrupting the stoichiometric H-PF4 complexes. This confirms that IgG antibodies responsible for HIT bind preferentially to PF4, to epitopes that are readily masked by low concentrations of heparin. These antibodies are at a much higher concentration than the current ones observed for HIT, keeping a strong reactivity even for plasma dilutions as high as 1/500 to 1/5,000, whilst the current dilution for testing heparin-dependent antibodies in HIT is 1/100. Although VITT anti-PF4 antibodies can be detected with the current anti-H-PF4 enzyme-linked immunosorbent assays (ELISAs) designed for HIT, some assays have low sensitivity or are unreactive, like lateral immunofiltration methods or chemiluminescent automated assays. The preferred method should concern the use of capture assays using PF4 coated solid surfaces. This report proposes that the immune response is only targeted to the binding domain of PF4 with the hexons present on the adenovirus vector, through an epitope spreading mechanism, without any exposure of neo-epitopes on PF4 protein.

[Names] => Jean Amiral ... Gwenaëlle Renaud [Doi] => 10.37349/ei.2022.00071 [Published] => August 31, 2022 [Viewed] => 905 [Downloaded] => 31 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00071 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:604–621 [Recommend] => 0 [Keywords] => Thrombosis, thrombocytopenia, severe acute respiratory syndrome coronavirus-2, adenovirus vector vaccines, platelet factor 4, autoantibodies, vaccine-induced immune thrombotic thrombocytopenia [DetailTitle] => [DetailUrl] => [Id] => 100371 [ris] => https://www.explorationpub.com/uploads/Article/A100371/86ecea5b5b1ecb59773c24a8b57c16c2.ris [bib] => https://www.explorationpub.com/uploads/Article/A100371/dacd2cad9aa82814aab51d5f6ffa2245.bib [ens] => [Cited] => 2 [Cited_Time] => 2024-04-25 [CitethisArticle] => Amiral J, Legros E, Vivant M, Rossi D, Renaud G. Vaccine induced thrombotic thrombocytopenia: development and reactivity of anti-platelet factor 4 antibodies and immune pathogenic mechanisms. Explor Immunol. 2022;2:604–21. https://doi.org/10.37349/ei.2022.00071 [Jindex] => 0 [CName] => JeanAmiral, [CEmail] => jean.amiral@scientific-hemostasis.com, [Ris_Time] => 2022-08-31 00:56:57 [Bib_Time] => 2022-08-31 00:56:57 [KeysWordContens] => Vaccine induced thrombotic thrombocytopenia: development and reactivity of anti-platelet factor 4 antibodies and immune pathogenic mechanisms, Thrombosis, thrombocytopenia, severe acute respiratory syndrome coronavirus-2, adenovirus vector vaccines, platelet factor 4, autoantibodies, vaccine-induced immune thrombotic thrombocytopenia, In ultrarare cases, patients vaccinated with DNA adenovirus vector vaccine against severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), develop a vaccine-induced immune thrombotic thrombocytopenia (VITT), with a high incidence of fatal cases. The causative agent is the development of platelet factor 4 (PF4)-dependent antibodies that resemble heparin-induced thrombocytopenia (HIT) complication, although many differences can be noticed in clinical presentation, antibody reactivity, involved epitopes on the PF4 protein, and pathological mechanisms. From the literature review, and the experience of HIT and testing a few plasmas from patients with VITT, this review analyzes the possible mechanisms, which show the strong immunoglobulin G (IgG) antibody reactivity to PF4 alone, in the absence of heparin, and to a lesser extend to stoichiometric complexes of PF4 and heparin (H-PF4). In addition, much lower heparin concentrations are required for inhibiting antibody binding to PF4. These concentrations are much lower than those required for disrupting the stoichiometric H-PF4 complexes. This confirms that IgG antibodies responsible for HIT bind preferentially to PF4, to epitopes that are readily masked by low concentrations of heparin. These antibodies are at a much higher concentration than the current ones observed for HIT, keeping a strong reactivity even for plasma dilutions as high as 1/500 to 1/5,000, whilst the current dilution for testing heparin-dependent antibodies in HIT is 1/100. Although VITT anti-PF4 antibodies can be detected with the current anti-H-PF4 enzyme-linked immunosorbent assays (ELISAs) designed for HIT, some assays have low sensitivity or are unreactive, like lateral immunofiltration methods or chemiluminescent automated assays. The preferred method should concern the use of capture assays using PF4 coated solid surfaces. This report proposes that the immune response is only targeted to the binding domain of PF4 with the hexons present on the adenovirus vector, through an epitope spreading mechanism, without any exposure of neo-epitopes on PF4 protein. ,Jean Amiral ... Gwenaëlle Renaud [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [71] => Array ( [ArticleId] => 385 [Create_Time] => 2022-08-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202303/20230301095829.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100372/100372.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100372/100372.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100372/100372_cover.png [JournalsId] => 5 [Title] => A non-redundant role of complement protein C1q in normal and adverse pregnancy [Abstract] => Complement component 1q (C1q) is the recognition molecule of the classical pathway of the complement system that can bind to an array of closely spaced antigen-bound immunoglobulin G (IgG) and IgM a [AbstractComplete] =>

Complement component 1q (C1q) is the recognition molecule of the classical pathway of the complement system that can bind to an array of closely spaced antigen-bound immunoglobulin G (IgG) and IgM antibodies. In addition to its involvement in defence against a range of pathogens and clearance of apoptotic and necrotic cells, C1q has also been implicated in immune and non-immune homeostasis. C1q is locally produced by immune cells such as monocytes, macrophages, and dendritic cells. C1q is also synthesized by decidual endothelial cells, thus acting as a link between decidual cells and trophoblasts, as well as contributing to the remodelling of spiral arteries. Furthermore, C1q is produced by the extravillous trophoblasts (EVTs) invading the decidua. As a pro-angiogenic molecule, C1q is also important for normal placentation processes as it favors the active angiogenesis in the developing decidua. These observations have been validated by C1q gene knock-out mice which showed pre-eclampsia (PE)-like symptoms, characterized by hypertension, proteinuria, glomerular endotheliosis, and increased soluble fms-like tyrosine kinase-1 (sFlt-1)/placental growth factor (PlGF) ratio, and increased oxidative stress. The role of C1q in normal and adverse human pregnancy is being studied extensively due to its absence or low level as a likely precipitating factor for the development of PE.

[Names] => Chiara Agostinis ... Roberta Bulla [Doi] => 10.37349/ei.2022.00072 [Published] => August 31, 2022 [Viewed] => 1747 [Downloaded] => 59 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00072 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:622–636 [Recommend] => 1 [Keywords] => C1q, complement system, pregnancy, pre-eclampsia [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100372 [ris] => https://www.explorationpub.com/uploads/Article/A100372/022a84262cd471a2bcc0ce30dcb7fbd6.ris [bib] => https://www.explorationpub.com/uploads/Article/A100372/155c7f430eb2d66800e5c813986edba8.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-26 [CitethisArticle] => Agostinis C, Mangogna A, Balduit A, Kishore U, Bulla R. A non-redundant role of complement protein C1q in normal and adverse pregnancy. Explor Immunol. 2022;2:622–36. https://doi.org/10.37349/ei.2022.00072 [Jindex] => 0 [CName] => AndreaBalduit,RobertaBulla, [CEmail] => abalduit@units.it,rbulla@units.it, [Ris_Time] => 2022-08-31 05:42:23 [Bib_Time] => 2022-08-31 05:42:23 [KeysWordContens] => A non-redundant role of complement protein C1q in normal and adverse pregnancy, C1q, complement system, pregnancy, pre-eclampsia, Complement component 1q (C1q) is the recognition molecule of the classical pathway of the complement system that can bind to an array of closely spaced antigen-bound immunoglobulin G (IgG) and IgM antibodies. In addition to its involvement in defence against a range of pathogens and clearance of apoptotic and necrotic cells, C1q has also been implicated in immune and non-immune homeostasis. C1q is locally produced by immune cells such as monocytes, macrophages, and dendritic cells. C1q is also synthesized by decidual endothelial cells, thus acting as a link between decidual cells and trophoblasts, as well as contributing to the remodelling of spiral arteries. Furthermore, C1q is produced by the extravillous trophoblasts (EVTs) invading the decidua. As a pro-angiogenic molecule, C1q is also important for normal placentation processes as it favors the active angiogenesis in the developing decidua. These observations have been validated by C1q gene knock-out mice which showed pre-eclampsia (PE)-like symptoms, characterized by hypertension, proteinuria, glomerular endotheliosis, and increased soluble fms-like tyrosine kinase-1 (sFlt-1)/placental growth factor (PlGF) ratio, and increased oxidative stress. The role of C1q in normal and adverse human pregnancy is being studied extensively due to its absence or low level as a likely precipitating factor for the development of PE. ,Chiara Agostinis ... Roberta Bulla [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [72] => Array ( [ArticleId] => 386 [Create_Time] => 2022-09-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202208/20220831064438.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100373/100373.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100373/100373.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100373/100373_cover.png [JournalsId] => 5 [Title] => Chemokines and nanomaterials: interaction for useful immune-applications [Abstract] => Chemokines are homeostatic or inflammatory small proteins regulating immune cell migration and are structurally characterized by cysteine disulfide bridges. Around 50 human chemokines binding almost [AbstractComplete] =>

Chemokines are homeostatic or inflammatory small proteins regulating immune cell migration and are structurally characterized by cysteine disulfide bridges. Around 50 human chemokines binding almost 20 seven-transmembrane G-protein coupled receptors have been discovered. The finding that two of them were the main human immunodeficiency virus (HIV) co-receptors intensified the research on the binding mechanism to block the viral entrance. Blockade of chemokine/chemokine receptor signaling ultimately modulates cell migration, then immune responses. Particular nanotechnologies can be designed to interfere with chemokine signaling or to exploit the ligand-receptor interaction. Surface chemical modification of nanomaterials with chemokines or specific peptides can find several applications in bio-medicine, from tissue-specific drug delivery to reduced cell migration in pathological conditions. Recent highlights on peculiar chemokine-nanoparticle design and their potential to modulate immune responses will be discussed.

[Names] => Giuseppe Bardi [Doi] => 10.37349/ei.2022.00073 [Published] => August 31, 2022 [Viewed] => 1914 [Downloaded] => 181 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00073 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 81 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:637–647 [Recommend] => 1 [Keywords] => Chemokines, nanoparticles, inflammation, chemokine receptors, protein corona [DetailTitle] => Nanomaterials interaction with chemokines: perspectives for applied immunology [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/81 [Id] => 100373 [ris] => https://www.explorationpub.com/uploads/Article/A100373/39599d0821b3f25b92ab6c6f3e0e3fb0.ris [bib] => https://www.explorationpub.com/uploads/Article/A100373/cf6d65795032bbdf9952c1c8b2326d92.bib [ens] => [Cited] => 2 [Cited_Time] => 2024-04-26 [CitethisArticle] => Bardi G. Chemokines and nanomaterials: interaction for useful immune-applications. Explor Immunol. 2022;2:637–47. https://doi.org/10.37349/ei.2022.00073 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-08-31 01:54:34 [Bib_Time] => 2022-08-31 01:54:34 [KeysWordContens] => Chemokines and nanomaterials: interaction for useful immune-applications, Chemokines, nanoparticles, inflammation, chemokine receptors, protein corona, Chemokines are homeostatic or inflammatory small proteins regulating immune cell migration and are structurally characterized by cysteine disulfide bridges. Around 50 human chemokines binding almost 20 seven-transmembrane G-protein coupled receptors have been discovered. The finding that two of them were the main human immunodeficiency virus (HIV) co-receptors intensified the research on the binding mechanism to block the viral entrance. Blockade of chemokine/chemokine receptor signaling ultimately modulates cell migration, then immune responses. Particular nanotechnologies can be designed to interfere with chemokine signaling or to exploit the ligand-receptor interaction. Surface chemical modification of nanomaterials with chemokines or specific peptides can find several applications in bio-medicine, from tissue-specific drug delivery to reduced cell migration in pathological conditions. Recent highlights on peculiar chemokine-nanoparticle design and their potential to modulate immune responses will be discussed. ,Giuseppe Bardi [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [73] => Array ( [ArticleId] => 388 [Create_Time] => 2022-09-21 [zipUrl] => https://www.explorationpub.com/uploads/zip/202211/20221104063144.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100374/100374.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100374/100374.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100374/100374_cover.png [JournalsId] => 5 [Title] => Immune responses to SARS-CoV-2 infection and COVID-19 vaccines [Abstract] => Coronavirus disease 2019 (COVID-19) is currently a major public health concern causing devastating sociological, economic, and psychological damage to livelihood all over the world. The most intense [AbstractComplete] =>

Coronavirus disease 2019 (COVID-19) is currently a major public health concern causing devastating sociological, economic, and psychological damage to livelihood all over the world. The most intense severity of COVID-19 is not only acute respiratory distress syndrome (ARDS), it also causes multi-organ failure, the post-infection secondary effect as well as death. The fast-mutating ability and high transmissibility rate of the virus cause emergence of the new variants and also the occurrence of breakthrough infections. Evidence suggests that vaccination against COVID-19 has been effective at preventing the severity of illness, hospitalization, and death. The efficacy of vaccines depends on multiple factors including the host’s ability to mount a robust and sustainable immune response, the virus’s ability to mutate its genome, and programmatic factors such as vaccine dose, storage, dosing schedules, etc. In this article, an overview of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, its pathogenesis, host immune responses to infection, and different type of COVID-19 vaccines, including vaccine efficacy and adverse effects are described.

[Names] => Basista Rabina Sharma, P. Veeranna Ravindra [Doi] => 10.37349/ei.2022.00074 [Published] => September 21, 2022 [Viewed] => 1246 [Downloaded] => 49 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00074 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 47 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:648–664 [Recommend] => 0 [Keywords] => Coronavirus disease 2019, vaccines, immune response, efficacy, adverse effect [DetailTitle] => Vaccine-induced Immune Responses Against SARS-CoV-2 Infections [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/47 [Id] => 100374 [ris] => https://www.explorationpub.com/uploads/Article/A100374/aa2729685a58f612a3eaba3064c4c411.ris [bib] => https://www.explorationpub.com/uploads/Article/A100374/a971da54445b0ef66cda7116a3e49674.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-26 [CitethisArticle] => Sharma BR, Ravindra PV. Immune responses to SARS-CoV-2 infection and COVID-19 vaccines. Explor Immunol. 2022;2:648–64. https://doi.org/10.37349/ei.2022.00074 [Jindex] => 0 [CName] => P. VeerannaRavindra, [CEmail] => raviravindra1@gmail.com, [Ris_Time] => 2022-09-19 05:34:43 [Bib_Time] => 2022-09-19 05:34:43 [KeysWordContens] => Immune responses to SARS-CoV-2 infection and COVID-19 vaccines, Coronavirus disease 2019, vaccines, immune response, efficacy, adverse effect, Coronavirus disease 2019 (COVID-19) is currently a major public health concern causing devastating sociological, economic, and psychological damage to livelihood all over the world. The most intense severity of COVID-19 is not only acute respiratory distress syndrome (ARDS), it also causes multi-organ failure, the post-infection secondary effect as well as death. The fast-mutating ability and high transmissibility rate of the virus cause emergence of the new variants and also the occurrence of breakthrough infections. Evidence suggests that vaccination against COVID-19 has been effective at preventing the severity of illness, hospitalization, and death. The efficacy of vaccines depends on multiple factors including the host’s ability to mount a robust and sustainable immune response, the virus’s ability to mutate its genome, and programmatic factors such as vaccine dose, storage, dosing schedules, etc. In this article, an overview of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, its pathogenesis, host immune responses to infection, and different type of COVID-19 vaccines, including vaccine efficacy and adverse effects are described. ,Basista Rabina Sharma, P. Veeranna Ravindra [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [74] => Array ( [ArticleId] => 401 [Create_Time] => 2022-10-25 [zipUrl] => https://www.explorationpub.com/uploads/zip/202210/20221031063726.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100375/100375.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100375/100375.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100375/100375_cover.png [JournalsId] => 5 [Title] => The progression of sepsis from physiologic systemic inflammatory response to immune dysregulation due to life-threatening infections [Abstract] => Sepsis was defined in 1991 by the systemic inflammatory response syndrome (SIRS) criteria which consisted mostly of physiologic responses to infection or inflammation (fever, tachycardia, tachypnea, [AbstractComplete] =>

Sepsis was defined in 1991 by the systemic inflammatory response syndrome (SIRS) criteria which consisted mostly of physiologic responses to infection or inflammation (fever, tachycardia, tachypnea, and leukocytosis). These criteria were initially proposed to identify patients with gram-negative bloodstream infection (BSI). However, most patients with BSI are not critically ill at initial presentation using objective clinical scores for acute severity of illness, such as the Pitt bacteremia score (PBS). Lack of specificity and low positive predictive value (PPV) are other pitfalls of the SIRS criteria. Moreover, the implementation of sepsis interventions based on this outdated definition failed to improve patients’ outcomes and in some settings was associated with increased use of broad-spectrum antibiotics and Clostridioides difficile (C. difficile) infection. In 2016, sepsis was redefined as a dysregulatory host response to life-threatening infections using quick sequential organ failure assessment (qSOFA) score. The presence of two of three bedside clinical variables (hypotension, respiratory distress, and altered mental status) that have consistently predicted mortality in patients with infections now constitutes sepsis. The scientific debate continues in the medical literature regarding the performance of the new criteria. Some medical professionals and quality organizations consider these changes to the sepsis definition too revolutionary and are resistant to altering existing medical practice. This narrative review presents infection as a continuum from localized to systemic infection (pre-sepsis) with the potential progression into sepsis and septic shock if appropriate antibiotic therapy and source control are delayed. The review assesses host and microbial factors that may influence the rate of progression through the sepsis cascade and proposes diagnostic considerations and management decisions at each step of the way. It emphasizes the need to utilize precision medicine concepts in selecting empirical antibiotic therapy based on patient-specific risk factors for infections due to resistant bacteria and potential benefits from appropriate therapy across the sepsis spectrum.

[Names] => Nicholas Daering, Majdi N. Al-Hasan [Doi] => 10.37349/ei.2022.00075 [Published] => October 25, 2022 [Viewed] => 827 [Downloaded] => 30 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00075 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 53 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:665–676 [Recommend] => 0 [Keywords] => Bacteremia, bloodstream infection, survival, precision medicine, antimicrobials [DetailTitle] => The Sepsis induced Immune Conundrum [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/53 [Id] => 100375 [ris] => https://www.explorationpub.com/uploads/Article/A100375/62fa49b56a39815c8073ef64f6e3848a.ris [bib] => https://www.explorationpub.com/uploads/Article/A100375/bb8e81a8c5bf7b9bea1589c176938688.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Daering N, Al-Hasan MN. The progression of sepsis from physiologic systemic inflammatory response to immune dysregulation due to life-threatening infections. Explor Immunol. 2022;2:665–76. https://doi.org/10.37349/ei.2022.00075 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-10-31 06:37:52 [Bib_Time] => 2022-10-31 06:37:52 [KeysWordContens] => The progression of sepsis from physiologic systemic inflammatory response to immune dysregulation due to life-threatening infections, Bacteremia, bloodstream infection, survival, precision medicine, antimicrobials, Sepsis was defined in 1991 by the systemic inflammatory response syndrome (SIRS) criteria which consisted mostly of physiologic responses to infection or inflammation (fever, tachycardia, tachypnea, and leukocytosis). These criteria were initially proposed to identify patients with gram-negative bloodstream infection (BSI). However, most patients with BSI are not critically ill at initial presentation using objective clinical scores for acute severity of illness, such as the Pitt bacteremia score (PBS). Lack of specificity and low positive predictive value (PPV) are other pitfalls of the SIRS criteria. Moreover, the implementation of sepsis interventions based on this outdated definition failed to improve patients’ outcomes and in some settings was associated with increased use of broad-spectrum antibiotics and Clostridioides difficile (C. difficile) infection. In 2016, sepsis was redefined as a dysregulatory host response to life-threatening infections using quick sequential organ failure assessment (qSOFA) score. The presence of two of three bedside clinical variables (hypotension, respiratory distress, and altered mental status) that have consistently predicted mortality in patients with infections now constitutes sepsis. The scientific debate continues in the medical literature regarding the performance of the new criteria. Some medical professionals and quality organizations consider these changes to the sepsis definition too revolutionary and are resistant to altering existing medical practice. This narrative review presents infection as a continuum from localized to systemic infection (pre-sepsis) with the potential progression into sepsis and septic shock if appropriate antibiotic therapy and source control are delayed. The review assesses host and microbial factors that may influence the rate of progression through the sepsis cascade and proposes diagnostic considerations and management decisions at each step of the way. It emphasizes the need to utilize precision medicine concepts in selecting empirical antibiotic therapy based on patient-specific risk factors for infections due to resistant bacteria and potential benefits from appropriate therapy across the sepsis spectrum. ,Nicholas Daering, Majdi N. Al-Hasan [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [75] => Array ( [ArticleId] => 403 [Create_Time] => 2022-10-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202305/20230522055620.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100376/100376.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100376/100376.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100376/100376_cover.png [JournalsId] => 5 [Title] => Do endometrial immune changes with age prior to menopause compromise fertility in women? [Abstract] => Menopause signals the end of the reproductive period in women. However, fertility and fecundity decrease with increasing age prior to menopause demonstrating that changes in the premenopausal female [AbstractComplete] =>

Menopause signals the end of the reproductive period in women. However, fertility and fecundity decrease with increasing age prior to menopause demonstrating that changes in the premenopausal female reproductive tract (FRT) are already occurring that negatively impact reproductive success. The effects of age on the endometrium are poorly understood, in contrast to the ovary where changes occur with increasing age that negatively affect successful reproduction. The endometrial immune system is essential for generating a receptive endometrium, but the link between the immune and reproductive systems in the endometrium in the years prior to menopause has not been well-defined. Since the endometrial immune system is tightly regulated to maximize reproductive success and pathogen protection, changes in immune function with increasing premenopausal age have the potential to impact reproduction.

[Names] => Mickey V. Patel ... Charles R. Wira [Doi] => 10.37349/ei.2022.00076 [Published] => October 29, 2022 [Viewed] => 927 [Downloaded] => 18 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00076 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:677–692 [Recommend] => 0 [Keywords] => Endometrium, aging, immunity, reproduction, implantation, epithelial cells, CD8+ T cells, menopause [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100376 [ris] => https://www.explorationpub.com/uploads/Article/A100376/55a062797a73994207169fd7a4767d9c.ris [bib] => https://www.explorationpub.com/uploads/Article/A100376/3e99f01620e443c775d060325f6d2c58.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-25 [CitethisArticle] => Patel MV, Shen Z, Wira CR. Do endometrial immune changes with age prior to menopause compromise fertility in women? Explor Immunol. 2022;2:677–92. https://doi.org/10.37349/ei.2022.00076 [Jindex] => 0 [CName] => Charles R.Wira, [CEmail] => Charles.R.Wira@Dartmouth.edu, [Ris_Time] => 2022-10-21 06:41:18 [Bib_Time] => 2022-10-21 06:41:18 [KeysWordContens] => Do endometrial immune changes with age prior to menopause compromise fertility in women?, Endometrium, aging, immunity, reproduction, implantation, epithelial cells, CD8+ T cells, menopause, Menopause signals the end of the reproductive period in women. However, fertility and fecundity decrease with increasing age prior to menopause demonstrating that changes in the premenopausal female reproductive tract (FRT) are already occurring that negatively impact reproductive success. The effects of age on the endometrium are poorly understood, in contrast to the ovary where changes occur with increasing age that negatively affect successful reproduction. The endometrial immune system is essential for generating a receptive endometrium, but the link between the immune and reproductive systems in the endometrium in the years prior to menopause has not been well-defined. Since the endometrial immune system is tightly regulated to maximize reproductive success and pathogen protection, changes in immune function with increasing premenopausal age have the potential to impact reproduction. ,Mickey V. Patel ... Charles R. Wira [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [76] => Array ( [ArticleId] => 407 [Create_Time] => 2022-10-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202211/20221104065038.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100377/100377.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100377/100377.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100377/100377_cover.png [JournalsId] => 5 [Title] => Natural killer cell-mediated immunopathology in recurrent pregnancy losses [Abstract] => Natural killer (NK) cells have a dual role in human reproduction for maternal-fetal tolerance and protection from infection. During the ovarian cycle and pregnancy, peripheral NK (pNK) and uterine N [AbstractComplete] =>

Natural killer (NK) cells have a dual role in human reproduction for maternal-fetal tolerance and protection from infection. During the ovarian cycle and pregnancy, peripheral NK (pNK) and uterine NK (uNK) cells dynamically change their proportions and cytotoxicities to prepare and accommodate invading trophoblast and maintain pregnancy. However, dysregulated pNK and uNK cell proportions and cytotoxic activities have been associated with aberrant spiral artery remodeling and trophoblast invasion, leading to implantation failures and recurrent pregnancy losses (RPLs). This review will focus on the role of NK cells in RPLs reviewing the ontogeny of NK cells, changes in pNK and uNK cell levels, and activities during the ovarian cycle, normal pregnancy, and RPL. In addition, the immunopathological role of NK cells in endometrial/decidual vascular development and killer immunoglobin-like receptor (KIR) and human leukocyte antigen (HLA)-C interactions are discussed.

[Names] => Thanh Luu ... Joanne Kwak-Kim [Doi] => 10.37349/ei.2022.00077 [Published] => October 30, 2022 [Viewed] => 1616 [Downloaded] => 46 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00077 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 46 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:693–722 [Recommend] => 0 [Keywords] => Natural killer cells, recurrent pregnancy loss, decidual natural killer, peripheral blood natural killer, natural killer cytotoxicity [DetailTitle] => Human Reproduction: Involvement of the Immune System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/46 [Id] => 100377 [ris] => https://www.explorationpub.com/uploads/Article/A100377/b5e556585f3e63d4d32596dd2ba84bc5.ris [bib] => https://www.explorationpub.com/uploads/Article/A100377/ade177deda9bf19465359bd04a78e262.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-25 [CitethisArticle] => Luu T, AlSubki L, Wolf K, Thees A, Ganieva U, Dambaeva S, et al. Natural killer cell-mediated immunopathology in recurrent pregnancy losses. Explor Immunol. 2022;2:693–722. https://doi.org/10.37349/ei.2022.00077 [Jindex] => 0 [CName] => JoanneKwak-Kim, [CEmail] => joanne.kwakkim@rosalindfranklin.edu, [Ris_Time] => 2022-10-23 07:14:23 [Bib_Time] => 2022-10-23 07:14:23 [KeysWordContens] => Natural killer cell-mediated immunopathology in recurrent pregnancy losses, Natural killer cells, recurrent pregnancy loss, decidual natural killer, peripheral blood natural killer, natural killer cytotoxicity, Natural killer (NK) cells have a dual role in human reproduction for maternal-fetal tolerance and protection from infection. During the ovarian cycle and pregnancy, peripheral NK (pNK) and uterine NK (uNK) cells dynamically change their proportions and cytotoxicities to prepare and accommodate invading trophoblast and maintain pregnancy. However, dysregulated pNK and uNK cell proportions and cytotoxic activities have been associated with aberrant spiral artery remodeling and trophoblast invasion, leading to implantation failures and recurrent pregnancy losses (RPLs). This review will focus on the role of NK cells in RPLs reviewing the ontogeny of NK cells, changes in pNK and uNK cell levels, and activities during the ovarian cycle, normal pregnancy, and RPL. In addition, the immunopathological role of NK cells in endometrial/decidual vascular development and killer immunoglobin-like receptor (KIR) and human leukocyte antigen (HLA)-C interactions are discussed. ,Thanh Luu ... Joanne Kwak-Kim [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [77] => Array ( [ArticleId] => 411 [Create_Time] => 2022-10-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202211/20221104065757.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100378/100378.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100378/100378.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100378/100378_cover.png [JournalsId] => 5 [Title] => Utilization of formalin-fixed paraffin-embedded specimens for microbiota characterization in cancer: utility and concern [Abstract] => Microbiome research has enormous potential in cancer research and the use of formalin-fixed paraffin-embedded (FFPE) tissues could offer many advantages. The tumor microenvironment represents a suit [AbstractComplete] =>

Microbiome research has enormous potential in cancer research and the use of formalin-fixed paraffin-embedded (FFPE) tissues could offer many advantages. The tumor microenvironment represents a suitable niche for specific microbes and evidence proves the presence of an endogenous tumor microbiota, here referred to as oncobiota. Awareness of the oncobiota role in tumorigenesis could have a large influence on cancer care, in terms of diagnosis, prevention, and treatment. Moreover, understanding the microbial-related tumor microenvironment, and its influence on tumor immune response and cancer cells will help define important pathogenetic mechanisms in cancer starting or progression. Routine collection of histopathological FFPE samples provides a large availability of specimens essential for affordable and impactful retrospective analyses and for getting robust statistical results. The FFPE tissues are common in the analysis of tumor biopsies including the tumor microbiota characterization which has an important role in the modulation of our immune system and consequently of tumor cells. However, the microbiota analysis starting from FFPE tissues presents methodological pitfalls and limits that may negatively affect the oncobiota research. After examining the methodological and analytical difficulties of this approach, this work seeks to offer workable solutions to promote that research area.

[Names] => Leandro Di Gloria, Elena Niccolai [Doi] => 10.37349/ei.2022.00078 [Published] => October 31, 2022 [Viewed] => 926 [Downloaded] => 28 [Subject] => Perspective [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00078 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 59 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:723–730 [Recommend] => 0 [Keywords] => Microbiome, formalin-fixed paraffin-embedded, cancer, oncobiota [DetailTitle] => New insights in cancer immunology: the role of microbiota from immunosurveillance to immunotherapy [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/59 [Id] => 100378 [ris] => https://www.explorationpub.com/uploads/Article/A100378/33a09c9d368415ccbe3a6ec0e89ff334.ris [bib] => https://www.explorationpub.com/uploads/Article/A100378/229c2213686224b30b2c3c87ab0c6aff.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Di Gloria L, Niccolai E. Utilization of formalin-fixed paraffin-embedded specimens for microbiota characterization in cancer: utility and concern. Explor Immunol. 2022;2:723-30. https://doi.org/10.37349/ei.2022.00078 [Jindex] => 0 [CName] => ElenaNiccolai, [CEmail] => elena.niccolai@unifi.it, [Ris_Time] => 2022-10-23 07:15:04 [Bib_Time] => 2022-10-23 07:15:04 [KeysWordContens] => Utilization of formalin-fixed paraffin-embedded specimens for microbiota characterization in cancer: utility and concern, Microbiome, formalin-fixed paraffin-embedded, cancer, oncobiota, Microbiome research has enormous potential in cancer research and the use of formalin-fixed paraffin-embedded (FFPE) tissues could offer many advantages. The tumor microenvironment represents a suitable niche for specific microbes and evidence proves the presence of an endogenous tumor microbiota, here referred to as oncobiota. Awareness of the oncobiota role in tumorigenesis could have a large influence on cancer care, in terms of diagnosis, prevention, and treatment. Moreover, understanding the microbial-related tumor microenvironment, and its influence on tumor immune response and cancer cells will help define important pathogenetic mechanisms in cancer starting or progression. Routine collection of histopathological FFPE samples provides a large availability of specimens essential for affordable and impactful retrospective analyses and for getting robust statistical results. The FFPE tissues are common in the analysis of tumor biopsies including the tumor microbiota characterization which has an important role in the modulation of our immune system and consequently of tumor cells. However, the microbiota analysis starting from FFPE tissues presents methodological pitfalls and limits that may negatively affect the oncobiota research. After examining the methodological and analytical difficulties of this approach, this work seeks to offer workable solutions to promote that research area. ,Leandro Di Gloria, Elena Niccolai [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [78] => Array ( [ArticleId] => 424 [Create_Time] => 2022-10-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202303/20230301100856.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100379/100379.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100379/100379.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100379/100379_cover.png [JournalsId] => 5 [Title] => Fight fire with fire: the need for a vaccine based on intrinsic disorder and structural flexibility [Abstract] => The absence of advancement in finding efficient vaccines for several human viruses, such as hepatitis C virus (HCV), human immunodeficiency virus type 1 (HIV-1), and herpes simplex viruses (HSVs) de [AbstractComplete] =>

The absence of advancement in finding efficient vaccines for several human viruses, such as hepatitis C virus (HCV), human immunodeficiency virus type 1 (HIV-1), and herpes simplex viruses (HSVs) despite 30, 40, and even 60 years of research, respectively, is unnerving. Among objective reasons for such failure are the highly glycosylated nature of proteins used as primary vaccine targets against these viruses and the presence of neotopes and cryptotopes, as well as high mutation rates of the RNA viruses HCV and HIV-1 and the capability to establish latency by HSVs. However, the lack of success in utilization of the structure-based reverse vaccinology for these viruses is likely to be related to the presence of highly flexible and intrinsically disordered regions in human antibodies (Abs) and the major immunogens of HIV-1, HCV, and HSVs, their surface glycoproteins. This clearly calls for moving from the rational structure-based vaccinology to the unstructural vaccinology based on the utilization of tools designed for the analysis of disordered and flexible proteins, while looking at intrinsically disordered viral antigens and their interactions with intrinsically disordered/flexible Abs.

[Names] => Vladimir N. Uversky [Doi] => 10.37349/ei.2022.00079 [Published] => October 31, 2022 [Viewed] => 1052 [Downloaded] => 53 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00079 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 63 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:731–748 [Recommend] => 0 [Keywords] => Reverse vaccinology, intrinsically disordered protein, antibody, antigen, structural flexibility [DetailTitle] => Old and New Paradigms in Viral Vaccinology [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/63 [Id] => 100379 [ris] => https://www.explorationpub.com/uploads/Article/A100379/8e220c7f4498fc33b81bf923083533a8.ris [bib] => https://www.explorationpub.com/uploads/Article/A100379/c905b02dca7011e93727e844f5c3e9c6.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Uversky VN. Fight fire with fire: the need for a vaccine based on intrinsic disorder and structural flexibility. Explor Immunol. 2022;2:731–48. https://doi.org/10.37349/ei.2022.00079 [Jindex] => 0 [CName] => Vladimir N.Uversky, [CEmail] => vuversky@usf.edu, [Ris_Time] => 2022-10-28 05:40:38 [Bib_Time] => 2022-10-28 05:40:38 [KeysWordContens] => Fight fire with fire: the need for a vaccine based on intrinsic disorder and structural flexibility, Reverse vaccinology, intrinsically disordered protein, antibody, antigen, structural flexibility, The absence of advancement in finding efficient vaccines for several human viruses, such as hepatitis C virus (HCV), human immunodeficiency virus type 1 (HIV-1), and herpes simplex viruses (HSVs) despite 30, 40, and even 60 years of research, respectively, is unnerving. Among objective reasons for such failure are the highly glycosylated nature of proteins used as primary vaccine targets against these viruses and the presence of neotopes and cryptotopes, as well as high mutation rates of the RNA viruses HCV and HIV-1 and the capability to establish latency by HSVs. However, the lack of success in utilization of the structure-based reverse vaccinology for these viruses is likely to be related to the presence of highly flexible and intrinsically disordered regions in human antibodies (Abs) and the major immunogens of HIV-1, HCV, and HSVs, their surface glycoproteins. This clearly calls for moving from the rational structure-based vaccinology to the unstructural vaccinology based on the utilization of tools designed for the analysis of disordered and flexible proteins, while looking at intrinsically disordered viral antigens and their interactions with intrinsically disordered/flexible Abs. ,Vladimir N. Uversky [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [79] => Array ( [ArticleId] => 426 [Create_Time] => 2022-11-02 [zipUrl] => https://www.explorationpub.com/uploads/zip/202305/20230523020231.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100380/100380.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100380/100380.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100380/100380_cover.png [JournalsId] => 5 [Title] => Distributing human leukocyte antigen (HLA) database in histocompatibility: a shift in HLA data governance [Abstract] => Aim: Human leukocyte antigen (HLA) population genetics has been a historical field centralizing data resource. HLA genetics databases typically facilitate access to frequencies of allele, haploty [AbstractComplete] =>

Aim:

Human leukocyte antigen (HLA) population genetics has been a historical field centralizing data resource. HLA genetics databases typically facilitate access to frequencies of allele, haplotype, and genotype format information. Among many resources, the Allele Frequency Net Database (AFND) is a typical centralized repository that allows users to research and analyze immune gene frequencies in different populations around the world. With the massive increase in medical data and the strengthening of data governance laws, the proposal for a new distributed and secure model for the historical centralization method in population genetics has become important. In this paper, a new model of HLA population genetic resources, an alternative distributed version of HLA databases has been developed. It allows users to perform the same research and analysis with other remote sites without sharing their original data and monitoring data access.

Methods:

This new version uses the Master/Worker distributed model and offers distributed algorithms for the calculation of allelic frequencies, haplotypic frequencies and for individual genotypic calculations. The new model was evaluated on a distributed testbed for experiment-driven research Grid’5000 and has obtained good results of accuracy and execution time compared to the original centralized scheme used by researchers.

Results:

The results show that distributed algorithm applied to HLA population genetics resources enables usage control and enables enforcing the security framework of the data-owning institution. It gives the same results for all counting methods in population immunogenetics. With the same frequencies’ estimations, it yields a much quicker computation time in many cases, in particular for large samples.

Conclusions:

Distributing previously centralized resources is an interesting perspective enhancing better control of data sharing.

[Names] => Sirine Sayadi ... Pierre-Antoine Gourraud [Doi] => 10.37349/ei.2022.00080 [Published] => November 01, 2022 [Viewed] => 1040 [Downloaded] => 46 [Subject] => Original Article [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00080 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 80 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:749–759 [Recommend] => 0 [Keywords] => Distributed analysis, precision medicine, data governance, security, allele frequency, haplotype, genotype [DetailTitle] => Bioinformatics, Big Data, AI: Exploring Immunology [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/80 [Id] => 100380 [ris] => https://www.explorationpub.com/uploads/Article/A100380/b98d02cf59bf17cfcb898595314e04ea.ris [bib] => https://www.explorationpub.com/uploads/Article/A100380/d0a0c22f7cdd276181ecc6fc15337b3c.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Sayadi S, Douillard V, Vince N, Südholt M, Gourraud PA. Distributing human leukocyte antigen (HLA) database in histocompatibility: a shift in HLA data governance. Explor Immunol. 2022;2:749–59. https://doi.org/10.37349/ei.2022.00080 [Jindex] => 0 [CName] => MarioSüdholt,Pierre-AntoineGourraud, [CEmail] => mario.sudholt@imt-atlantique.fr,pierre-antoine.gourraud@univ-nantes.fr, [Ris_Time] => 2022-10-28 01:16:26 [Bib_Time] => 2022-10-28 01:16:26 [KeysWordContens] => Distributing human leukocyte antigen (HLA) database in histocompatibility: a shift in HLA data governance, Distributed analysis, precision medicine, data governance, security, allele frequency, haplotype, genotype, Aim: Human leukocyte antigen (HLA) population genetics has been a historical field centralizing data resource. HLA genetics databases typically facilitate access to frequencies of allele, haplotype, and genotype format information. Among many resources, the Allele Frequency Net Database (AFND) is a typical centralized repository that allows users to research and analyze immune gene frequencies in different populations around the world. With the massive increase in medical data and the strengthening of data governance laws, the proposal for a new distributed and secure model for the historical centralization method in population genetics has become important. In this paper, a new model of HLA population genetic resources, an alternative distributed version of HLA databases has been developed. It allows users to perform the same research and analysis with other remote sites without sharing their original data and monitoring data access. Methods: This new version uses the Master/Worker distributed model and offers distributed algorithms for the calculation of allelic frequencies, haplotypic frequencies and for individual genotypic calculations. The new model was evaluated on a distributed testbed for experiment-driven research Grid’5000 and has obtained good results of accuracy and execution time compared to the original centralized scheme used by researchers. Results: The results show that distributed algorithm applied to HLA population genetics resources enables usage control and enables enforcing the security framework of the data-owning institution. It gives the same results for all counting methods in population immunogenetics. With the same frequencies’ estimations, it yields a much quicker computation time in many cases, in particular for large samples. Conclusions: Distributing previously centralized resources is an interesting perspective enhancing better control of data sharing. ,Sirine Sayadi ... Pierre-Antoine Gourraud [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [80] => Array ( [ArticleId] => 445 [Create_Time] => 2022-12-27 [zipUrl] => https://www.explorationpub.com/uploads/zip/202212/20221228010013.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100381/100381.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100381/100381.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100381/100381_cover.png [JournalsId] => 5 [Title] => Role of tyrosine kinase 2 signals during progression of psoriasis [Abstract] => Psoriasis is a skin disease characterized by scaly erythema, parakeratosis, and epidermal hyperplasia. Application of imiquimod (IMQ), a ligand for Toll-like receptor 7, produces a mouse model for psoriasis. IMQ application induces scaling, erythema, and thickness in skin lesions, and the symptoms are milder in interleukin-23 p19 (Il23p19)-deficient and Il17a-deficient mice than in wild-type mice; [AbstractComplete] =>

Psoriasis is a skin disease characterized by scaly erythema, parakeratosis, and epidermal hyperplasia. Application of imiquimod (IMQ), a ligand for Toll-like receptor 7, produces a mouse model for psoriasis. IMQ application induces scaling, erythema, and thickness in skin lesions, and the symptoms are milder in interleukin-23 p19 (Il23p19)-deficient and Il17a-deficient mice than in wild-type mice; this suggests that the interleukin-23 (IL-23)/T helper 17 (Th17) axis and Th17 cell-secreting cytokines play essential roles in the IMQ-induced psoriasis model. It is notable that a genome-wide association study identified the human tyrosine kinase 2 (TYK2) gene within the psoriasis susceptibility locus. After IMQ application, mice lacking Tyk2, a mouse homologue of the human TYK2 gene, exhibited significantly lower symptom scores of psoriasis and diminished inflammatory cell infiltration in the skin lesions. Tyk2-deficient mice also failed to increase CD4+IL-17+ or CD4+ interferon-γ+ (IFN-γ+) T cells in the draining lymph nodes or to produce Th17 cell-related cytokines after IMQ application. Furthermore, Tyk2 deficiency led to diminished skin inflammation induced by IL-23 and IL-22 injections. These results indicate that Tyk2-mediated signals in mice contribute to multiple steps of immune and inflammatory responses during the development of psoriasis; therefore, TYK2 targeting may be a promising strategy to treat patients with psoriasis. Recent clinical trials have shown that TYK2 inhibitors have a high overall response rate with good tolerability in the management of psoriasis. This review describes the fundamental mechanisms of Tyk2 inhibition in immune/inflammatory diseases.

[Names] => Ryuta Muromoto ... Tadashi Matsuda [Doi] => 10.37349/ei.2022.00081 [Published] => December 27, 2022 [Viewed] => 1125 [Downloaded] => 42 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00081 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 92 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:760–770 [Recommend] => 0 [Keywords] => Tyrosine kinase 2 (TYK2), interleukin-23 (IL-23), interleukin-17 (IL-17), T helper 1 (Th1), T helper 17 (Th17), signal transducer and activator of transcription 3 (STAT3), inhibitor of nuclear factor κB kinase-ζ(IκB-ζ), psor [DetailTitle] => Cytokines and Skin Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/92 [Id] => 100381 [ris] => https://www.explorationpub.com/uploads/Article/A100381/6c527e18d1be19eba9a4fe56c7b87941.ris [bib] => https://www.explorationpub.com/uploads/Article/A100381/3a720147ccc18f46a63dad61801b40e6.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Muromoto R, Oritani K, Matsuda T. Role of tyrosine kinase 2 signals during progression of psoriasis. Explor Immunol. 2022;2:760–70. https://doi.org/10.37349/ei.2022.00081 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-12-27 06:10:10 [Bib_Time] => 2022-12-27 06:10:10 [KeysWordContens] => Role of tyrosine kinase 2 signals during progression of psoriasis, Tyrosine kinase 2 (TYK2), interleukin-23 (IL-23), interleukin-17 (IL-17), T helper 1 (Th1), T helper 17 (Th17), signal transducer and activator of transcription 3 (STAT3), inhibitor of nuclear factor κB kinase-ζ(IκB-ζ), psoriasis, Psoriasis is a skin disease characterized by scaly erythema, parakeratosis, and epidermal hyperplasia. Application of imiquimod (IMQ), a ligand for Toll-like receptor 7, produces a mouse model for psoriasis. IMQ application induces scaling, erythema, and thickness in skin lesions, and the symptoms are milder in interleukin-23 p19 (Il23p19)-deficient and Il17a-deficient mice than in wild-type mice; this suggests that the interleukin-23 (IL-23)/T helper 17 (Th17) axis and Th17 cell-secreting cytokines play essential roles in the IMQ-induced psoriasis model. It is notable that a genome-wide association study identified the human tyrosine kinase 2 (TYK2) gene within the psoriasis susceptibility locus. After IMQ application, mice lacking Tyk2, a mouse homologue of the human TYK2 gene, exhibited significantly lower symptom scores of psoriasis and diminished inflammatory cell infiltration in the skin lesions. Tyk2-deficient mice also failed to increase CD4+IL-17+ or CD4+ interferon-γ+ (IFN-γ+) T cells in the draining lymph nodes or to produce Th17 cell-related cytokines after IMQ application. Furthermore, Tyk2 deficiency led to diminished skin inflammation induced by IL-23 and IL-22 injections. These results indicate that Tyk2-mediated signals in mice contribute to multiple steps of immune and inflammatory responses during the development of psoriasis; therefore, TYK2 targeting may be a promising strategy to treat patients with psoriasis. Recent clinical trials have shown that TYK2 inhibitors have a high overall response rate with good tolerability in the management of psoriasis. This review describes the fundamental mechanisms of Tyk2 inhibition in immune/inflammatory diseases. ,Ryuta Muromoto ... Tadashi Matsuda [PublishedText] => Published [IsEdit] => 0 [AccountId] => 24 [Zh] => 1 ) [81] => Array ( [ArticleId] => 448 [Create_Time] => 2022-12-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202212/20221227081134.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100382/100382.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100382/100382.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100382/100382_cover.png [JournalsId] => 5 [Title] => Signal-transducing adaptor protein-2 modulates T-cell functions [Abstract] => Immune responses are orchestrated by controlling the initiation, magnitude, and duration of various signaling pathways. Adaptor proteins act as positive or negative regulators by targeting critical [AbstractComplete] =>

Immune responses are orchestrated by controlling the initiation, magnitude, and duration of various signaling pathways. Adaptor proteins act as positive or negative regulators by targeting critical molecules of signaling cascades. Signal-transducing adaptor protein-2 (STAP-2) contains typical features of adaptor proteins, like a pleckstrin homology (PH) domain in the N-terminal region and a Src homology 2 (SH2) domain in the central region. STAP-2 binds to a variety of signaling or transcriptional molecules to control multiple steps of inflammatory/immune responses. STAP-2 enhances T-cell receptor (TCR)-mediated signaling via the association with TCR-proximal CD3ζ immunoreceptor tyrosine-based activation motifs (ITAMs) and lymphocyte-specific protein tyrosine kinase (Lck). STAP-2 decreases adherence of T-cells to fibronectin (FN) through an association with focal adhesion kinase (Fak) and Casitas B-lineage Lymphoma (c-Cbl), and increases chemotaxis of T-cells toward stromal cell-derived factor-1α (SDF-1α) through interactions with Vav1 and Ras-related C3 botulinum toxin substrate 1 (Rac1). STAP-2 positively regulates activation-induced cell deathrough the association with Fas and caspase-8. This review describes the current knowledge of the roles of STAP-2 in T-cell-dependent immune responses and the possible clinical utility of STAP-2-targeting therapies.

[Names] => Tadashi Matsuda ... Kenji Oritani [Doi] => 10.37349/ei.2022.00082 [Published] => December 27, 2022 [Viewed] => 806 [Downloaded] => 30 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00082 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 94 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:771–782 [Recommend] => 0 [Keywords] => Signal-transducing adaptor protein, adaptor protein, signal transduction, T-cell, immune response, autoimmunity, chimeric antigen receptor T-cells [DetailTitle] => The Role of Adaptor Proteins in Lymphoid Cell Signaling [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/94 [Id] => 100382 [ris] => https://www.explorationpub.com/uploads/Article/A100382/ac400df22e865da45c778aa414b4faf2.ris [bib] => https://www.explorationpub.com/uploads/Article/A100382/f2d9d738f1e5fa8edecfc65049cbf080.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Matsuda T, Sasaki Y, Kagohashi K, Saitoh K, Sekine Y, Kashiwakura JI, et al. Signal-transducing adaptor protein-2 modulates T-cell functions. Explor Immunol. 2022;2:771–82. https://doi.org/10.37349/ei.2022.00082 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2022-12-26 06:23:57 [Bib_Time] => 2022-12-26 06:23:57 [KeysWordContens] => Signal-transducing adaptor protein-2 modulates T-cell functions, Signal-transducing adaptor protein, adaptor protein, signal transduction, T-cell, immune response, autoimmunity, chimeric antigen receptor T-cells, Immune responses are orchestrated by controlling the initiation, magnitude, and duration of various signaling pathways. Adaptor proteins act as positive or negative regulators by targeting critical molecules of signaling cascades. Signal-transducing adaptor protein-2 (STAP-2) contains typical features of adaptor proteins, like a pleckstrin homology (PH) domain in the N-terminal region and a Src homology 2 (SH2) domain in the central region. STAP-2 binds to a variety of signaling or transcriptional molecules to control multiple steps of inflammatory/immune responses. STAP-2 enhances T-cell receptor (TCR)-mediated signaling via the association with TCR-proximal CD3ζ immunoreceptor tyrosine-based activation motifs (ITAMs) and lymphocyte-specific protein tyrosine kinase (Lck). STAP-2 decreases adherence of T-cells to fibronectin (FN) through an association with focal adhesion kinase (Fak) and Casitas B-lineage Lymphoma (c-Cbl), and increases chemotaxis of T-cells toward stromal cell-derived factor-1α (SDF-1α) through interactions with Vav1 and Ras-related C3 botulinum toxin substrate 1 (Rac1). STAP-2 positively regulates activation-induced cell deathrough the association with Fas and caspase-8. This review describes the current knowledge of the roles of STAP-2 in T-cell-dependent immune responses and the possible clinical utility of STAP-2-targeting therapies. ,Tadashi Matsuda ... Kenji Oritani [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 ) [82] => Array ( [ArticleId] => 462 [Create_Time] => 2022-12-29 [zipUrl] => https://www.explorationpub.com/uploads/zip/202305/20230530055522.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100383/100383.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100383/100383.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100383/100383_cover.png [JournalsId] => 5 [Title] => The synergistic effects of the constant region and variable heavy chain families of multimeric immunoglobulin M on its interaction with Fc-mu receptor and antigen [Abstract] => Aim: As the primary response antibody with increasing use as a therapeutic immunoglobulin (Ig) format, IgM is also the largest antibody structure among the five major human isotypes. Spontaneousl [AbstractComplete] =>

Aim:

As the primary response antibody with increasing use as a therapeutic immunoglobulin (Ig) format, IgM is also the largest antibody structure among the five major human isotypes. Spontaneously formed pentamers and hexamers of IgM have avidity effects that could compensate for weaker interactions in monomeric Igs. However, this advantage is counterbalanced by potential steric clashes when binding to multiple large antigens. Recent findings have challenged the expected canonical independence of Fc receptor (FcR) binding at the heavy chain constant (C)-region where the heavy chain C-region isotypes affected antigen binding at the variable (V)-regions, and the variable heavy (VH) families of the V-region affected FcR engagement at the antibody C-regions. With such effects found on other Ig isotypes, IgM candidates need to be investigated with regards to such effects, especially when considering its natural oligomerisation at the C-region that can amplify or modulate such allosteric effects.

Methods:

Through a panel of 14 recombinant complementarity determining regions (CDRs)-grafted trastuzumab and pertuzumab VH1-7 IgMs subjected to bio-layer interferometry measurements, the interactions with the antigen human epidermal growth factor receptor 2 (Her2), Fc-mu receptor (FcμR), and superantigen Protein L (PpL) were investigated.

Results:

Significant effects from the V-regions to mitigate FcμR binding and the IgM C-region bidirectional effect modulating Her2 antigen engagements at the V-regions were found. Additional modulatory effects from superantigen PpL binding on the V-region of the kappa chain (Vκ) mitigating antigen binding were also found, revealing possible novel mechanisms of antibody superantigens that can be moderated by the antibody VH frameworks.

Conclusions:

These findings show that the oligomerisation of IgMs plays a significant role in FcμR, antigen, and superantigen binding that made IgM distinct from the other antibody isotypes and how these features should be considered during further development and protein engineering of IgM therapeutics.

[Names] => Wei-Li Ling, Samuel Ken-En Gan [Doi] => 10.37349/ei.2022.00083 [Published] => December 29, 2022 [Viewed] => 862 [Downloaded] => 36 [Subject] => Original Article [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00083 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:783–793 [Recommend] => 0 [Keywords] => Immunoglobulin M, Fc-mu receptor, human epidermal growth factor receptor 2, avidity, hexamers, equilibrium dissociation constant, bio-layer interferometry, Protein L [DetailTitle] => [DetailUrl] => [Id] => 100383 [ris] => https://www.explorationpub.com/uploads/Article/A100383/3538370755a11a2564d9e1f4c97e0771.ris [bib] => https://www.explorationpub.com/uploads/Article/A100383/265eacf43ee20a6c94aac6f24996c4f1.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Ling WL, Gan SKE. The synergistic effects of the constant region and variable heavy chain families of multimeric immunoglobulin M on its interaction with Fc-mu receptor and antigen. Explor Immunol. 2022;2:783–93. https://doi.org/10.37349/ei.2022.00083 [Jindex] => 0 [CName] => Samuel Ken-EnGan, [CEmail] => samgan@apdskeg.com, [Ris_Time] => 2022-12-29 02:50:06 [Bib_Time] => 2022-12-29 02:50:06 [KeysWordContens] => The synergistic effects of the constant region and variable heavy chain families of multimeric immunoglobulin M on its interaction with Fc-mu receptor and antigen, Immunoglobulin M, Fc-mu receptor, human epidermal growth factor receptor 2, avidity, hexamers, equilibrium dissociation constant, bio-layer interferometry, Protein L, Aim: As the primary response antibody with increasing use as a therapeutic immunoglobulin (Ig) format, IgM is also the largest antibody structure among the five major human isotypes. Spontaneously formed pentamers and hexamers of IgM have avidity effects that could compensate for weaker interactions in monomeric Igs. However, this advantage is counterbalanced by potential steric clashes when binding to multiple large antigens. Recent findings have challenged the expected canonical independence of Fc receptor (FcR) binding at the heavy chain constant (C)-region where the heavy chain C-region isotypes affected antigen binding at the variable (V)-regions, and the variable heavy (VH) families of the V-region affected FcR engagement at the antibody C-regions. With such effects found on other Ig isotypes, IgM candidates need to be investigated with regards to such effects, especially when considering its natural oligomerisation at the C-region that can amplify or modulate such allosteric effects. Methods: Through a panel of 14 recombinant complementarity determining regions (CDRs)-grafted trastuzumab and pertuzumab VH1-7 IgMs subjected to bio-layer interferometry measurements, the interactions with the antigen human epidermal growth factor receptor 2 (Her2), Fc-mu receptor (FcμR), and superantigen Protein L (PpL) were investigated. Results: Significant effects from the V-regions to mitigate FcμR binding and the IgM C-region bidirectional effect modulating Her2 antigen engagements at the V-regions were found. Additional modulatory effects from superantigen PpL binding on the V-region of the kappa chain (Vκ) mitigating antigen binding were also found, revealing possible novel mechanisms of antibody superantigens that can be moderated by the antibody VH frameworks. Conclusions: These findings show that the oligomerisation of IgMs plays a significant role in FcμR, antigen, and superantigen binding that made IgM distinct from the other antibody isotypes and how these features should be considered during further development and protein engineering of IgM therapeutics. ,Wei-Li Ling, Samuel Ken-En Gan [PublishedText] => Published [IsEdit] => 0 [AccountId] => 22 [Zh] => 1 ) [83] => Array ( [ArticleId] => 466 [Create_Time] => 2022-12-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202302/20230228033823.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100384/100384.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100384/100384.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100384/100384_cover.png [JournalsId] => 5 [Title] => Incursions by severe acute respiratory syndrome coronavirus-2 on the host anti-viral immunity during mild, moderate, and severe coronavirus disease 2019 disease [Abstract] => The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection in the human host can lead to various clinical manifestations, from symptomless carriers to mild to moderate to severe/critical illness. Therefore, the clinical classification of SARS-CoV-2 disease, based on severity, is a reliable way to predict disease states in SARS-CoV-2 infection. Recent studies on genomics, transcriptomics, epigenomics, and immunogenomics, along with spatial analysis of immune cells have delineated and defined the categorization of these disease groups using these high throughout technologies. These technologies hold the promise of providing not only a detailed but a holistic view of SARS-CoV-2-led pathogenesis. The main genomic, cellular, and immunologic features of each disease category, and what separates them spatially and molecularly are discussed in this brief review to provide a foundational spatial understanding of SARS-CoV-2 immunopathogenesis. [AbstractComplete] =>

The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection in the human host can lead to various clinical manifestations, from symptomless carriers to mild to moderate to severe/critical illness. Therefore, the clinical classification of SARS-CoV-2 disease, based on severity, is a reliable way to predict disease states in SARS-CoV-2 infection. Recent studies on genomics, transcriptomics, epigenomics, and immunogenomics, along with spatial analysis of immune cells have delineated and defined the categorization of these disease groups using these high throughout technologies. These technologies hold the promise of providing not only a detailed but a holistic view of SARS-CoV-2-led pathogenesis. The main genomic, cellular, and immunologic features of each disease category, and what separates them spatially and molecularly are discussed in this brief review to provide a foundational spatial understanding of SARS-CoV-2 immunopathogenesis.

[Names] => Nitin Saksena ... Thyago H. Cardoso [Doi] => 10.37349/ei.2022.00084 [Published] => December 29, 2022 [Viewed] => 1215 [Downloaded] => 47 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2022.00084 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 64 [TitleAbbr] => Explor Immunol. [Pages] => 2022;2:794–811 [Recommend] => 0 [Keywords] => Severe acute respiratory syndrome coronavirus-2, anti-viral immunity, genomics, interferons, immune cells, tropism [DetailTitle] => Immunology, Immunopathology and Genomics of SARS-COV-2 [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/64 [Id] => 100384 [ris] => https://www.explorationpub.com/uploads/Article/A100384/7870455dabd0816c6ef907f33fb4bd8d.ris [bib] => https://www.explorationpub.com/uploads/Article/A100384/d0a710fe4e2dc6751898773215342fdc.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-26 [CitethisArticle] => Saksena N, Bonam SR, Miranda-Saksena M, Cardoso TH. Incursions by severe acute respiratory syndrome coronavirus-2 on the host anti-viral immunity during mild, moderate, and severe coronavirus disease 2019 disease. Explor Immunol. 2022;2:794–811. https://doi.org/10.37349/ei.2022.00084 [Jindex] => 0 [CName] => NitinSaksena, [CEmail] => nitin.saksena@bigpond.com, [Ris_Time] => 2022-12-29 02:52:06 [Bib_Time] => 2022-12-29 02:52:06 [KeysWordContens] => Incursions by severe acute respiratory syndrome coronavirus-2 on the host anti-viral immunity during mild, moderate, and severe coronavirus disease 2019 disease, Severe acute respiratory syndrome coronavirus-2, anti-viral immunity, genomics, interferons, immune cells, tropism, The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection in the human host can lead to various clinical manifestations, from symptomless carriers to mild to moderate to severe/critical illness. Therefore, the clinical classification of SARS-CoV-2 disease, based on severity, is a reliable way to predict disease states in SARS-CoV-2 infection. Recent studies on genomics, transcriptomics, epigenomics, and immunogenomics, along with spatial analysis of immune cells have delineated and defined the categorization of these disease groups using these high throughout technologies. These technologies hold the promise of providing not only a detailed but a holistic view of SARS-CoV-2-led pathogenesis. The main genomic, cellular, and immunologic features of each disease category, and what separates them spatially and molecularly are discussed in this brief review to provide a foundational spatial understanding of SARS-CoV-2 immunopathogenesis. ,Nitin Saksena ... Thyago H. Cardoso [PublishedText] => Published [IsEdit] => 0 [AccountId] => 47 [Zh] => 1 ) [84] => Array ( [ArticleId] => 469 [Create_Time] => 2023-02-24 [zipUrl] => https://www.explorationpub.com/uploads/zip/202302/20230228065435.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100385/100385.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100385/100385.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100385/100385_cover.png [JournalsId] => 5 [Title] => Immunoinformatics and tick vaccinology [Abstract] => Immunoinformatics is an emerging area focused on development and applications of methods used to facilitate vaccine development. There is a growing interest in the field of vaccinology cente [AbstractComplete] =>

Immunoinformatics is an emerging area focused on development and applications of methods used to facilitate vaccine development. There is a growing interest in the field of vaccinology centered on the new omic science named ‘vaccinomics’. However, this approach has not succeeded to provide a solution against major infections affecting both animals and humans, since tick vaccines are still being developed based on conventional biochemical or immunological methods to dissect the molecular structure of the pathogen, looking for a candidate antigen. The availability of complete genomes and the novel advanced technologies, such as data mining, bioinformatics, microarrays, and proteomics, have revolutionized the approach to vaccine development and provided a new impulse to tick research. The aim of this review is to explore how modern vaccinology will contribute to the discovery of new candidate antigens and to understand the research process to improve existing vaccines. Under this concept, the omic age of ticks will make it possible to design vaccines starting from a prediction based on the in silico analysis of gene sequences obtained by data mining using computer algorithms, without the need to keep the pathogen growing in vitro. This new genome-based approach has been named “reverse vaccinology 3.0” or “vaccinomics 1.0” and can be applied to ticks.

[Names] => Rodrigo Rosario-Cruz ... Fernando Rosario-Domínguez [Doi] => 10.37349/ei.2023.00085 [Published] => February 24, 2023 [Viewed] => 979 [Downloaded] => 42 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00085 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 80 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:1–16 [Recommend] => 0 [Keywords] => Rhipicephalus microplus, tick vaccines, reverse vaccinology, vaccinomics, systems biology [DetailTitle] => Bioinformatics, Big Data, AI: Exploring Immunology [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/80 [Id] => 100385 [ris] => https://www.explorationpub.com/uploads/Article/A100385/1ad115700924f082cb4bed3c1d222901.ris [bib] => https://www.explorationpub.com/uploads/Article/A100385/92742b1f8de6aa9a89c1d580fdff5209.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Rosario-Cruz R, Domínguez-García DI, López-Silva S, Rosario-Domínguez F. Immunoinformatics and tick vaccinology. Explor Immunol. 2023;3:1–16. https://doi.org/10.37349/ei.2023.00085 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-02-27 02:47:04 [Bib_Time] => 2023-02-27 02:47:04 [KeysWordContens] => Immunoinformatics and tick vaccinology, Rhipicephalus microplus, tick vaccines, reverse vaccinology, vaccinomics, systems biology, Immunoinformatics is an emerging area focused on development and applications of methods used to facilitate vaccine development. There is a growing interest in the field of vaccinology centered on the new omic science named ‘vaccinomics’. However, this approach has not succeeded to provide a solution against major infections affecting both animals and humans, since tick vaccines are still being developed based on conventional biochemical or immunological methods to dissect the molecular structure of the pathogen, looking for a candidate antigen. The availability of complete genomes and the novel advanced technologies, such as data mining, bioinformatics, microarrays, and proteomics, have revolutionized the approach to vaccine development and provided a new impulse to tick research. The aim of this review is to explore how modern vaccinology will contribute to the discovery of new candidate antigens and to understand the research process to improve existing vaccines. Under this concept, the omic age of ticks will make it possible to design vaccines starting from a prediction based on the in silico analysis of gene sequences obtained by data mining using computer algorithms, without the need to keep the pathogen growing in vitro. This new genome-based approach has been named “reverse vaccinology 3.0” or “vaccinomics 1.0” and can be applied to ticks. ,Rodrigo Rosario-Cruz ... Fernando Rosario-Domínguez [PublishedText] => Published [IsEdit] => 0 [AccountId] => 38 [Zh] => 1 ) [85] => Array ( [ArticleId] => 485 [Create_Time] => 2023-02-24 [zipUrl] => https://www.explorationpub.com/uploads/zip/202302/20230224004309.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100386/100386.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100386/100386.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100386/100386_Cover.png [JournalsId] => 5 [Title] => Cytomegalovirus at the crossroads of immunosenescence and oncogenesis [Abstract] => Human cytomegalovirus (HCMV), whose genome is around 235 kb, is a ubiquitous human herpesvirus that infects between 40% and 95% of the population. Though HCMV infection is co [AbstractComplete] =>

Human cytomegalovirus (HCMV), whose genome is around 235 kb, is a ubiquitous human herpesvirus that infects between 40% and 95% of the population. Though HCMV infection is commonly asymptomatic and leads to subtle clinical symptoms, it can promote robust immune responses and establish lifelong latency. In addition, in immunocompromised hosts, including individuals with acquired immunodeficiency syndrome (AIDS), transplant recipients, and developing fetuses it can lead to severe diseases. Immunosenescence, well-defined as the alterations in the immune system, is linked mainly to aging and has been recently gathering considerable attention. Senescence was characterized by an elevated inflammation and hence considered a powerful contributor to “inflammaging” that is measured mainly by tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and C-reactive protein (CRP) levels as well as latent viral infections, for instance, cytomegalovirus (CMV). Inflammaging resulted in a senescence-associated secretory phenotype (SASP). HCMV is markedly associated with accelerated aging of the immune system as well as several age-associated diseases that accumulate and subsequently deteriorate the immune responses, thus have been linked to mortality, declined vaccine efficacy, serious diseases, and tumors in the elderly. HCMV triggers or exacerbates immunosenescence; on the other hand, the weakened immune responses and inflammaging favor viral reactivation and highlight the role of HCMV in aging as well as viral-associated tumors. HCMV reactivation resulting in sequential lytic and latent viral cycles could contribute to HCMV genomic variability. Besides the oncomodulatory role and transforming capacities of HCMV, the immune-privileged tumor microenvironment has been considered the main element in tumor progression and aggressiveness. Therefore, the interplay between HCMV, immunosenescence, and cancer will aid in discovering new therapeutic approaches that target HCMV and act as immune response boosters mainly to fight cancers of poor prognosis, particularly in the elderly population.

[Names] => Fidaa Bouezzedine ... Georges Herbein [Doi] => 10.37349/ei.2023.00086 [Published] => February 24, 2023 [Viewed] => 660 [Downloaded] => 20 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00086 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 111 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:17–27 [Recommend] => 0 [Keywords] => Cytomegalovirus, immunosenescence, oncomodulation, oncogenesis, inflammaging, tumor microenvironment [DetailTitle] => Immunosenescence: Mechanisms and Its Impact [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/111 [Id] => 100386 [ris] => https://www.explorationpub.com/uploads/Article/A100386/37537a25d8fc688cb974ba1e4f71fb9d.ris [bib] => https://www.explorationpub.com/uploads/Article/A100386/3e9ee0630b6a9efd48f3de8950607c89.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Bouezzedine F, El Baba R, Morot-Bizot S, Diab-Assaf M, Herbein G. Cytomegalovirus at the crossroads of immunosenescence and oncogenesis. Explor Immunol. 2023;3:17–27. https://doi.org/10.37349/ei.2023.00086 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-02-23 01:44:34 [Bib_Time] => 2023-02-23 01:44:34 [KeysWordContens] => Cytomegalovirus at the crossroads of immunosenescence and oncogenesis, Cytomegalovirus, immunosenescence, oncomodulation, oncogenesis, inflammaging, tumor microenvironment, Human cytomegalovirus (HCMV), whose genome is around 235 kb, is a ubiquitous human herpesvirus that infects between 40% and 95% of the population. Though HCMV infection is commonly asymptomatic and leads to subtle clinical symptoms, it can promote robust immune responses and establish lifelong latency. In addition, in immunocompromised hosts, including individuals with acquired immunodeficiency syndrome (AIDS), transplant recipients, and developing fetuses it can lead to severe diseases. Immunosenescence, well-defined as the alterations in the immune system, is linked mainly to aging and has been recently gathering considerable attention. Senescence was characterized by an elevated inflammation and hence considered a powerful contributor to “inflammaging” that is measured mainly by tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and C-reactive protein (CRP) levels as well as latent viral infections, for instance, cytomegalovirus (CMV). Inflammaging resulted in a senescence-associated secretory phenotype (SASP). HCMV is markedly associated with accelerated aging of the immune system as well as several age-associated diseases that accumulate and subsequently deteriorate the immune responses, thus have been linked to mortality, declined vaccine efficacy, serious diseases, and tumors in the elderly. HCMV triggers or exacerbates immunosenescence; on the other hand, the weakened immune responses and inflammaging favor viral reactivation and highlight the role of HCMV in aging as well as viral-associated tumors. HCMV reactivation resulting in sequential lytic and latent viral cycles could contribute to HCMV genomic variability. Besides the oncomodulatory role and transforming capacities of HCMV, the immune-privileged tumor microenvironment has been considered the main element in tumor progression and aggressiveness. Therefore, the interplay between HCMV, immunosenescence, and cancer will aid in discovering new therapeutic approaches that target HCMV and act as immune response boosters mainly to fight cancers of poor prognosis, particularly in the elderly population. ,Fidaa Bouezzedine ... Georges Herbein [PublishedText] => Published [IsEdit] => 0 [AccountId] => 55 [Zh] => 1 ) [86] => Array ( [ArticleId] => 487 [Create_Time] => 2023-02-27 [zipUrl] => https://www.explorationpub.com/uploads/zip/202302/20230227024632.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100387/100387.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100387/100387.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100387/100387_cover.png [JournalsId] => 5 [Title] => Innate immune cell and severe acute respiratory syndrome coronavirus 2 interaction [Abstract] => Coronavirus disease caused by the recently emerged severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) represents a major public health that has submerged the world into a crisis unpreceden [AbstractComplete] =>

Coronavirus disease caused by the recently emerged severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) represents a major public health that has submerged the world into a crisis unprecedented in the modern era. A better understanding of the innate immune response could help to fight this pandemic and be better prepared for potential future outbreaks. Interestingly, innate immune cells can develop a non-specific memory termed trained immunity. This review details recent evidence concerning the interaction of SARS-CoV-2 with innate immune cells, in particular those in which the trained immunity activity has been demonstrated.

[Names] => Naima G. Cortes-Perez [Doi] => 10.37349/ei.2023.00087 [Published] => February 26, 2023 [Viewed] => 559 [Downloaded] => 12 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00087 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 64 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:28–39 [Recommend] => 0 [Keywords] => Innate, immune, severe acute respiratory syndrome coronavirus 2, productive infection [DetailTitle] => Immunology, Immunopathology and Genomics of SARS-COV-2 [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/64 [Id] => 100387 [ris] => https://www.explorationpub.com/uploads/Article/A100387/2754a8003beff6f4145f01254149b63d.ris [bib] => https://www.explorationpub.com/uploads/Article/A100387/6a698b8e39edef85d92f71841b6d0eac.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Cortes-Perez NG. Innate immune cell and severe acute respiratory syndrome coronavirus 2 interaction. Explor Immunol. 2023;3:28–39. https://doi.org/10.37349/ei.2023.00087 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-02-25 04:07:32 [Bib_Time] => 2023-02-25 04:07:32 [KeysWordContens] => Innate immune cell and severe acute respiratory syndrome coronavirus 2 interaction, Innate, immune, severe acute respiratory syndrome coronavirus 2, productive infection, Coronavirus disease caused by the recently emerged severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) represents a major public health that has submerged the world into a crisis unprecedented in the modern era. A better understanding of the innate immune response could help to fight this pandemic and be better prepared for potential future outbreaks. Interestingly, innate immune cells can develop a non-specific memory termed trained immunity. This review details recent evidence concerning the interaction of SARS-CoV-2 with innate immune cells, in particular those in which the trained immunity activity has been demonstrated. ,Naima G. Cortes-Perez [PublishedText] => Published [IsEdit] => 0 [AccountId] => 58 [Zh] => 1 ) [87] => Array ( [ArticleId] => 503 [Create_Time] => 2023-02-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202302/20230228020038.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100388/100388.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100388/100388.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100388/100388_cover.png [JournalsId] => 5 [Title] => Role of tumor necrosis factor receptor-associated factor 5 in B- and T-lymphocytes [Abstract] => Tumor necrosis factor receptor (TNFR)-associated factors (TRAFs) are a family of intracellular signaling adaptors that associate with the cytoplasmic tails of a diverse range of lymphocyte receptors [AbstractComplete] =>

Tumor necrosis factor receptor (TNFR)-associated factors (TRAFs) are a family of intracellular signaling adaptors that associate with the cytoplasmic tails of a diverse range of lymphocyte receptors, including members of the TNFR superfamily, the Toll-like receptor (TLR)/interleukin-1 (IL-1) receptor superfamily, and the IL-6 receptor family that are major targets for therapeutic intervention for inflammatory diseases. TRAF5 is one of the seven family members of the TRAF family and is highly expressed by B- and T-lymphocytes. As compared to other family members, the biological and pathophysiological functions of TRAF5 have remained ambiguous since its discovery. TRAF5 promotes lymphocyte signaling for the TNFR family molecules such as glucocorticoid-induced TNFR family-related protein (GITR), CD27, and CD40. In contrast, TRAF5 limits the activity of the common signaling receptor subunit glycoprotein 130 kDa (gp130) in CD4+ T cells that requires signaling by IL-6 and IL-27. TRAF5 also restrains TLR signaling in B cells. Thus, TRAF5 regulates lymphocyte signaling in both positive and negative ways. This review will summarize the findings of recent studies of TRAF5 in terms of how TRAF5 regulates signaling in lymphocytes and other cell types and how TRAF5 expression contributes to inflammatory and autoimmune diseases in mice and humans.

[Names] => Mari Hikosaka Kuniishi ... Takanori So [Doi] => 10.37349/ei.2023.00088 [Published] => February 27, 2023 [Viewed] => 702 [Downloaded] => 24 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00088 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 94 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:40–55 [Recommend] => 0 [Keywords] => Tumor necrosis factor receptor-associated factor 5, interleukin-6, Janus kinase, signal transducer and activator of transcription, Toll-like receptor, tumor necrosis factor receptor superfamily, inflammation, autoimmunity [DetailTitle] => The Role of Adaptor Proteins in Lymphoid Cell Signaling [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/94 [Id] => 100388 [ris] => https://www.explorationpub.com/uploads/Article/A100388/57d5ff8a5505ceece13a52d285469ac8.ris [bib] => https://www.explorationpub.com/uploads/Article/A100388/9a935760e168fe3ecc564ee1d3360a9d.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Hikosaka Kuniishi M, Ishii N, So T. Role of tumor necrosis factor receptor-associated factor 5 in B- and T-lymphocytes. Explor Immunol. 2023;3:40–55. https://doi.org/10.37349/ei.2023.00088 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-02-27 07:24:55 [Bib_Time] => 2023-02-27 07:24:55 [KeysWordContens] => Role of tumor necrosis factor receptor-associated factor 5 in B- and T-lymphocytes, Tumor necrosis factor receptor-associated factor 5, interleukin-6, Janus kinase, signal transducer and activator of transcription, Toll-like receptor, tumor necrosis factor receptor superfamily, inflammation, autoimmunity, Tumor necrosis factor receptor (TNFR)-associated factors (TRAFs) are a family of intracellular signaling adaptors that associate with the cytoplasmic tails of a diverse range of lymphocyte receptors, including members of the TNFR superfamily, the Toll-like receptor (TLR)/interleukin-1 (IL-1) receptor superfamily, and the IL-6 receptor family that are major targets for therapeutic intervention for inflammatory diseases. TRAF5 is one of the seven family members of the TRAF family and is highly expressed by B- and T-lymphocytes. As compared to other family members, the biological and pathophysiological functions of TRAF5 have remained ambiguous since its discovery. TRAF5 promotes lymphocyte signaling for the TNFR family molecules such as glucocorticoid-induced TNFR family-related protein (GITR), CD27, and CD40. In contrast, TRAF5 limits the activity of the common signaling receptor subunit glycoprotein 130 kDa (gp130) in CD4+ T cells that requires signaling by IL-6 and IL-27. TRAF5 also restrains TLR signaling in B cells. Thus, TRAF5 regulates lymphocyte signaling in both positive and negative ways. This review will summarize the findings of recent studies of TRAF5 in terms of how TRAF5 regulates signaling in lymphocytes and other cell types and how TRAF5 expression contributes to inflammatory and autoimmune diseases in mice and humans. ,Mari Hikosaka Kuniishi ... Takanori So [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 ) [88] => Array ( [ArticleId] => 516 [Create_Time] => 2023-03-15 [zipUrl] => https://www.explorationpub.com/uploads/zip/202303/20230317025956.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100390/100390.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100390/100390.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100390/100390_cover.png [JournalsId] => 5 [Title] => Inflammasomes driven inflammation in lung cancer revisited: a short review [Abstract] => Lung cancer is the leading cause of cancer-related deaths worldwide. The main risk factor for lung cancer is exposure to chemicals present in cigarettes and atmospheric pollutants, which, among othe [AbstractComplete] =>

Lung cancer is the leading cause of cancer-related deaths worldwide. The main risk factor for lung cancer is exposure to chemicals present in cigarettes and atmospheric pollutants, which, among other mechanisms, can increase the risk of cancer by inducing pulmonary inflammation. Among the complex features of inflammatory processes, the role of inflammasomes has attracted increasing attention due to their role in different stages of carcinogenesis. Inflammasomes are intracellular multiprotein complexes that when activated promote the maturation of interleukin-1beta (IL-1β) and IL-18, pro-inflammatory cytokines involved in the promotion, progression, epithelial-mesenchymal transition, metastasis, and resistance to therapy of lung cancer. In this way, this review summarizes the recent findings of inflammasome research in different stages of lung cancer, with a focus on non-small cell lung carcinoma (NSCLC), and highlights these multiprotein complexes as promising targets for cancer therapy.

[Names] => Vitor Rodrigues da Costa ... Rodrigo Pinheiro Araldi [Doi] => 10.37349/ei.2023.00090 [Published] => March 14, 2023 [Viewed] => 1064 [Downloaded] => 44 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00090 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 65 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:70–81 [Recommend] => 0 [Keywords] => Lung cancer, inflammation, inflammasomes, interleukin-1 beta, interleukin-18 [DetailTitle] => DNA Sensing in Lung Inflammation [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/65 [Id] => 100390 [ris] => https://www.explorationpub.com/uploads/Article/A100390/d2318e4402a52317c7da43e19ab3111f.ris [bib] => https://www.explorationpub.com/uploads/Article/A100390/5f06bf1d831700ac31cb49a4ebd530f9.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => da Costa VR, Souza OF, Teixeira MR, Alievi AL, Vigerelli H, Araldi RP. Inflammasomes driven inflammation in lung cancer revisited: a short review. Explor Immunol. 2023;3:70–81. https://doi.org/10.37349/ei.2023.00090 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-03-08 01:38:14 [Bib_Time] => 2023-03-08 01:38:14 [KeysWordContens] => Inflammasomes driven inflammation in lung cancer revisited: a short review, Lung cancer, inflammation, inflammasomes, interleukin-1 beta, interleukin-18, Lung cancer is the leading cause of cancer-related deaths worldwide. The main risk factor for lung cancer is exposure to chemicals present in cigarettes and atmospheric pollutants, which, among other mechanisms, can increase the risk of cancer by inducing pulmonary inflammation. Among the complex features of inflammatory processes, the role of inflammasomes has attracted increasing attention due to their role in different stages of carcinogenesis. Inflammasomes are intracellular multiprotein complexes that when activated promote the maturation of interleukin-1beta (IL-1β) and IL-18, pro-inflammatory cytokines involved in the promotion, progression, epithelial-mesenchymal transition, metastasis, and resistance to therapy of lung cancer. In this way, this review summarizes the recent findings of inflammasome research in different stages of lung cancer, with a focus on non-small cell lung carcinoma (NSCLC), and highlights these multiprotein complexes as promising targets for cancer therapy. ,Vitor Rodrigues da Costa ... Rodrigo Pinheiro Araldi [PublishedText] => Published [IsEdit] => 0 [AccountId] => 57 [Zh] => 1 ) [89] => Array ( [ArticleId] => 512 [Create_Time] => 2023-03-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202302/20230228085815.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100389/100389.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100389/100389.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100389/100389_cover.png [JournalsId] => 5 [Title] => SARS-CoV-2 infection activates the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes pathway in the lung: a review [Abstract] => The infection of COVID-19 is directly linked to the destruction of lung epithelial cells, and the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes (cGAS [AbstractComplete] =>

The infection of COVID-19 is directly linked to the destruction of lung epithelial cells, and the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes (cGAS-STING) system has been implicated in the pathology of respiratory infections. This study aimed to systematize the relationship between the pathophysiology of COVID-19 and the cGAS-STING system’s activation in the lungs. Severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) is an RNA virus that belongs to the Coronaviridae family whose genetic material is produced by a single positive RNA molecule (RNA+). The cGAS-STING signaling pathway has emerged as a key mediator of injury caused by infection and cellular or tissue stress. The cGAS-STING cyclic pathway is part of innate immunity and is activated from cytosolic DNA responses present in newly formed syncytia, by cell-to-cell fusion, in target of angiotensin-converting enzyme 2 (ACE2) expression and SARS-CoV-2 Spike protein. Although this pathway is canonically understood to be responsive to both pathogen-derived and host-derived DNA, it has been demonstrated to cross-communicate with the retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs). cGAS-STING activation is significant to interferon production, mainly type-I interferons (IFN-I), in a SARS-CoV-2 infection scenario, indicating a major antiviral role of the cGAS-STING pathway. It was identified that in SARS-CoV-2 the cGAS-STING axis is activated, but the inflammatory response could be specific for nuclear factor-κB (NF-κB) in infected cells, and that this axis is potentiated by a cytokine storm produced by the immune system’s cells.

[Names] => Gislei F. Aragão ... Sara Lívia M. Teixeira [Doi] => 10.37349/ei.2023.00089 [Published] => February 28, 2023 [Viewed] => 866 [Downloaded] => 35 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00089 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 65 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:56–69 [Recommend] => 0 [Keywords] => SARS-CoV-2, COVID-19, cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes pathway, lung damage, interferon, cytokines [DetailTitle] => DNA Sensing in Lung Inflammation [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/65 [Id] => 100389 [ris] => https://www.explorationpub.com/uploads/Article/A100389/55a2094193aa4da7c66250248dc64943.ris [bib] => https://www.explorationpub.com/uploads/Article/A100389/6b85530275261d70f45623d1b6e586dc.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Aragão GF, Feitosa SG, Veras HN, de Lima Filho CGAP, Assunção KS, Arrais LM, et al. SARS-CoV-2 infection activates the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes pathway in the lung: a review. Explor Immunol. 2023;3:56–69. https://doi.org/10.37349/ei.2023.00089 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-02-27 03:47:37 [Bib_Time] => 2023-02-27 03:47:37 [KeysWordContens] => SARS-CoV-2 infection activates the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes pathway in the lung: a review, SARS-CoV-2, COVID-19, cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes pathway, lung damage, interferon, cytokines, The infection of COVID-19 is directly linked to the destruction of lung epithelial cells, and the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes (cGAS-STING) system has been implicated in the pathology of respiratory infections. This study aimed to systematize the relationship between the pathophysiology of COVID-19 and the cGAS-STING system’s activation in the lungs. Severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) is an RNA virus that belongs to the Coronaviridae family whose genetic material is produced by a single positive RNA molecule (RNA+). The cGAS-STING signaling pathway has emerged as a key mediator of injury caused by infection and cellular or tissue stress. The cGAS-STING cyclic pathway is part of innate immunity and is activated from cytosolic DNA responses present in newly formed syncytia, by cell-to-cell fusion, in target of angiotensin-converting enzyme 2 (ACE2) expression and SARS-CoV-2 Spike protein. Although this pathway is canonically understood to be responsive to both pathogen-derived and host-derived DNA, it has been demonstrated to cross-communicate with the retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs). cGAS-STING activation is significant to interferon production, mainly type-I interferons (IFN-I), in a SARS-CoV-2 infection scenario, indicating a major antiviral role of the cGAS-STING pathway. It was identified that in SARS-CoV-2 the cGAS-STING axis is activated, but the inflammatory response could be specific for nuclear factor-κB (NF-κB) in infected cells, and that this axis is potentiated by a cytokine storm produced by the immune system’s cells. ,Gislei F. Aragão ... Sara Lívia M. Teixeira [PublishedText] => Published [IsEdit] => 0 [AccountId] => 57 [Zh] => 1 ) [90] => Array ( [ArticleId] => 549 [Create_Time] => 2023-04-25 [zipUrl] => https://www.explorationpub.com/uploads/zip/202304/20230427002730.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100391/100391.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100391/100391.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100391/100391_Cover.png [JournalsId] => 5 [Title] => Beyond MHC binding: immunogenicity prediction tools to refine neoantigen selection in cancer patients [Abstract] => In the last years, multiple efforts have been made to accurately predict neoantigens derived from somatic mutations in cancer patients, either to develop personalized therapeutic vaccines or to stud [AbstractComplete] =>

In the last years, multiple efforts have been made to accurately predict neoantigens derived from somatic mutations in cancer patients, either to develop personalized therapeutic vaccines or to study immune responses after cancer immunotherapy. In this context, the increasing accessibility of paired whole-exome sequencing (WES) of tumor biopsies and matched normal tissue as well as RNA sequencing (RNA-Seq) has provided a basis for the development of bioinformatics tools that predict and prioritize neoantigen candidates. Most pipelines rely on the binding prediction of candidate peptides to the patient’s major histocompatibility complex (MHC), but these methods return a high number of false positives since they lack information related to other features that influence T cell responses to neoantigens. This review explores available computational methods that incorporate information on T cell preferences to predict their activation after encountering a peptide-MHC complex. Specifically, methods that predict i) biological features that may increase the availability of a neopeptide to be exposed to the immune system, ii) metrics of self-similarity representing the chances of a neoantigen to break immune tolerance, iii) pathogen immunogenicity, and iv) tumor immunogenicity. Also, this review describes the characteristics of these tools and addresses their performance in the context of a novel benchmark dataset of experimentally validated neoantigens from patients treated with a melanoma vaccine (VACCIMEL) in a phase II clinical study. The overall results of the evaluation indicate that current tools have a limited ability to predict the activation of a cytotoxic response against neoantigens. Based on this result, the limitations that make this problem an unsolved challenge in immunoinformatics are discussed.

[Names] => Ibel Carri ... María Marcela Barrio [Doi] => 10.37349/ei.2023.00091 [Published] => April 25, 2023 [Viewed] => 1096 [Downloaded] => 43 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00091 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 80 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:82–103 [Recommend] => 0 [Keywords] => Neoantigen, cancer vaccine, melanoma, machine learning, neoepitope prediction [DetailTitle] => Bioinformatics, Big Data, AI: Exploring Immunology [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/80 [Id] => 100391 [ris] => https://www.explorationpub.com/uploads/Article/A100391/f71dba11e7dd60e96c6062eeae49497c.ris [bib] => https://www.explorationpub.com/uploads/Article/A100391/89c52e8d5beb95e40f371a61bf937fa9.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-25 [CitethisArticle] => Carri I, Schwab E, Podaza E, Garcia Alvarez HM, Mordoh J, Nielsen M, et al. Beyond MHC binding: immunogenicity prediction tools to refine neoantigen selection in cancer patients. Explor Immunol. 2023;3:82–103. https://doi.org/10.37349/ei.2023.00091 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-04-23 02:09:13 [Bib_Time] => 2023-04-23 02:09:13 [KeysWordContens] => Beyond MHC binding: immunogenicity prediction tools to refine neoantigen selection in cancer patients, Neoantigen, cancer vaccine, melanoma, machine learning, neoepitope prediction, In the last years, multiple efforts have been made to accurately predict neoantigens derived from somatic mutations in cancer patients, either to develop personalized therapeutic vaccines or to study immune responses after cancer immunotherapy. In this context, the increasing accessibility of paired whole-exome sequencing (WES) of tumor biopsies and matched normal tissue as well as RNA sequencing (RNA-Seq) has provided a basis for the development of bioinformatics tools that predict and prioritize neoantigen candidates. Most pipelines rely on the binding prediction of candidate peptides to the patient’s major histocompatibility complex (MHC), but these methods return a high number of false positives since they lack information related to other features that influence T cell responses to neoantigens. This review explores available computational methods that incorporate information on T cell preferences to predict their activation after encountering a peptide-MHC complex. Specifically, methods that predict i) biological features that may increase the availability of a neopeptide to be exposed to the immune system, ii) metrics of self-similarity representing the chances of a neoantigen to break immune tolerance, iii) pathogen immunogenicity, and iv) tumor immunogenicity. Also, this review describes the characteristics of these tools and addresses their performance in the context of a novel benchmark dataset of experimentally validated neoantigens from patients treated with a melanoma vaccine (VACCIMEL) in a phase II clinical study. The overall results of the evaluation indicate that current tools have a limited ability to predict the activation of a cytotoxic response against neoantigens. Based on this result, the limitations that make this problem an unsolved challenge in immunoinformatics are discussed. ,Ibel Carri ... María Marcela Barrio [PublishedText] => Published [IsEdit] => 0 [AccountId] => 38 [Zh] => 1 ) [91] => Array ( [ArticleId] => 567 [Create_Time] => 2023-04-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202304/20230428015306.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100394/100394.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100394/100394.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100394/100394_cover.png [JournalsId] => 5 [Title] => Localization in vesicles, clusters and supramolecular complexes as key elements of LAT function [Abstract] => Linker for activation of T cells (LAT) is a central adaptor protein in proximal T cell activation. A key element of its adaptor function is the efficiency with which LAT interacts with its binding p [AbstractComplete] =>

Linker for activation of T cells (LAT) is a central adaptor protein in proximal T cell activation. A key element of its adaptor function is the efficiency with which LAT interacts with its binding partners. Such efficiency is controlled by the local concentration of LAT as well as the vicinity to up- and downstream interaction partners, i.e. LAT localization. Several factors control LAT localization. LAT is a palmitoylated transmembrane protein and traffics between vesicular compartments and the plasma membrane. Membrane heterogeneity and protein-protein interactions can drive LAT clustering, at scales from a few to hundreds if not more molecules. LAT vesicular trafficking through the small, crowded cytoplasm of a T cell and the commonly nm scale clusters are difficult to access experimentally, in particular in the physiological interaction of T cells binding to antigen presenting cells (APCs) with a highly undulating interface. Only in recent years have technological advances begun to provide better access. Based on such advances, three elements of LAT localization are discussed in conjunction: vesicular trafficking as it regulates LAT transport towards, insertion into, and removal from the plasma membrane; LAT clustering as it increases local LAT concentrations; LAT-anchored supramolecular signaling complexes as they embed LAT in a dense network of interaction partners. Consistent with the important role of LAT localization for its function, each of these processes regulates LAT activity and the efficiency of T cell activation.

[Names] => Laura E. McMillan, Christoph Wülfing [Doi] => 10.37349/ei.2023.00094 [Published] => April 27, 2023 [Viewed] => 561 [Downloaded] => 24 [Subject] => Perspective [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00094 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 94 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:148–157 [Recommend] => 0 [Keywords] => T cell, linker for activation of T cells, vesicular trafficking, microcluster, supramolecular [DetailTitle] => The Role of Adaptor Proteins in Lymphoid Cell Signaling [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/94 [Id] => 100394 [ris] => https://www.explorationpub.com/uploads/Article/A100394/c52437a7e2cf347d048308c484dbd489.ris [bib] => https://www.explorationpub.com/uploads/Article/A100394/d38ebe63d3e09b1c5a6a6b95b827a175.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => McMillan LE, Wülfing C. Localization in vesicles, clusters and supramolecular complexes as key elements of LAT function. Explor Immunol. 2023;3:148–57. https://doi.org/10.37349/ei.2023.00094 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-04-26 01:32:18 [Bib_Time] => 2023-04-26 01:32:18 [KeysWordContens] => Localization in vesicles, clusters and supramolecular complexes as key elements of LAT function, T cell, linker for activation of T cells, vesicular trafficking, microcluster, supramolecular, Linker for activation of T cells (LAT) is a central adaptor protein in proximal T cell activation. A key element of its adaptor function is the efficiency with which LAT interacts with its binding partners. Such efficiency is controlled by the local concentration of LAT as well as the vicinity to up- and downstream interaction partners, i.e. LAT localization. Several factors control LAT localization. LAT is a palmitoylated transmembrane protein and traffics between vesicular compartments and the plasma membrane. Membrane heterogeneity and protein-protein interactions can drive LAT clustering, at scales from a few to hundreds if not more molecules. LAT vesicular trafficking through the small, crowded cytoplasm of a T cell and the commonly nm scale clusters are difficult to access experimentally, in particular in the physiological interaction of T cells binding to antigen presenting cells (APCs) with a highly undulating interface. Only in recent years have technological advances begun to provide better access. Based on such advances, three elements of LAT localization are discussed in conjunction: vesicular trafficking as it regulates LAT transport towards, insertion into, and removal from the plasma membrane; LAT clustering as it increases local LAT concentrations; LAT-anchored supramolecular signaling complexes as they embed LAT in a dense network of interaction partners. Consistent with the important role of LAT localization for its function, each of these processes regulates LAT activity and the efficiency of T cell activation. ,Laura E. McMillan, Christoph Wülfing [PublishedText] => Published [IsEdit] => 0 [AccountId] => 57 [Zh] => 1 ) [92] => Array ( [ArticleId] => 556 [Create_Time] => 2023-04-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202304/20230428012337.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100392/100392.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100392/100392.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100392/100392_cover.png [JournalsId] => 5 [Title] => Mesenchymal stem cells—the master immunomodulators [Abstract] => Mesenchymal stem/stromal cells (MSCs) are known as multipotent cells due to their ability to differentiate into various cell lineages of mesoderm origin. Recent developments in stem cell biology hav [AbstractComplete] =>

Mesenchymal stem/stromal cells (MSCs) are known as multipotent cells due to their ability to differentiate into various cell lineages of mesoderm origin. Recent developments in stem cell biology have provided a new ray of hope for the treatment of diseases and disorders that are yet to be treated. These cells have been widely used in animals and clinical trials in humans. To date, there are more than 920 clinical trials on humans related to MSCs as cell-based therapy in various conditions. The purpose of this review is to provide a summary of the characteristics of MSCs, evaluate their immunological properties, activation of MSCs that dictate their soluble factors, possible pathway, and mechanisms involved by MSCs and immune cell interaction, and various application of MSCs in different diseases.

[Names] => Mehak Vohra, Sunil K. Arora [Doi] => 10.37349/ei.2023.00092 [Published] => April 27, 2023 [Viewed] => 794 [Downloaded] => 23 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.0009 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 77 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:104–122 [Recommend] => 0 [Keywords] => Mesenchymal stem cells, immunomodulation, regenerative medicine, animal model, cell-based therapy [DetailTitle] => Interplay of Stem Cells and Immunology in Regenerative Medicine [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/77 [Id] => 100392 [ris] => https://www.explorationpub.com/uploads/Article/A100392/582614248942783219c0df7d03c8e836.ris [bib] => https://www.explorationpub.com/uploads/Article/A100392/5b821c46b0ca334d9a3a7e32c0fa2e66.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Vohra M, Arora SK. Mesenchymal stem cells—the master immunomodulators. Explor Immunol. 2023;3:104–22. https://doi.org/10.37349/ei.2023.00092 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-04-28 01:08:10 [Bib_Time] => 2023-04-28 01:08:10 [KeysWordContens] => Mesenchymal stem cells—the master immunomodulators, Mesenchymal stem cells, immunomodulation, regenerative medicine, animal model, cell-based therapy, Mesenchymal stem/stromal cells (MSCs) are known as multipotent cells due to their ability to differentiate into various cell lineages of mesoderm origin. Recent developments in stem cell biology have provided a new ray of hope for the treatment of diseases and disorders that are yet to be treated. These cells have been widely used in animals and clinical trials in humans. To date, there are more than 920 clinical trials on humans related to MSCs as cell-based therapy in various conditions. The purpose of this review is to provide a summary of the characteristics of MSCs, evaluate their immunological properties, activation of MSCs that dictate their soluble factors, possible pathway, and mechanisms involved by MSCs and immune cell interaction, and various application of MSCs in different diseases. ,Mehak Vohra, Sunil K. Arora [PublishedText] => Published [IsEdit] => 0 [AccountId] => 69 [Zh] => 1 ) [93] => Array ( [ArticleId] => 561 [Create_Time] => 2023-04-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202304/20230428015122.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100393/100393.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100393/100393.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100393/100393_ccver.png [JournalsId] => 5 [Title] => Chemokine-targeted nanoparticles: stimulation of the immune system in cancer immunotherapy [Abstract] => Surgery, chemotherapy, radiation therapy, and immunotherapy are potential therapeutic choices for many malignant and metastatic cancers. Despite adverse side effects and pain, surgery and chemothera [AbstractComplete] =>

Surgery, chemotherapy, radiation therapy, and immunotherapy are potential therapeutic choices for many malignant and metastatic cancers. Despite adverse side effects and pain, surgery and chemotherapy continue to be the most common cancer treatments. However, patients treated with immunotherapy had better cancer control than those who got other treatments. There are two methods to activate immunological pathways: systemically and locally. To modify the tumor microenvironment (TME), the former uses systemic cytokine/chemokine (CK) delivery, whilst the latter uses immunological checkpoints or small molecule inhibitors. Organic and inorganic nanomaterials (NMs) enhanced the efficacy of cancer immunotherapy. NMs can transmit drugs, peptides, antigens, antibodies, whole cell membranes, etc. Surface-modified NMs precisely target and enter the tissues. The inner core of surface-modified NMs is composed of chemicals with limited bioavailability and biocompatibility, resulting in prolonged blood retention and decreased renal clearance. These platforms hinder or prevent many immune cell activities and modify the TME, enhancing the efficiency of cancer immunotherapy. By inhibiting CK/CK receptor signaling, cell migration and other immune responses could be controlled. Developing CK-targeted nanoparticles (NPs) that inhibit CK signaling or take advantage of the ligand-receptor connection is possible. Surface chemical modification of NMs with CKs or specific peptides has several medicinal applications, including tissue-specific drug delivery and limited cell migration in cancer-afflicted conditions. This review covers current developments in the role of different groups of CK-loaded NP in tumor therapy targeting immune cells and cancer. It also covers the role of NP targeting CK signaling which aids in immunogenic cell death (ICD) and induction of antitumor immunity. In addition, CK gene silencing and its capacity to prevent cancer metastasis as well as inhibition of immune cell migration to modulate the TME are discussed.

[Names] => Ranjeet Singh ... Partha Pratim Manna [Doi] => 10.37349/ei.2023.00093 [Published] => April 27, 2023 [Viewed] => 1539 [Downloaded] => 46 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00093 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 81 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:123–147 [Recommend] => 0 [Keywords] => Chemokine, immunogenic cell death, chemokine receptors, nanomaterials, cancer, therapeutic relevance [DetailTitle] => Nanomaterials interaction with chemokines: perspectives for applied immunology [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/81 [Id] => 100393 [ris] => https://www.explorationpub.com/uploads/Article/A100393/722376f2ca8e36cb01540d94f56286ae.ris [bib] => https://www.explorationpub.com/uploads/Article/A100393/75c7ebba2ae19c5148c2c0e811f2077d.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Singh R, Srivastava P, Manna PP. Chemokine-targeted nanoparticles: stimulation of the immune system in cancer immunotherapy. Explor Immunol. 2023;3:123–47. https://doi.org/10.37349/emed.2023.00093 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-04-26 08:59:33 [Bib_Time] => 2023-04-26 08:59:33 [KeysWordContens] => Chemokine-targeted nanoparticles: stimulation of the immune system in cancer immunotherapy, Chemokine, immunogenic cell death, chemokine receptors, nanomaterials, cancer, therapeutic relevance, Surgery, chemotherapy, radiation therapy, and immunotherapy are potential therapeutic choices for many malignant and metastatic cancers. Despite adverse side effects and pain, surgery and chemotherapy continue to be the most common cancer treatments. However, patients treated with immunotherapy had better cancer control than those who got other treatments. There are two methods to activate immunological pathways: systemically and locally. To modify the tumor microenvironment (TME), the former uses systemic cytokine/chemokine (CK) delivery, whilst the latter uses immunological checkpoints or small molecule inhibitors. Organic and inorganic nanomaterials (NMs) enhanced the efficacy of cancer immunotherapy. NMs can transmit drugs, peptides, antigens, antibodies, whole cell membranes, etc. Surface-modified NMs precisely target and enter the tissues. The inner core of surface-modified NMs is composed of chemicals with limited bioavailability and biocompatibility, resulting in prolonged blood retention and decreased renal clearance. These platforms hinder or prevent many immune cell activities and modify the TME, enhancing the efficiency of cancer immunotherapy. By inhibiting CK/CK receptor signaling, cell migration and other immune responses could be controlled. Developing CK-targeted nanoparticles (NPs) that inhibit CK signaling or take advantage of the ligand-receptor connection is possible. Surface chemical modification of NMs with CKs or specific peptides has several medicinal applications, including tissue-specific drug delivery and limited cell migration in cancer-afflicted conditions. This review covers current developments in the role of different groups of CK-loaded NP in tumor therapy targeting immune cells and cancer. It also covers the role of NP targeting CK signaling which aids in immunogenic cell death (ICD) and induction of antitumor immunity. In addition, CK gene silencing and its capacity to prevent cancer metastasis as well as inhibition of immune cell migration to modulate the TME are discussed. ,Ranjeet Singh ... Partha Pratim Manna [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 ) [94] => Array ( [ArticleId] => 580 [Create_Time] => 2023-04-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202304/20230428062612.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100395/100395.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100395/100395.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100395/100395_cover.png [JournalsId] => 5 [Title] => Role of Vav1, a hematopoietic signal transduction molecule, as an adaptor protein in health and disease [Abstract] => The growth and differentiation of normal cells are controlled by protein-tyrosine kinases, which serve as receptors for a wide variety of external signals. Small protein modules called Src homology [AbstractComplete] =>

The growth and differentiation of normal cells are controlled by protein-tyrosine kinases, which serve as receptors for a wide variety of external signals. Small protein modules called Src homology 2 (SH2) and SH3 domains mediate protein-protein interactions in signaling pathways that are triggered by protein tyrosine kinases. The SH2 domain, a protein module of around 100 amino acids, is present in tyrosine kinase targets within the cell. SH2 domains are recruited to activated and autophosphorylated growth factor receptors by directly recognizing tyrosine phosphorylation sites. Growth factor receptors and other phosphoproteins have short phosphotyrosine (pTyr)-containing sequences that are bound by SH2 domains. The SH3 domain, a distinct element of approximately 50 residues that recognizes proline-rich and hydrophobic-amino-acid-containing regions, is frequently found in SH2-containing proteins. Tyrosine kinases can be coupled to downstream targets with SH3-binding sites by proteins with SH2 and SH3 domains acting as adaptors. These intricate and precise biochemical signaling pathways result in the regulation of gene expression, cytoskeletal architecture, and cell metabolism. The role of SH2/SH3 proteins in T cell signaling will be discussed. A special focus will be on the role of the hematopoietic signal transducer with SH2/SH3 domains, Vav1, in health and cancer.

[Names] => Shulamit Katzav [Doi] => 10.37349/ei.2023.00095 [Published] => April 28, 2023 [Viewed] => 633 [Downloaded] => 30 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00095 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 94 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:158–173 [Recommend] => 0 [Keywords] => Src homology 2 domain, Src homology 3 domain, Vav1, T cells [DetailTitle] => The Role of Adaptor Proteins in Lymphoid Cell Signaling [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/94 [Id] => 100395 [ris] => https://www.explorationpub.com/uploads/Article/A100395/8ff83e5be7527137e390882490be2606.ris [bib] => https://www.explorationpub.com/uploads/Article/A100395/34836c128f31ea293143a50b49247b59.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Katzav S. Role of Vav1, a hematopoietic signal transduction molecule, as an adaptor protein in health and disease. Explor Immunol. 2023;3:158–73. https://doi.org/10.37349/ei.2023.00095 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-04-27 04:43:37 [Bib_Time] => 2023-04-27 04:43:37 [KeysWordContens] => Role of Vav1, a hematopoietic signal transduction molecule, as an adaptor protein in health and disease, Src homology 2 domain, Src homology 3 domain, Vav1, T cells, The growth and differentiation of normal cells are controlled by protein-tyrosine kinases, which serve as receptors for a wide variety of external signals. Small protein modules called Src homology 2 (SH2) and SH3 domains mediate protein-protein interactions in signaling pathways that are triggered by protein tyrosine kinases. The SH2 domain, a protein module of around 100 amino acids, is present in tyrosine kinase targets within the cell. SH2 domains are recruited to activated and autophosphorylated growth factor receptors by directly recognizing tyrosine phosphorylation sites. Growth factor receptors and other phosphoproteins have short phosphotyrosine (pTyr)-containing sequences that are bound by SH2 domains. The SH3 domain, a distinct element of approximately 50 residues that recognizes proline-rich and hydrophobic-amino-acid-containing regions, is frequently found in SH2-containing proteins. Tyrosine kinases can be coupled to downstream targets with SH3-binding sites by proteins with SH2 and SH3 domains acting as adaptors. These intricate and precise biochemical signaling pathways result in the regulation of gene expression, cytoskeletal architecture, and cell metabolism. The role of SH2/SH3 proteins in T cell signaling will be discussed. A special focus will be on the role of the hematopoietic signal transducer with SH2/SH3 domains, Vav1, in health and cancer. ,Shulamit Katzav [PublishedText] => Published [IsEdit] => 0 [AccountId] => 38 [Zh] => 1 ) [95] => Array ( [ArticleId] => 594 [Create_Time] => 2023-06-12 [zipUrl] => https://www.explorationpub.com/uploads/zip/202307/20230701032815.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100396/100396.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100396/100396.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100396/100396_cover.png [JournalsId] => 5 [Title] => STIM/Orai-mediated calcium entry elicits spontaneous TSLP overproduction in epidermal cells of atopic dermatitis mice [Abstract] => Aim: Atopic dermatitis (AD) is a pruritic, chronic inflammatory skin disease. Thymic stromal lymphopoietin (TSLP) is highly expressed in the epidermis of patients with AD and induces T helper 2 ( [AbstractComplete] =>

Aim:

Atopic dermatitis (AD) is a pruritic, chronic inflammatory skin disease. Thymic stromal lymphopoietin (TSLP) is highly expressed in the epidermis of patients with AD and induces T helper 2 (Th2) immune responses and itching. Although the mechanism underlying the stimulus-induced TSLP production in normal keratinocytes has been intensively studied, whether the production capability of TSLP is naturally enhanced in epidermal cells in AD conditions remains unclear. Previous studies demonstrated that a deficiency of polyunsaturated fatty acid (PUFA) causes AD-like pruritic skin inflammation in special diet-fed hairless mice. The aim of the study was to examine the TSLP production capability of epidermal cells isolated from diet-induced AD mouse model and its mechanism.

Methods:

Epidermal cells were isolated from normal and AD mice and incubated under unstimulated culture conditions to assess spontaneous TSLP production. Messenger ribonucleic acid (mRNA) and protein levels of TSLP were determined by real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA), respectively.

Results:

TSLP level was markedly increased in the skin of AD mice. When epidermal cells were isolated from AD mice and cultured without stimulation, Tslp gene expression was upregulated, and a large amount of TSLP protein was extracellularly released. Such TSLP overproduction was not observed in the epidermal cells of normal mice. TSLP overproduction in AD epidermal cells was almost completely inhibited by extracellular calcium chelation, interference with plasma membrane interaction of stromal interaction molecule 1 (STIM1), blockade of the calcium release-activated calcium (CRAC) channels Orai1 and Orai2, or treatment with a PUFA γ-linolenic acid (GLA).

Conclusions:

Epidermal cells isolated from AD mice can spontaneously produce TSLP through STIM/Orai-mediated calcium entry, and GLA may negatively regulate this TSLP production.

[Names] => Masanori Fujii ... Susumu Ohya [Doi] => 10.37349/ei.2023.00096 [Published] => June 11, 2023 [Viewed] => 1307 [Downloaded] => 29 [Subject] => Original Article [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00096 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 92 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:174–185 [Recommend] => 0 [Keywords] => Atopic dermatitis, thymic stromal lymphopoietin, epidermal cells, calcium entry, stromal interaction molecule, Orai, polyunsaturated fatty acid [DetailTitle] => Cytokines and Skin Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/92 [Id] => 100396 [ris] => https://www.explorationpub.com/uploads/Article/A100396/1faefcbf7cc6b63a055e6592acee5cf7.ris [bib] => https://www.explorationpub.com/uploads/Article/A100396/880551eeae13b4039d5d292186a23590.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Fujii M, Kobayashi S, Ueda A, Sakagami M, Matsui R, Yamada Y, et al. STIM/Orai-mediated calcium entry elicits spontaneous TSLP overproduction in epidermal cells of atopic dermatitis mice. Explor Immunol. 2023;3:174–85. https://doi.org/10.37349/ei.2023.00096 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-05-30 07:02:37 [Bib_Time] => 2023-05-30 07:02:37 [KeysWordContens] => STIM/Orai-mediated calcium entry elicits spontaneous TSLP overproduction in epidermal cells of atopic dermatitis mice, Atopic dermatitis, thymic stromal lymphopoietin, epidermal cells, calcium entry, stromal interaction molecule, Orai, polyunsaturated fatty acid, Aim: Atopic dermatitis (AD) is a pruritic, chronic inflammatory skin disease. Thymic stromal lymphopoietin (TSLP) is highly expressed in the epidermis of patients with AD and induces T helper 2 (Th2) immune responses and itching. Although the mechanism underlying the stimulus-induced TSLP production in normal keratinocytes has been intensively studied, whether the production capability of TSLP is naturally enhanced in epidermal cells in AD conditions remains unclear. Previous studies demonstrated that a deficiency of polyunsaturated fatty acid (PUFA) causes AD-like pruritic skin inflammation in special diet-fed hairless mice. The aim of the study was to examine the TSLP production capability of epidermal cells isolated from diet-induced AD mouse model and its mechanism. Methods: Epidermal cells were isolated from normal and AD mice and incubated under unstimulated culture conditions to assess spontaneous TSLP production. Messenger ribonucleic acid (mRNA) and protein levels of TSLP were determined by real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Results: TSLP level was markedly increased in the skin of AD mice. When epidermal cells were isolated from AD mice and cultured without stimulation, Tslp gene expression was upregulated, and a large amount of TSLP protein was extracellularly released. Such TSLP overproduction was not observed in the epidermal cells of normal mice. TSLP overproduction in AD epidermal cells was almost completely inhibited by extracellular calcium chelation, interference with plasma membrane interaction of stromal interaction molecule 1 (STIM1), blockade of the calcium release-activated calcium (CRAC) channels Orai1 and Orai2, or treatment with a PUFA γ-linolenic acid (GLA). Conclusions: Epidermal cells isolated from AD mice can spontaneously produce TSLP through STIM/Orai-mediated calcium entry, and GLA may negatively regulate this TSLP production. ,Masanori Fujii ... Susumu Ohya [PublishedText] => Published [IsEdit] => 0 [AccountId] => 22 [Zh] => 1 ) [96] => Array ( [ArticleId] => 600 [Create_Time] => 2023-06-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230628063552.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100397/100397.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100397/100397.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100397/100397_cover.png [JournalsId] => 5 [Title] => Role of an adaptor protein human germinal center-associated lymphoma (HGAL) in cell signaling and lymphomagenesis [Abstract] => Human germinal center (GC)-associated lymphoma (HGAL) is a multi-domain adaptor protein expressed in GC B lymphocytes, T follicular helper (Tfh) cells and lymphomas derived from these cells. HGAL ex [AbstractComplete] =>

Human germinal center (GC)-associated lymphoma (HGAL) is a multi-domain adaptor protein expressed in GC B lymphocytes, T follicular helper (Tfh) cells and lymphomas derived from these cells. HGAL expression is an independent predictor of longer survival of diffuse large B-cell lymphoma (DLBCL) and classical Hodgkin’s lymphoma (HL) patients. HGAL regulates B cell receptor (BCR) signaling and immunological synapse formation by binding to either the downstream effectors [e.g., spleen tyrosine kinase (Syk)] or other signaling regulators [e.g., growth factor receptor-bound protein 2 (Grb2)]. HGAL regulates the cytoskeleton that reshapes B cell morphology during BCR signaling and cell motility by at least two molecular mechanisms: enhanced Ras homolog gene family member A (RhoA) signaling and inhibition of myosin-actin translocation. These effects on the cytoskeleton decrease lymphoma dissemination in animal models and contribute to decreased lymphoma dissemination in patients. The latter may contribute to the association of HGAL protein expression with longer survival of patients with DLBCL and HL tumors. The ability to regulate multiple and distinct functions simultaneously in B cells implies that the HGAL protein level is tightly regulated. It was demonstrated that HGAL can be regulated by PR/SET domain 1 (PRDM1)/B lymphocyte-induced maturation protein-1 (BLIMP1) and interleukin-4 (IL-4) at the transcription level, by microRNA-155 (miR-155) at the post-transcriptional level, and by F-box protein 10 (FBXO10) at the post-translational level. Constitutive enforced expression of HGAL at physiological levels leads to lymphoid hyperplasia and DLBCL in mice. Future studies need to focus on identifying HGAL interactome, dissecting its interaction network, and understanding HGAL spatiotemporal signaling in live cells in physiological conditions. Further, the recent demonstration of HGAL expression in Tfh cells requires the determination of its function in these cells. These studies will contribute to new insights into the biology of these cellular subsets and how immune dysregulation contributes to lymphomagenesis.

[Names] => Xiaoyu Jiang, Izidore S. Lossos [Doi] => 10.37349/ei.2023.00097 [Published] => June 28, 2023 [Viewed] => 655 [Downloaded] => 21 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00097 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 94 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:186–206 [Recommend] => 0 [Keywords] => Human germinal center-associated lymphoma, motility, B cell receptor, lymphomagenesis [DetailTitle] => The Role of Adaptor Proteins in Lymphoid Cell Signaling [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/94 [Id] => 100397 [ris] => https://www.explorationpub.com/uploads/Article/A100397/b0e72e70105e8b1e20b74a5dddb7de2e.ris [bib] => https://www.explorationpub.com/uploads/Article/A100397/65deb468eef9d831fe8dbc0a50d828ce.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Jiang X, Lossos IS. Role of an adaptor protein human germinal center-associated lymphoma (HGAL) in cell signaling and lymphomagenesis. Explor Immunol. 2023;3:186–206. https://doi.org/10.37349/ei.2023.00097 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-06-16 01:07:02 [Bib_Time] => 2023-06-16 01:07:02 [KeysWordContens] => Role of an adaptor protein human germinal center-associated lymphoma (HGAL) in cell signaling and lymphomagenesis, Human germinal center-associated lymphoma, motility, B cell receptor, lymphomagenesis, Human germinal center (GC)-associated lymphoma (HGAL) is a multi-domain adaptor protein expressed in GC B lymphocytes, T follicular helper (Tfh) cells and lymphomas derived from these cells. HGAL expression is an independent predictor of longer survival of diffuse large B-cell lymphoma (DLBCL) and classical Hodgkin’s lymphoma (HL) patients. HGAL regulates B cell receptor (BCR) signaling and immunological synapse formation by binding to either the downstream effectors [e.g., spleen tyrosine kinase (Syk)] or other signaling regulators [e.g., growth factor receptor-bound protein 2 (Grb2)]. HGAL regulates the cytoskeleton that reshapes B cell morphology during BCR signaling and cell motility by at least two molecular mechanisms: enhanced Ras homolog gene family member A (RhoA) signaling and inhibition of myosin-actin translocation. These effects on the cytoskeleton decrease lymphoma dissemination in animal models and contribute to decreased lymphoma dissemination in patients. The latter may contribute to the association of HGAL protein expression with longer survival of patients with DLBCL and HL tumors. The ability to regulate multiple and distinct functions simultaneously in B cells implies that the HGAL protein level is tightly regulated. It was demonstrated that HGAL can be regulated by PR/SET domain 1 (PRDM1)/B lymphocyte-induced maturation protein-1 (BLIMP1) and interleukin-4 (IL-4) at the transcription level, by microRNA-155 (miR-155) at the post-transcriptional level, and by F-box protein 10 (FBXO10) at the post-translational level. Constitutive enforced expression of HGAL at physiological levels leads to lymphoid hyperplasia and DLBCL in mice. Future studies need to focus on identifying HGAL interactome, dissecting its interaction network, and understanding HGAL spatiotemporal signaling in live cells in physiological conditions. Further, the recent demonstration of HGAL expression in Tfh cells requires the determination of its function in these cells. These studies will contribute to new insights into the biology of these cellular subsets and how immune dysregulation contributes to lymphomagenesis. ,Xiaoyu Jiang, Izidore S. Lossos [PublishedText] => Published [IsEdit] => 0 [AccountId] => 57 [Zh] => 1 ) [97] => Array ( [ArticleId] => 601 [Create_Time] => 2023-06-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230630051320.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100398/100398.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100398/100398.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100398/100398_cover.png [JournalsId] => 5 [Title] => The aging process and its relation to periodontal conditions [Abstract] => Periodontal tissue destruction can cause complaints for sufferers. Inflammatory conditions of the gingiva, bleeding gums, and even tooth loss are clinical features of the destruction of the periodon [AbstractComplete] =>

Periodontal tissue destruction can cause complaints for sufferers. Inflammatory conditions of the gingiva, bleeding gums, and even tooth loss are clinical features of the destruction of the periodontal tissues. Periodontitis is an inflammatory disease involving the periodontal tissues. The prevalence of periodontium destruction increases with aging. Changes in innate and adaptive immunity that occur in the elderly also play a role in the severity of periodontitis. “Inflammaging” is a chronic inflammatory state associated with old age in humans. Periodontitis contributes to inflammaging since periodontitis in the elderly is associated with increased markers of systemic inflammation. Age-related changes also affect neutrophil function, especially antimicrobial activity, so neutrophils may become more pathological. After infiltration into the tissue, neutrophils are equipped with several antimicrobial strategies to reduce the number of antigens. Phagocytosis is the ability of neutrophils to engulf and kill microbes, but neutrophil phagocytosis is weakened in the elderly. Age-related changes affecting neutrophils, macrophages, and T cells appear to promote pathogenic immune responses and contribute to the increased prevalence of periodontal disease in aging individuals. Proper regulation of the host immune response is critical in maintaining periodontal health. This paper aims to describe the aging process and its relation to periodontal conditions.

[Names] => Pitu Wulandari [Doi] => 10.37349/ei.2023.00098 [Published] => June 30, 2023 [Viewed] => 718 [Downloaded] => 20 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00098 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 111 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:207–216 [Recommend] => 0 [Keywords] => Periodontal, inflammation, aging, immunity, periodontitis [DetailTitle] => Immunosenescence: Mechanisms and Its Impact [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/111 [Id] => 100398 [ris] => https://www.explorationpub.com/uploads/Article/A100398/6b1cfd7fb555fe0d6c305827444a38ac.ris [bib] => https://www.explorationpub.com/uploads/Article/A100398/7297167b38c343b4231d7a16ae0db3f7.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Wulandari P. The aging process and its relation to periodontal conditions. Explor Immunol. 2023;3:207–16. https://doi.org/10.37349/ei.2023.00098 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-06-16 01:11:11 [Bib_Time] => 2023-06-16 01:11:11 [KeysWordContens] => The aging process and its relation to periodontal conditions, Periodontal, inflammation, aging, immunity, periodontitis, Periodontal tissue destruction can cause complaints for sufferers. Inflammatory conditions of the gingiva, bleeding gums, and even tooth loss are clinical features of the destruction of the periodontal tissues. Periodontitis is an inflammatory disease involving the periodontal tissues. The prevalence of periodontium destruction increases with aging. Changes in innate and adaptive immunity that occur in the elderly also play a role in the severity of periodontitis. “Inflammaging” is a chronic inflammatory state associated with old age in humans. Periodontitis contributes to inflammaging since periodontitis in the elderly is associated with increased markers of systemic inflammation. Age-related changes also affect neutrophil function, especially antimicrobial activity, so neutrophils may become more pathological. After infiltration into the tissue, neutrophils are equipped with several antimicrobial strategies to reduce the number of antigens. Phagocytosis is the ability of neutrophils to engulf and kill microbes, but neutrophil phagocytosis is weakened in the elderly. Age-related changes affecting neutrophils, macrophages, and T cells appear to promote pathogenic immune responses and contribute to the increased prevalence of periodontal disease in aging individuals. Proper regulation of the host immune response is critical in maintaining periodontal health. This paper aims to describe the aging process and its relation to periodontal conditions. ,Pitu Wulandari [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 ) [98] => Array ( [ArticleId] => 631 [Create_Time] => 2023-06-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230630053120.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100399/100399.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100399/100399.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100399/ei-03-100399_cover.png [JournalsId] => 5 [Title] => Conformational and functional regulation of the chicken tumor virus number 10 (CT10) regulator of kinase II (CrkII) adaptor protein by cyclophilin A [Abstract] => The Src homology 2 (SH2) and SH3 domain-containing chicken tumor virus number 10 (CT10) regulator of kinase (Crk) adaptor proteins include three cellular members that serve as integral constituents [AbstractComplete] =>

The Src homology 2 (SH2) and SH3 domain-containing chicken tumor virus number 10 (CT10) regulator of kinase (Crk) adaptor proteins include three cellular members that serve as integral constituents of multiple receptor-linked signal transduction pathways. CrkI and CrkII are products of alternative RNA-splicing which is transcribed from a single gene, while Crk-like (CrkL), which is highly homologous to CrkII, is encoded by a different gene. Thanks to their modular structure, the Crk adaptor proteins can simultaneously interact with activated receptors and a wide range of effector molecules, and orchestrate the assembly of complexes containing enzymes and substrates at the receptor site. They are involved in the regulation of a large number of cellular processes which control cell growth, differentiation, transformation, and apoptosis. Cell activation-dependent tyrosine phosphorylation of CrkII and CrkL serves as a major posttranslational modification mechanism that introduces conformational changes in the proteins by promoting an intramolecular interaction between the phosphotyrosine and the self SH2 domain. The resulting conformational change induces downregulation of CrkII- and CrkL-dependent biological processes. A second type of posttranslational modification mechanism regulates the structure and function of the CrkII adaptor protein by immunophilin-mediated protein isomerization. Two of the most abundant immunophilins in T lymphocytes which function as peptidyl-prolyl cis-trans isomerases (PPIases), namely cyclophilin A (CypA) and FK506-binding proteins (FKBPs), can associate with CrkII and catalyze its reciprocal cis-trans isomerization. This mechanism is of special importance for the regulation of T lymphocyte functions and for T cell-mediated immune responses, since immunophilin inhibitors, such as cyclosporin A (CsA) and FK506, function as immunosuppressive drugs that can prevent allotransplanted graft rejection. The present manuscript focuses on selected functions of Crk adaptor proteins, predominantly in T lymphocytes, and reviews in more detail the current knowledge on the immunophilin-dependent regulation of the structure and function of the CrkII adaptor protein.

[Names] => Noah Isakov [Doi] => 10.37349/ei.2023.00099 [Published] => June 30, 2023 [Viewed] => 544 [Downloaded] => 15 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00099 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 94 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:217–232 [Recommend] => 0 [Keywords] => Chicken tumor virus number 10 (CT10) regulator of kinase II (CrkII), Crk adaptor protein, peptidyl-prolyl cis-trans isomerase (PPIase), immunophilin, cyclophilin A (CypA), cyclosporin A (CsA), T cell activation, signal transduction [DetailTitle] => The Role of Adaptor Proteins in Lymphoid Cell Signaling [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/94 [Id] => 100399 [ris] => https://www.explorationpub.com/uploads/Article/A100399/b3967620cbb63433b137ae47141fda36.ris [bib] => https://www.explorationpub.com/uploads/Article/A100399/0fbbdb85e0a6562e45fc99855d5c7985.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Isakov N. Conformational and functional regulation of the chicken tumor virus number 10 (CT10) regulator of kinase II (CrkII) adaptor protein by cyclophilin A. Explor Immunol. 2023;3:217–32. https://doi.org/10.37349/ei.2023.00099 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-06-29 05:17:30 [Bib_Time] => 2023-06-29 05:17:30 [KeysWordContens] => Conformational and functional regulation of the chicken tumor virus number 10 (CT10) regulator of kinase II (CrkII) adaptor protein by cyclophilin A, Chicken tumor virus number 10 (CT10) regulator of kinase II (CrkII), Crk adaptor protein, peptidyl-prolyl cis-trans isomerase (PPIase), immunophilin, cyclophilin A (CypA), cyclosporin A (CsA), T cell activation, signal transduction, The Src homology 2 (SH2) and SH3 domain-containing chicken tumor virus number 10 (CT10) regulator of kinase (Crk) adaptor proteins include three cellular members that serve as integral constituents of multiple receptor-linked signal transduction pathways. CrkI and CrkII are products of alternative RNA-splicing which is transcribed from a single gene, while Crk-like (CrkL), which is highly homologous to CrkII, is encoded by a different gene. Thanks to their modular structure, the Crk adaptor proteins can simultaneously interact with activated receptors and a wide range of effector molecules, and orchestrate the assembly of complexes containing enzymes and substrates at the receptor site. They are involved in the regulation of a large number of cellular processes which control cell growth, differentiation, transformation, and apoptosis. Cell activation-dependent tyrosine phosphorylation of CrkII and CrkL serves as a major posttranslational modification mechanism that introduces conformational changes in the proteins by promoting an intramolecular interaction between the phosphotyrosine and the self SH2 domain. The resulting conformational change induces downregulation of CrkII- and CrkL-dependent biological processes. A second type of posttranslational modification mechanism regulates the structure and function of the CrkII adaptor protein by immunophilin-mediated protein isomerization. Two of the most abundant immunophilins in T lymphocytes which function as peptidyl-prolyl cis-trans isomerases (PPIases), namely cyclophilin A (CypA) and FK506-binding proteins (FKBPs), can associate with CrkII and catalyze its reciprocal cis-trans isomerization. This mechanism is of special importance for the regulation of T lymphocyte functions and for T cell-mediated immune responses, since immunophilin inhibitors, such as cyclosporin A (CsA) and FK506, function as immunosuppressive drugs that can prevent allotransplanted graft rejection. The present manuscript focuses on selected functions of Crk adaptor proteins, predominantly in T lymphocytes, and reviews in more detail the current knowledge on the immunophilin-dependent regulation of the structure and function of the CrkII adaptor protein. ,Noah Isakov [PublishedText] => Published [IsEdit] => 0 [AccountId] => 24 [Zh] => 1 ) [99] => Array ( [ArticleId] => 637 [Create_Time] => 2023-06-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230630062049.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003100/1003100.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003100/1003100.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003100/1003100_cover.png [JournalsId] => 5 [Title] => Immune response: the Achilles’ heel of the stem cell-based regenerative therapies [Abstract] => Besides trauma, several pathological conditions which directly affect the normal functioning of organs, require new therapeutic strategies to repair damaged or diseased tissues. Tissue regeneration [AbstractComplete] =>

Besides trauma, several pathological conditions which directly affect the normal functioning of organs, require new therapeutic strategies to repair damaged or diseased tissues. Tissue regeneration is a complex and spatiotemporal process involving a plethora of cell types, including various immune cells and stem cells in a synchronized relationship. However, individual parameters, namely ageing, obesity, diabetes, and chronic conditions, have been intrinsically correlated with poor regenerative properties of adult tissues. While vast progress has been made regarding stem cell-based therapy to direct self-healing, the immune response is still the Achilles’ heel of such strategies. Whereas the role of effector immune cells has been well defined along the regenerative process, an understanding of the behavior of the main adult stem cells, namely mesenchymal stem cells (MSCs) and hematopoietic stem and progenitor cells (HSPCs), along the different phases of the regenerative process could clarify how these stem cells can be used to positively influence the immune response. In this scope, this review highlights the main interactions between these stem cells and immune cells during tissue repair, exploring the most important regenerative properties of stem cells and correlating them with the modulation of the immune response during tissue regeneration. Furthermore, the utmost strategies used to explore how the behavior and stem cell fate are affected by specific microenvironments and/or stimuli usually found during a regenerative process, are emphasized. This clarification may provide critical insight into the molecular mechanisms by which stem cells modulate the immune response in a positive feedback loop toward tissue repair.

[Names] => Cláudia S. Oliveira, Freni K. Tavaria [Doi] => 10.37349/ei.2023.00100 [Published] => June 30, 2023 [Viewed] => 950 [Downloaded] => 43 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00100 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 77 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:233–254 [Recommend] => 0 [Keywords] => Mesenchymal stem cells, hematopoietic stem cells, tissue regeneration, immune response, immunomodulation, stem cell-based therapies, regenerative properties [DetailTitle] => Interplay of Stem Cells and Immunology in Regenerative Medicine [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/77 [Id] => 1003100 [ris] => https://www.explorationpub.com/uploads/Article/A1003100/63d91acd66fe20f03124e9262a64e7c9.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003100/57c6e8a22cfc7d67468deabd03d99c8a.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Oliveira CS, Tavaria FK. Immune response: the Achilles’ heel of the stem cell-based regenerative therapies. Explor Immunol. 2023;3:233–54. https://doi.org/10.37349/ei.2023.00100 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-06-29 05:13:16 [Bib_Time] => 2023-06-29 05:13:16 [KeysWordContens] => Immune response: the Achilles’ heel of the stem cell-based regenerative therapies, Mesenchymal stem cells, hematopoietic stem cells, tissue regeneration, immune response, immunomodulation, stem cell-based therapies, regenerative properties, Besides trauma, several pathological conditions which directly affect the normal functioning of organs, require new therapeutic strategies to repair damaged or diseased tissues. Tissue regeneration is a complex and spatiotemporal process involving a plethora of cell types, including various immune cells and stem cells in a synchronized relationship. However, individual parameters, namely ageing, obesity, diabetes, and chronic conditions, have been intrinsically correlated with poor regenerative properties of adult tissues. While vast progress has been made regarding stem cell-based therapy to direct self-healing, the immune response is still the Achilles’ heel of such strategies. Whereas the role of effector immune cells has been well defined along the regenerative process, an understanding of the behavior of the main adult stem cells, namely mesenchymal stem cells (MSCs) and hematopoietic stem and progenitor cells (HSPCs), along the different phases of the regenerative process could clarify how these stem cells can be used to positively influence the immune response. In this scope, this review highlights the main interactions between these stem cells and immune cells during tissue repair, exploring the most important regenerative properties of stem cells and correlating them with the modulation of the immune response during tissue regeneration. Furthermore, the utmost strategies used to explore how the behavior and stem cell fate are affected by specific microenvironments and/or stimuli usually found during a regenerative process, are emphasized. This clarification may provide critical insight into the molecular mechanisms by which stem cells modulate the immune response in a positive feedback loop toward tissue repair. ,Cláudia S. Oliveira, Freni K. Tavaria [PublishedText] => Published [IsEdit] => 0 [AccountId] => 45 [Zh] => 1 ) [100] => Array ( [ArticleId] => 665 [Create_Time] => 2023-08-04 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230816005056.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003101/1003101.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003101/1003101.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003101/1003101_cover.png [JournalsId] => 5 [Title] => COVID-19 induced ARDS: immunopathology and therapeutics [Abstract] => The coronavirus disease-2019 (COVID-19) pandemic is a significant threat in the modern era. Clinical studies show that the most common symptom of severe COVID-19 is viral pneumonia-induced acute res [AbstractComplete] =>

The coronavirus disease-2019 (COVID-19) pandemic is a significant threat in the modern era. Clinical studies show that the most common symptom of severe COVID-19 is viral pneumonia-induced acute respiratory distress syndrome (ARDS). The underlying mechanisms by which severe respiratory disease syndrome-coronavirus-2 (SARS-CoV-2) results in ARDS and how certain host factors confer an increased risk of developing severe disease remain unknown. Therefore, identifying the distinctive features of this severe and fatal disease and the therapeutic approaches to COVID-19-induced ARDS remains an immediate need to serve as a basis for best practice models of standardized ARDS treatment. This review article aims to comprehensively discuss the immunopathology of ARDS and provides an overview of the precise role of both the innate and adaptive immune system, with emphasis on the current treatment strategies being tested in the COVID-19-induced ARDS patients. This knowledge will supposedly help in revealing further mechanistic insights into understanding COVID-19-induced ARDS.

[Names] => Sneha Das ... Rupesh K. Srivastava [Doi] => 10.37349/ei.2023.00101 [Published] => August 04, 2023 [Viewed] => 505 [Downloaded] => 29 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00101 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 64 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:255–275 [Recommend] => 0 [Keywords] => Coronavirus disease-2019, acute respiratory distress syndrome, immunopathology, innate, adaptive, therapeutics [DetailTitle] => Immunology, Immunopathology and Genomics of SARS-COV-2 [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/64 [Id] => 1003101 [ris] => https://www.explorationpub.com/uploads/Article/A1003101/60ccc11c6a8b75916c1895ec7b1f616f.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003101/dde66e11af81578387000cec87f4008d.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Das S, Sharma T, Bhardwaj A, Srivastava RK. COVID-19 induced ARDS: immunopathology and therapeutics. Explor Immunol. 2023;3:255–75. https://doi.org/10.37349/ei.2023.00101 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-08-04 07:09:47 [Bib_Time] => 2023-08-04 07:09:47 [KeysWordContens] => COVID-19 induced ARDS: immunopathology and therapeutics, Coronavirus disease-2019, acute respiratory distress syndrome, immunopathology, innate, adaptive, therapeutics, The coronavirus disease-2019 (COVID-19) pandemic is a significant threat in the modern era. Clinical studies show that the most common symptom of severe COVID-19 is viral pneumonia-induced acute respiratory distress syndrome (ARDS). The underlying mechanisms by which severe respiratory disease syndrome-coronavirus-2 (SARS-CoV-2) results in ARDS and how certain host factors confer an increased risk of developing severe disease remain unknown. Therefore, identifying the distinctive features of this severe and fatal disease and the therapeutic approaches to COVID-19-induced ARDS remains an immediate need to serve as a basis for best practice models of standardized ARDS treatment. This review article aims to comprehensively discuss the immunopathology of ARDS and provides an overview of the precise role of both the innate and adaptive immune system, with emphasis on the current treatment strategies being tested in the COVID-19-induced ARDS patients. This knowledge will supposedly help in revealing further mechanistic insights into understanding COVID-19-induced ARDS. ,Sneha Das ... Rupesh K. Srivastava [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 ) [101] => Array ( [ArticleId] => 1258 [Create_Time] => 2024-04-26 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240426024300.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003139/1003139.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003139/1003139.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003139/1003139_cover.png [JournalsId] => 5 [Title] => Filoviridae: insights into immune responses to Ebola virus [Abstract] => Ebola virus (EBOV) is a zoonotic virus comprising of six known different species, designated within the family Filoviridae and genus Ebolavirus. The first recorded outbreak of an EBOV disease (EVD) [AbstractComplete] =>

Ebola virus (EBOV) is a zoonotic virus comprising of six known different species, designated within the family Filoviridae and genus Ebolavirus. The first recorded outbreak of an EBOV disease (EVD) was in Yambuku, Zaire EBOV (ZEBOV) in 1976, followed by the Sudan EBOV (SUDV) later that year. Outbreaks have been increasing throughout the 21st century, and mortality rates can reach up to 90%. Such extraordinary virulence is evidenced by a few pathogens, similar to the Marburg virus (MARV) that originated in Uganda and was first detected in Germany in 1967. The virulent nature of filovirus disease has established these related viruses as a formidable global concern. There are currently four types of Ebolaviridae species known to infect humans, with two more recently identified in other animals that are genomically different concerning cellular pathogenesis or aetiology of disease. Recent advances in understanding the pathogenesis of filovirus disease infections have been remarkable, yet the immunological response to filovirus infection remains unknown. Scientific analysis of cellular mechanisms can provide insight into virulence factors utilised by other pathogenic viruses that also cause febrile illness with occasional haemorrhagic fever in humans. In this review, a brief summary of EBOV protein structure and functional cellular effects is covered. The role of innate and adaptive immune cells known since 1976 is considered with the relevance and implications of immunological proteins measured by cluster of differentiation (CD) molecule, alongside cytokine, chemokine, and other biologically relevant pathways, and through genetic research. A thorough understanding of immunological correlates affecting host responses to EBOV will facilitate clinical and applied research knowledge, contributing to protection against potential public health threats.

[Names] => Brent Brown ... Ingo Fricke [Doi] => 10.37349/ei.2024.00139 [Published] => April 25, 2024 [Viewed] => 18 [Downloaded] => 5 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2024.00139 [Inline] => 1 [Type] => 0 [Issue] => 0 [Topic] => 63 [TitleAbbr] => Explor Immunol. [Pages] => 2024;4:238–266 [Recommend] => 0 [Keywords] => Adaptive, Ebola, cellular, Filoviridae , immunology, innate, molecular [DetailTitle] => Old and New Paradigms in Viral Vaccinology [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/63 [Id] => 1003139 [ris] => https://www.explorationpub.com/uploads/Article/A1003139/6fbef0685af70da3b8f4997f79e0008e.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003139/8fc74440cb10f4ef0fdd45e7f46c4229.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Brown B, Imarogbe C, Chacon-Cruz E, Fricke I. Filoviridae: insights into immune responses to Ebola virus. Explor Immunol. 2024;4:238–66. https://doi.org/10.37349/ei.2024.00139 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-04-23 05:33:52 [Bib_Time] => 2024-04-23 05:33:52 [KeysWordContens] => Filoviridae: insights into immune responses to Ebola virus, Adaptive, Ebola, cellular, Filoviridae , immunology, innate, molecular, Ebola virus (EBOV) is a zoonotic virus comprising of six known different species, designated within the family Filoviridae and genus Ebolavirus. The first recorded outbreak of an EBOV disease (EVD) was in Yambuku, Zaire EBOV (ZEBOV) in 1976, followed by the Sudan EBOV (SUDV) later that year. Outbreaks have been increasing throughout the 21st century, and mortality rates can reach up to 90%. Such extraordinary virulence is evidenced by a few pathogens, similar to the Marburg virus (MARV) that originated in Uganda and was first detected in Germany in 1967. The virulent nature of filovirus disease has established these related viruses as a formidable global concern. There are currently four types of Ebolaviridae species known to infect humans, with two more recently identified in other animals that are genomically different concerning cellular pathogenesis or aetiology of disease. Recent advances in understanding the pathogenesis of filovirus disease infections have been remarkable, yet the immunological response to filovirus infection remains unknown. Scientific analysis of cellular mechanisms can provide insight into virulence factors utilised by other pathogenic viruses that also cause febrile illness with occasional haemorrhagic fever in humans. In this review, a brief summary of EBOV protein structure and functional cellular effects is covered. The role of innate and adaptive immune cells known since 1976 is considered with the relevance and implications of immunological proteins measured by cluster of differentiation (CD) molecule, alongside cytokine, chemokine, and other biologically relevant pathways, and through genetic research. A thorough understanding of immunological correlates affecting host responses to EBOV will facilitate clinical and applied research knowledge, contributing to protection against potential public health threats. ,Brent Brown ... Ingo Fricke [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 0 ) [102] => Array ( [ArticleId] => 701 [Create_Time] => 2023-08-24 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230824054055.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003102/1003102.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003102/1003102.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003102/1003102_cover.png [JournalsId] => 5 [Title] => Trained-immunity and cross-reactivity for protection: insights from the coronavirus disease 2019 and monkeypox emergencies for vaccine development [Abstract] => The emergence and re-emergence of pathogens is a public-health concern, which has become more evident after the coronavirus disease 2019 (COVID-19) pandemic and the monkeypox outbreaks in early 2022 [AbstractComplete] =>

The emergence and re-emergence of pathogens is a public-health concern, which has become more evident after the coronavirus disease 2019 (COVID-19) pandemic and the monkeypox outbreaks in early 2022. Given that vaccines are the more effective and affordable tools to control infectious diseases, the authors reviewed two heterologous effects of vaccines: the trained immunity and the cross-reactivity. Trained immunity, provided by attenuated vaccines, was exemplified in this article by the decreased the burden of COVID-19 in populations with high Bacille Calmette-Guerin (BCG) coverage. Cross-reactive responses were exemplified here by the studies which suggested that vaccinia could help controlling the monkeypox outbreak, because of common epitopes shared by orthopoxviruses. Although modern vaccination is likely to use subunit vaccines, the authors discussed how adjuvants might be the key to induce trained immunity and improve cross-reactive responses, ensuring that heterologous effects would improve the vaccine’s response.

[Names] => Amanda Izeli Portilho, Elizabeth De Gaspari [Doi] => 10.37349/ei.2023.00102 [Published] => August 24, 2023 [Viewed] => 503 [Downloaded] => 13 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00102 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 159 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:276–285 [Recommend] => 0 [Keywords] => Coronavirus disease 2019, monkeypox, trained-immunity, cross-immunity, adjuvants [DetailTitle] => Mucosal Immune Cells - Border Protection or Entrance Gate? [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/159 [Id] => 1003102 [ris] => https://www.explorationpub.com/uploads/Article/A1003102/0188f45806fb6ed67f3c5fee3faedafe.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003102/c043a7d4741f9a440630e1fd9e9bc8e7.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Portilho AI, De Gaspari E. Trained-immunity and cross-reactivity for protection: insights from the coronavirus disease 2019 and monkeypox emergencies for vaccine development. Explor Immunol. 2023;3:276–85. https://doi.org/10.37349/ei.2023.00102 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-08-23 10:16:32 [Bib_Time] => 2023-08-23 10:16:32 [KeysWordContens] => Trained-immunity and cross-reactivity for protection: insights from the coronavirus disease 2019 and monkeypox emergencies for vaccine development, Coronavirus disease 2019, monkeypox, trained-immunity, cross-immunity, adjuvants, The emergence and re-emergence of pathogens is a public-health concern, which has become more evident after the coronavirus disease 2019 (COVID-19) pandemic and the monkeypox outbreaks in early 2022. Given that vaccines are the more effective and affordable tools to control infectious diseases, the authors reviewed two heterologous effects of vaccines: the trained immunity and the cross-reactivity. Trained immunity, provided by attenuated vaccines, was exemplified in this article by the decreased the burden of COVID-19 in populations with high Bacille Calmette-Guerin (BCG) coverage. Cross-reactive responses were exemplified here by the studies which suggested that vaccinia could help controlling the monkeypox outbreak, because of common epitopes shared by orthopoxviruses. Although modern vaccination is likely to use subunit vaccines, the authors discussed how adjuvants might be the key to induce trained immunity and improve cross-reactive responses, ensuring that heterologous effects would improve the vaccine’s response. ,Amanda Izeli Portilho, Elizabeth De Gaspari [PublishedText] => Published [IsEdit] => 0 [AccountId] => 45 [Zh] => 1 ) [103] => Array ( [ArticleId] => 709 [Create_Time] => 2023-08-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230830055932.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003103/1003103.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003103/1003103.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003103/1003103_cover.png [JournalsId] => 5 [Title] => Considerations for simultaneous detection of autoantibodies to coagulation factor and lupus anticoagulant [Abstract] => In patients with autoimmune coagulation factor deficiency (AiCFD), the production of autoantibodies that inhibit coagulation factors in the blood reduces the activity of those relevant coagulation f [AbstractComplete] =>

In patients with autoimmune coagulation factor deficiency (AiCFD), the production of autoantibodies that inhibit coagulation factors in the blood reduces the activity of those relevant coagulation factors, resulting in severe bleeding symptoms. Recently, reports of patients with AiCFD have noted the concomitant detection of lupus anticoagulant (LA), a risk factor for thrombosis. LA-positive patients may show bleeding symptoms due to decreased activity of coagulation factor II (FII) caused by autoantibodies against FII, in addition to thrombotic symptoms, a condition termed LA-hypoprothrombinemia syndrome (LAHPS). Anti-FII antibodies in LAHPS cases are frequently cleared antibodies that can be detected using immunological techniques, such as enzyme-linked immunosorbent assay (ELISA). Recently, several cases of coagulation FV inhibitors, known as autoimmune FV deficiency, have been reported. Some of these cases may be complicated by LA, which can cause thrombosis. False-positive results for anticoagulant inhibitors are known to occur in LA cases; therefore, immunological confirmation of antibodies against coagulation factors is recommended. Additionally, acquired hemophilia A (AHA), caused by autoantibodies against FVIII, is a typical acquired hemorrhagic diathesis, although affected patients may present with thrombosis associated with LA. Thus, it is important to remember that hemorrhagic diathesis due to autoantibodies against clotting factors can also result in thrombosis, as demonstrated by the co-detection of LA. When clotting factor inhibitors are detected in LA-positive individuals, it is important to confirm the presence of autoantibodies against coagulation factors using immunological methods, such as ELISA, to avoid false-positive results.

[Names] => Masahiro Ieko ... Akitada Ichinose [Doi] => 10.37349/ei.2023.00103 [Published] => August 30, 2023 [Viewed] => 449 [Downloaded] => 15 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00103 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 112 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:286–299 [Recommend] => 0 [Keywords] => Lupus anticoagulant-hypoprothrombinemia syndrome, autoimmune coagulation factor deficiency, lupus anticoagulant-hypoprothrombinemia syndrome-V, acquired hemophilia A, lupus anticoagulant, thrombosis [DetailTitle] => Autoantibodies Associated to Thrombosis and Hemostasis [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/112 [Id] => 1003103 [ris] => https://www.explorationpub.com/uploads/Article/A1003103/76b6d9994ec6e4b420c6776b302b6bba.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003103/943e7f9867431c5f80e6ed5658d0f666.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Ieko M, Ohmura K, Naito S, Yoshida M, Sasaki H, Sato T, et al. Considerations for simultaneous detection of autoantibodies to coagulation factor and lupus anticoagulant. Explor Immunol. 2023;3:286–99. https://doi.org/10.37349/ei.2023.00103 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-08-24 05:11:02 [Bib_Time] => 2023-08-24 05:11:02 [KeysWordContens] => Considerations for simultaneous detection of autoantibodies to coagulation factor and lupus anticoagulant, Lupus anticoagulant-hypoprothrombinemia syndrome, autoimmune coagulation factor deficiency, lupus anticoagulant-hypoprothrombinemia syndrome-V, acquired hemophilia A, lupus anticoagulant, thrombosis, In patients with autoimmune coagulation factor deficiency (AiCFD), the production of autoantibodies that inhibit coagulation factors in the blood reduces the activity of those relevant coagulation factors, resulting in severe bleeding symptoms. Recently, reports of patients with AiCFD have noted the concomitant detection of lupus anticoagulant (LA), a risk factor for thrombosis. LA-positive patients may show bleeding symptoms due to decreased activity of coagulation factor II (FII) caused by autoantibodies against FII, in addition to thrombotic symptoms, a condition termed LA-hypoprothrombinemia syndrome (LAHPS). Anti-FII antibodies in LAHPS cases are frequently cleared antibodies that can be detected using immunological techniques, such as enzyme-linked immunosorbent assay (ELISA). Recently, several cases of coagulation FV inhibitors, known as autoimmune FV deficiency, have been reported. Some of these cases may be complicated by LA, which can cause thrombosis. False-positive results for anticoagulant inhibitors are known to occur in LA cases; therefore, immunological confirmation of antibodies against coagulation factors is recommended. Additionally, acquired hemophilia A (AHA), caused by autoantibodies against FVIII, is a typical acquired hemorrhagic diathesis, although affected patients may present with thrombosis associated with LA. Thus, it is important to remember that hemorrhagic diathesis due to autoantibodies against clotting factors can also result in thrombosis, as demonstrated by the co-detection of LA. When clotting factor inhibitors are detected in LA-positive individuals, it is important to confirm the presence of autoantibodies against coagulation factors using immunological methods, such as ELISA, to avoid false-positive results. ,Masahiro Ieko ... Akitada Ichinose [PublishedText] => Published [IsEdit] => 0 [AccountId] => 55 [Zh] => 1 ) [104] => Array ( [ArticleId] => 762 [Create_Time] => 2023-08-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230831061541.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003106/1003106.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003106/1003106.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003106/1003106_cover.png [JournalsId] => 5 [Title] => Vitamin D, ageing, and the immune system [Abstract] => Changes occurring in the immune system along the ageing process increase the risk of infection, susceptibility to tumor development, and autoimmunity. Interventions such as physical exercise, supple [AbstractComplete] =>

Changes occurring in the immune system along the ageing process increase the risk of infection, susceptibility to tumor development, and autoimmunity. Interventions such as physical exercise, supplements, and probiotics have been proposed in order to circumvent these conditions. Vitamin D supplementation could contribute to the immune system homeostasis in older adults since a large proportion of this population has low levels of circulating vitamin D. Additionally, observational studies have shown the association between vitamin D status and infections, chronic diseases such as cancer, diabetes, and cardiovascular disease. Recently it was observed that old patients with COVID-19 and vitamin D deficiency had enhanced severity of lung damage, longer stay at the hospital, and increased risk of death, suggesting that vitamin D plays an important role in the patient outcome from COVID-19. A high dose of vitamin D supplementation improved clinical recovery in a case-series report but in another study, no evident link between levels of vitamin D and risk of COVID-19 infection was found. Results also remain debatable for vitamin D supplements and improvement of immune response after vaccination, tuberculosis, pneumonia, and sepsis. It has been hypothesized that vitamin D could modulate the immune system and thus provide both efficacies in the immune response to pathogens/vaccinations and reduction of the inflammatory phenotype. This review will discuss vitamin D and homeostasis of the immune system; the literature-based clinical data on vitamin D and infections; and the possible link between vitamin D and immune response after vaccination.

[Names] => Valquiria Bueno [Doi] => 10.37349/ei.2023.00106 [Published] => August 31, 2023 [Viewed] => 714 [Downloaded] => 23 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00106 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 111 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:341–360 [Recommend] => 0 [Keywords] => Ageing, vitamin D, immune system, infections, vaccine, COVID-19 [DetailTitle] => Immunosenescence: Mechanisms and Its Impact [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/111 [Id] => 1003106 [ris] => https://www.explorationpub.com/uploads/Article/A1003106/ac52d29bf1bfcd3ddd22ac15bf72e7f5.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003106/22500a2f7c04597dee5ad4eb36a24e22.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Bueno V. Vitamin D, ageing, and the immune system. Explor Immunol. 2023;3:341–60. https://doi.org/10.37349/ei.2023.00106 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-08-29 09:41:47 [Bib_Time] => 2023-08-29 09:41:47 [KeysWordContens] => Vitamin D, ageing, and the immune system, Ageing, vitamin D, immune system, infections, vaccine, COVID-19, Changes occurring in the immune system along the ageing process increase the risk of infection, susceptibility to tumor development, and autoimmunity. Interventions such as physical exercise, supplements, and probiotics have been proposed in order to circumvent these conditions. Vitamin D supplementation could contribute to the immune system homeostasis in older adults since a large proportion of this population has low levels of circulating vitamin D. Additionally, observational studies have shown the association between vitamin D status and infections, chronic diseases such as cancer, diabetes, and cardiovascular disease. Recently it was observed that old patients with COVID-19 and vitamin D deficiency had enhanced severity of lung damage, longer stay at the hospital, and increased risk of death, suggesting that vitamin D plays an important role in the patient outcome from COVID-19. A high dose of vitamin D supplementation improved clinical recovery in a case-series report but in another study, no evident link between levels of vitamin D and risk of COVID-19 infection was found. Results also remain debatable for vitamin D supplements and improvement of immune response after vaccination, tuberculosis, pneumonia, and sepsis. It has been hypothesized that vitamin D could modulate the immune system and thus provide both efficacies in the immune response to pathogens/vaccinations and reduction of the inflammatory phenotype. This review will discuss vitamin D and homeostasis of the immune system; the literature-based clinical data on vitamin D and infections; and the possible link between vitamin D and immune response after vaccination. ,Valquiria Bueno [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 ) [105] => Array ( [ArticleId] => 724 [Create_Time] => 2023-08-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230831032503.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003104/1003104.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003104/1003104.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003104/1003104_cover.png [JournalsId] => 5 [Title] => Analytical dilemmas in lupus anticoagulant detection [Abstract] => Accurate lupus anticoagulant (LA) detection is crucial to antiphospholipid syndrome (APS) diagnosis. Detection is based on LA functional behavior in coagulation assays irrespective of epitope specif [AbstractComplete] =>

Accurate lupus anticoagulant (LA) detection is crucial to antiphospholipid syndrome (APS) diagnosis. Detection is based on LA functional behavior in coagulation assays irrespective of epitope specificity. LA screening tests employ dilute phospholipids to accentuate in vitro inhibition by LAs, although they are not LA-specific and can be elevated by other coagulation abnormalities. Elevated screening tests are reflexed to mixing tests to distinguish between factor deficiency and inhibition. Confirmatory tests with high phospholipid concentration swamp LA to generate shorter clotting times than screening tests, whilst prolongation persists with non-phospholipid-dependent inhibitors. LA heterogeneity means that no single screening test detects every LA and the screen/mix/confirm medley must be applied to at least two assay types, usually dilute Russell’s viper venom time (dRVVT) and an LA-sensitive activated partial thromboplastin time (aPTT). Most laboratories restrict LA testing to these two assays, yet others, such as dilute prothrombin time (dPT), can perform with equal diagnostic efficacy, and additionally detect LA unreactive with dRVVT and aPTT. Converting clotting times to normalized ratios improves assay performance, and practitioners must choose between normal pooled plasma (NPP) clotting time denominators to reflect on-the-day assay performance, or reference interval (RI) mean clotting times to negate the effects of NPP variation. Cut-offs can be generated parametrically from normally distributed data, or different percentiles applied depending on the preferred balance between sensitivity and specificity. Sourcing sufficient donors for accurate cut-off estimations is problematic and transference exercises can be undertaken on low donor numbers. Analytical limitations of mixing tests have led to the adoption of alternative algorithms to the screen/mix/confirm test order, whilst some continue to rigidly apply the latter despite those limitations. Strategies to reduce or eliminate the effects of therapeutic anticoagulation have limitations, whilst the Taipan snake venom time (TSVT) screening test with an ecarin time (ET) confirmatory test is insensitive to vitamin K antagonist (VKA) and direct activated factor X anticoagulation.

[Names] => Gary W. Moore [Doi] => 10.37349/ei.2023.00104 [Published] => August 31, 2023 [Viewed] => 753 [Downloaded] => 38 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00104 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 112 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:300–324 [Recommend] => 0 [Keywords] => Activated partial thromboplastin time, antiphospholipid antibodies, confirmatory test, dilute prothrombin time, dilute Russell’s viper venom time, mixing test, screening test, Taipan snake venom time [DetailTitle] => Autoantibodies Associated to Thrombosis and Hemostasis [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/112 [Id] => 1003104 [ris] => https://www.explorationpub.com/uploads/Article/A1003104/71a5e426df3707c2ec0a2aa6f3b8a324.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003104/bc7dea3b96f41cc5bdf80de2d94f8b2b.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Moore GW. Analytical dilemmas in lupus anticoagulant detection. Explor Immunol. 2023;3:300–24. https://doi.org/10.37349/ei.2023.00104 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-08-28 06:20:48 [Bib_Time] => 2023-08-28 06:20:48 [KeysWordContens] => Analytical dilemmas in lupus anticoagulant detection, Activated partial thromboplastin time, antiphospholipid antibodies, confirmatory test, dilute prothrombin time, dilute Russell’s viper venom time, mixing test, screening test, Taipan snake venom time, Accurate lupus anticoagulant (LA) detection is crucial to antiphospholipid syndrome (APS) diagnosis. Detection is based on LA functional behavior in coagulation assays irrespective of epitope specificity. LA screening tests employ dilute phospholipids to accentuate in vitro inhibition by LAs, although they are not LA-specific and can be elevated by other coagulation abnormalities. Elevated screening tests are reflexed to mixing tests to distinguish between factor deficiency and inhibition. Confirmatory tests with high phospholipid concentration swamp LA to generate shorter clotting times than screening tests, whilst prolongation persists with non-phospholipid-dependent inhibitors. LA heterogeneity means that no single screening test detects every LA and the screen/mix/confirm medley must be applied to at least two assay types, usually dilute Russell’s viper venom time (dRVVT) and an LA-sensitive activated partial thromboplastin time (aPTT). Most laboratories restrict LA testing to these two assays, yet others, such as dilute prothrombin time (dPT), can perform with equal diagnostic efficacy, and additionally detect LA unreactive with dRVVT and aPTT. Converting clotting times to normalized ratios improves assay performance, and practitioners must choose between normal pooled plasma (NPP) clotting time denominators to reflect on-the-day assay performance, or reference interval (RI) mean clotting times to negate the effects of NPP variation. Cut-offs can be generated parametrically from normally distributed data, or different percentiles applied depending on the preferred balance between sensitivity and specificity. Sourcing sufficient donors for accurate cut-off estimations is problematic and transference exercises can be undertaken on low donor numbers. Analytical limitations of mixing tests have led to the adoption of alternative algorithms to the screen/mix/confirm test order, whilst some continue to rigidly apply the latter despite those limitations. Strategies to reduce or eliminate the effects of therapeutic anticoagulation have limitations, whilst the Taipan snake venom time (TSVT) screening test with an ecarin time (ET) confirmatory test is insensitive to vitamin K antagonist (VKA) and direct activated factor X anticoagulation. ,Gary W. Moore [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 ) [106] => Array ( [ArticleId] => 790 [Create_Time] => 2023-08-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230831090236.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003109/1003109.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003109/1003109.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003109/1003109_cover.png [JournalsId] => 5 [Title] => Inflammatory immune mediators and Plasmodium falciparum infection: a cross-sectional study among Sudanese patients with severe and uncomplicated malaria [Abstract] => Aim: A number of questions remain unanswered concerning how infected individuals regulate their immune response to Plasmodium falciparum (P. falciparum) parasites at varying levels of exposure. D [AbstractComplete] =>

Aim:

A number of questions remain unanswered concerning how infected individuals regulate their immune response to Plasmodium falciparum (P. falciparum) parasites at varying levels of exposure. Due to the interactions of inflammatory mediators and cytokines with the P. falciparum parasite complex density, several mediators influence parasitaemia and may give some indications of disease severity and represent effective signs in clinical manifestations of malaria disease.

Methods:

In this study, various levels of immune response mediators of interleukin 8 (IL-8), tumor necrosis factor-beta (TNF-β, also known as lymphotoxin-α), interferon-gamma (IFN-γ), IL-6, and IL-10 were investigated to the different phases of infection with P. falciparum in hyperendemic states in Sudan (White Nile, Blue Nile). This study vetted the association between certain inflammatory mediators during malaria infection and parasite density. This study was based on a total of 108 cases, in which 86 patients (62.0%) were uncomplicated and (17.6%) were severe, all met the diagnostic criteria and were clinically admitted for malaria infections. Commercial enzyme-linked immunosorbent assay (ELISA) kits were employed to determine the inflammatory mediator’s serum concentration.

Results:

The analysis of data indicated that older infected children had substantially raised levels of IFN-γ (P < 0.05), among study groups, levels of IFN-γ, TNF-β, and IL-8 were strongly linked with the severity of malaria, in severe and uncomplicated cases (P < 0.001), IL-6 and IL-10 were significantly associated with severe malaria cases uniquely (P < 0.001). Furthermore, we reported a positive correlation between IL-8 and TNF-β during all infection cases (r = 0.760, P < 0.001). Additionally, in severe malaria cases IL-6 was positively correlated with IL-10 (r = 0.575, P = 0.010).

Conclusions:

Eliminating P. falciparum blood-stage infection needs effective, specific, and tuned immune response strategies, which may present in the mediator’s correlations and depend on the density of the infection. Besides the effective levels contribution of certain cytokines that play protective roles during different stages of an infection.

[Names] => Dia Aldeen Alfaki ... Mohamed Mubarak Elbasheir [Doi] => 10.37349/ei.2023.00109 [Published] => August 31, 2023 [Viewed] => 612 [Downloaded] => 18 [Subject] => Original Article [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00109 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:406–415 [Recommend] => 0 [Keywords] => Interferon-gamma, tumor necrosis factor-beta, interleukin 6, interleukin 8, interleukin 10, Plasmodium falciparum [DetailTitle] => [DetailUrl] => [Id] => 1003109 [ris] => https://www.explorationpub.com/uploads/Article/A1003109/541572f7a85b2ea395c00f2b251cc2f1.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003109/74121bec44720ffe63441dbd728e2302.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Alfaki DA, Hussein M, Hassan M, Eloraish AG, Elbasheir MM. Inflammatory immune mediators and Plasmodium falciparum infection: a cross-sectional study among Sudanese patients with severe and uncomplicated malaria. Explor Immunol. 2023;3:406–15. https://doi.org/10.37349/ei.2023.00109 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-08-31 06:04:59 [Bib_Time] => 2023-08-31 06:04:59 [KeysWordContens] => Inflammatory immune mediators and Plasmodium falciparum infection: a cross-sectional study among Sudanese patients with severe and uncomplicated malaria, Interferon-gamma, tumor necrosis factor-beta, interleukin 6, interleukin 8, interleukin 10, Plasmodium falciparum , Aim: A number of questions remain unanswered concerning how infected individuals regulate their immune response to Plasmodium falciparum (P. falciparum) parasites at varying levels of exposure. Due to the interactions of inflammatory mediators and cytokines with the P. falciparum parasite complex density, several mediators influence parasitaemia and may give some indications of disease severity and represent effective signs in clinical manifestations of malaria disease. Methods: In this study, various levels of immune response mediators of interleukin 8 (IL-8), tumor necrosis factor-beta (TNF-β, also known as lymphotoxin-α), interferon-gamma (IFN-γ), IL-6, and IL-10 were investigated to the different phases of infection with P. falciparum in hyperendemic states in Sudan (White Nile, Blue Nile). This study vetted the association between certain inflammatory mediators during malaria infection and parasite density. This study was based on a total of 108 cases, in which 86 patients (62.0%) were uncomplicated and (17.6%) were severe, all met the diagnostic criteria and were clinically admitted for malaria infections. Commercial enzyme-linked immunosorbent assay (ELISA) kits were employed to determine the inflammatory mediator’s serum concentration. Results: The analysis of data indicated that older infected children had substantially raised levels of IFN-γ (P < 0.05), among study groups, levels of IFN-γ, TNF-β, and IL-8 were strongly linked with the severity of malaria, in severe and uncomplicated cases (P < 0.001), IL-6 and IL-10 were significantly associated with severe malaria cases uniquely (P < 0.001). Furthermore, we reported a positive correlation between IL-8 and TNF-β during all infection cases (r = 0.760, P < 0.001). Additionally, in severe malaria cases IL-6 was positively correlated with IL-10 (r = 0.575, P = 0.010). Conclusions: Eliminating P. falciparum blood-stage infection needs effective, specific, and tuned immune response strategies, which may present in the mediator’s correlations and depend on the density of the infection. Besides the effective levels contribution of certain cytokines that play protective roles during different stages of an infection. ,Dia Aldeen Alfaki ... Mohamed Mubarak Elbasheir [PublishedText] => Published [IsEdit] => 0 [AccountId] => 83 [Zh] => 1 ) [107] => Array ( [ArticleId] => 757 [Create_Time] => 2023-08-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230831051858.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003105/1003105.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003105/1003105.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003105/1003105_cover.png [JournalsId] => 5 [Title] => Immune system rejuvenation—approaches and real achievements [Abstract] => Interest in the mechanisms of aging of the immune system has not faded over the past 100 years, and it is caused by the immune-mediated development of age-related pathology, including autoimmune org [AbstractComplete] =>

Interest in the mechanisms of aging of the immune system has not faded over the past 100 years, and it is caused by the immune-mediated development of age-related pathology, including autoimmune organ damage, reduced vaccination efficiency, atherosclerosis, the development of cardiovascular pathology, etc. In contrast to many other organs and systems, the immune system aging begins at an early age and has more pronounced changes that lead to the development of secondary pathology, which significantly affects life expectancy. But an effective strategy to restore immune function has not been developed yet. During this time, the mechanisms of age-related dysfunction of organs and cells of both the adaptive and innate immune systems were studied in detail—thymus involution, a decrease in the potential of hematopoietic stem cells, impaired differentiation and functions of immunocompetent cells, as well as the ways of their interaction. Numerous potential therapeutic targets have been identified and various approaches have been used to implement such therapeutic interventions. The review is devoted to replacement therapy using transplantation of hematopoietic stem cells (HSCs) and young lymphoid cells and tissues, cellular and systemic factor exchange in heterochronic parabiosis, and some other widely used life extension approaches. It has been proven that cell therapy using young cells to rejuvenate the old immune system, unfortunately, often turns out to be ineffective because it does not eliminate the root cause of age-related changes. The phenomenon of inflamm-aging that develops with age can significantly affect both the aging of the organism in general and the functioning of immunocompetent cells in particular. Therefore, the most promising direction in the restoration of immune functions during aging is systemic approaches that have a complex effect on the organism as a whole and can slow down the aging process.

[Names] => Iryna Pishel [Doi] => 10.37349/ei.2023.00105 [Published] => August 31, 2023 [Viewed] => 674 [Downloaded] => 13 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00105 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 111 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:325–340 [Recommend] => 0 [Keywords] => Aging, immune system, rejuvenation [DetailTitle] => Immunosenescence: Mechanisms and Its Impact [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/111 [Id] => 1003105 [ris] => https://www.explorationpub.com/uploads/Article/A1003105/857b52709fba33354ffd0174199f66a0.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003105/9770b47b6f69844ba63ffd7e4623155c.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Pishel I. Immune system rejuvenation—approaches and real achievements. Explor Immunol. 2023;3:325–40. https://doi.org/10.37349/ei.2023.00105 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-08-29 06:39:28 [Bib_Time] => 2023-08-29 06:39:28 [KeysWordContens] => Immune system rejuvenation—approaches and real achievements, Aging, immune system, rejuvenation, Interest in the mechanisms of aging of the immune system has not faded over the past 100 years, and it is caused by the immune-mediated development of age-related pathology, including autoimmune organ damage, reduced vaccination efficiency, atherosclerosis, the development of cardiovascular pathology, etc. In contrast to many other organs and systems, the immune system aging begins at an early age and has more pronounced changes that lead to the development of secondary pathology, which significantly affects life expectancy. But an effective strategy to restore immune function has not been developed yet. During this time, the mechanisms of age-related dysfunction of organs and cells of both the adaptive and innate immune systems were studied in detail—thymus involution, a decrease in the potential of hematopoietic stem cells, impaired differentiation and functions of immunocompetent cells, as well as the ways of their interaction. Numerous potential therapeutic targets have been identified and various approaches have been used to implement such therapeutic interventions. The review is devoted to replacement therapy using transplantation of hematopoietic stem cells (HSCs) and young lymphoid cells and tissues, cellular and systemic factor exchange in heterochronic parabiosis, and some other widely used life extension approaches. It has been proven that cell therapy using young cells to rejuvenate the old immune system, unfortunately, often turns out to be ineffective because it does not eliminate the root cause of age-related changes. The phenomenon of inflamm-aging that develops with age can significantly affect both the aging of the organism in general and the functioning of immunocompetent cells in particular. Therefore, the most promising direction in the restoration of immune functions during aging is systemic approaches that have a complex effect on the organism as a whole and can slow down the aging process. ,Iryna Pishel [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 ) [108] => Array ( [ArticleId] => 771 [Create_Time] => 2023-08-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230831064547.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003107/1003107.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003107/1003107.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003107/1003107_cover.png [JournalsId] => 5 [Title] => The emergence of nanovaccines as a new paradigm in virological vaccinology: a review [Abstract] => Vaccination has made an enormous contribution to global health. Treatment resistance for infectious diseases is growing quickly, and chemotherapeutic toxicity in cancer means that vaccines must be m [AbstractComplete] =>

Vaccination has made an enormous contribution to global health. Treatment resistance for infectious diseases is growing quickly, and chemotherapeutic toxicity in cancer means that vaccines must be made right away to save humanity. But subunit vaccinations alone don’t give enough strong and long-lasting protection against infections that can kill. Nanoparticle (NP)-based delivery vehicles, such as dendrimers, liposomes, micelles, virosomes, nanogels, and microemulsions, offer interesting ways to get around the problems with traditional vaccine adjuvants. The nanovaccines (50–250 nm in size) are most efficient in terms of tissue targeting, staying in the bloodstream for a long time. Nanovaccines can improve antigen presentation, targeted delivery, stimulation of the body’s innate immune system, and a strong T-cell response without putting people at risk. This can help fight infectious diseases and cancers. Also, nanovaccines can be very helpful for making cancer treatments that use immunotherapy. So, this review highlights the various types of NPs used in the techniques that have worked in the new paradigm in viral vaccinology for infectious diseases. It gives a full rundown of the current NP-based vaccines, their potential as adjuvants, and the ways they can be delivered to cells. In the future, the best nanovaccines will try to be more logically designed, have more antigens in them, be fully functionalized, and be given to the right people.

[Names] => Chittaranjan Baruah ... Bhabesh Deka [Doi] => 10.37349/ei.2023.00107 [Published] => August 31, 2023 [Viewed] => 813 [Downloaded] => 25 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00107 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 63 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:361–383 [Recommend] => 0 [Keywords] => Adjuvant, cancer, infection, nanoparticle, nanovaccine, non-neutralizing antibody, neutralizing antibody [DetailTitle] => Old and New Paradigms in Viral Vaccinology [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/63 [Id] => 1003107 [ris] => https://www.explorationpub.com/uploads/Article/A1003107/3a9e9cb81151c3c3f94cbb95716446e2.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003107/b838b06aafb58a5cd58a11aaee62e0c1.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Baruah C, Das P, Devi P, Saikia PM, Deka B. The emergence of nanovaccines as a new paradigm in virological vaccinology: a review. Explor Immunol. 2023;3:361–83. https://doi.org/10.37349/ei.2023.00107 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-08-30 05:47:44 [Bib_Time] => 2023-08-30 05:47:44 [KeysWordContens] => The emergence of nanovaccines as a new paradigm in virological vaccinology: a review, Adjuvant, cancer, infection, nanoparticle, nanovaccine, non-neutralizing antibody, neutralizing antibody, Vaccination has made an enormous contribution to global health. Treatment resistance for infectious diseases is growing quickly, and chemotherapeutic toxicity in cancer means that vaccines must be made right away to save humanity. But subunit vaccinations alone don’t give enough strong and long-lasting protection against infections that can kill. Nanoparticle (NP)-based delivery vehicles, such as dendrimers, liposomes, micelles, virosomes, nanogels, and microemulsions, offer interesting ways to get around the problems with traditional vaccine adjuvants. The nanovaccines (50–250 nm in size) are most efficient in terms of tissue targeting, staying in the bloodstream for a long time. Nanovaccines can improve antigen presentation, targeted delivery, stimulation of the body’s innate immune system, and a strong T-cell response without putting people at risk. This can help fight infectious diseases and cancers. Also, nanovaccines can be very helpful for making cancer treatments that use immunotherapy. So, this review highlights the various types of NPs used in the techniques that have worked in the new paradigm in viral vaccinology for infectious diseases. It gives a full rundown of the current NP-based vaccines, their potential as adjuvants, and the ways they can be delivered to cells. In the future, the best nanovaccines will try to be more logically designed, have more antigens in them, be fully functionalized, and be given to the right people. ,Chittaranjan Baruah ... Bhabesh Deka [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 ) [109] => Array ( [ArticleId] => 779 [Create_Time] => 2023-08-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202309/20230901011520.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003108/1003108.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003108/1003108.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003108/1003108_cover.png [JournalsId] => 5 [Title] => Immune evasion by cancer stem cells ensures tumor initiation and failure of immunotherapy [Abstract] => Cancer stem cells (CSCs) are a small subpopulation of cells that drive the formation and progression of tumors. However, during tumor initiation, how CSCs communicate with neighbouring immune cells [AbstractComplete] =>

Cancer stem cells (CSCs) are a small subpopulation of cells that drive the formation and progression of tumors. However, during tumor initiation, how CSCs communicate with neighbouring immune cells to overcome the powerful immune surveillance barrier in order to form, spread, and maintain the tumor, remains poorly understood. It is, therefore, absolutely necessary to understand how a small number of tumor-initiating cells (TICs) survive immune attack during (a) the “elimination phase” of “tumor immune-editing”, (b) the establishment of regional or distant tumor after metastasis, and (c) recurrence after therapy. Mounting evidence suggests that CSCs suppress the immune system through a variety of distinct mechanisms that ensure the survival of not only CSCs but also non-stem cancer cells (NSCCs), which eventually form the tumor mass. In this review article, the mechanisms via which CSCs change the immune landscape of the tissue of origin, which contains macrophages, dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), natural killer (NK) cells, and tumor-infiltrating lymphocytes, in favour of tumorigenesis were discussed. The failure of cancer immunotherapy might also be explained by such interaction between CSCs and immune cells. This review will shed light on the critical role of CSCs in tumor immune evasion and emphasize the importance of CSC-targeted immunotherapy as a cutting-edge technique for battling cancer by restricting communication between immune cells and CSCs.

[Names] => Sourio Chakraborty ... Tanya Das [Doi] => 10.37349/ei.2023.00108 [Published] => August 31, 2023 [Viewed] => 568 [Downloaded] => 21 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00108 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 77 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:384–405 [Recommend] => 0 [Keywords] => Antitumor immunity, cancer stem cells, cancer stem cell sensitizing therapy, metastasis, suppressive immune cells, tumor initiation, tumor-microenvironment, tumor relapse [DetailTitle] => Interplay of Stem Cells and Immunology in Regenerative Medicine [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/77 [Id] => 1003108 [ris] => https://www.explorationpub.com/uploads/Article/A1003108/adffcf0b906effd38c0d0b78723901d5.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003108/3117f13482d84e18940b92491597f6a5.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-26 [CitethisArticle] => Chakraborty S, Mukherjee S, Basak U, Pati S, Dutta A, Dutta S, et al. Immune evasion by cancer stem cells ensures tumor initiation and failure of immunotherapy. Explor Immunol. 2023;3:384–405. https://doi.org/10.37349/ei.2023.00108 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-08-31 00:58:44 [Bib_Time] => 2023-08-31 00:58:44 [KeysWordContens] => Immune evasion by cancer stem cells ensures tumor initiation and failure of immunotherapy, Antitumor immunity, cancer stem cells, cancer stem cell sensitizing therapy, metastasis, suppressive immune cells, tumor initiation, tumor-microenvironment, tumor relapse, Cancer stem cells (CSCs) are a small subpopulation of cells that drive the formation and progression of tumors. However, during tumor initiation, how CSCs communicate with neighbouring immune cells to overcome the powerful immune surveillance barrier in order to form, spread, and maintain the tumor, remains poorly understood. It is, therefore, absolutely necessary to understand how a small number of tumor-initiating cells (TICs) survive immune attack during (a) the “elimination phase” of “tumor immune-editing”, (b) the establishment of regional or distant tumor after metastasis, and (c) recurrence after therapy. Mounting evidence suggests that CSCs suppress the immune system through a variety of distinct mechanisms that ensure the survival of not only CSCs but also non-stem cancer cells (NSCCs), which eventually form the tumor mass. In this review article, the mechanisms via which CSCs change the immune landscape of the tissue of origin, which contains macrophages, dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), natural killer (NK) cells, and tumor-infiltrating lymphocytes, in favour of tumorigenesis were discussed. The failure of cancer immunotherapy might also be explained by such interaction between CSCs and immune cells. This review will shed light on the critical role of CSCs in tumor immune evasion and emphasize the importance of CSC-targeted immunotherapy as a cutting-edge technique for battling cancer by restricting communication between immune cells and CSCs. ,Sourio Chakraborty ... Tanya Das [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 ) [110] => Array ( [ArticleId] => 820 [Create_Time] => 2023-10-08 [zipUrl] => https://www.explorationpub.com/uploads/zip/202310/20231030084231.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003110/1003110.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003110/1003110.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003110/1003110_cover.png [JournalsId] => 5 [Title] => Update on laboratory practice for the diagnosis of lupus anticoagulant and the antiphospholipid syndrome [Abstract] => Antiphospholipid syndrome (APS) is defined as an autoimmune and prothrombotic disorder in patients with the persistent presence of antiphospholipid antibodies (aPLs). In the classification criteria, [AbstractComplete] =>

Antiphospholipid syndrome (APS) is defined as an autoimmune and prothrombotic disorder in patients with the persistent presence of antiphospholipid antibodies (aPLs). In the classification criteria, aPL expresses lupus anticoagulant (LA) activity, which is detected by prolongation of coagulation assays. The LA detection algorithm is a sequential flow including screening tests, mixing tests, and confirmatory tests to differentiate between LA-positive and other anticoagulant abnormalities. Two types of assays are used, like dilute Russell’s viper venom time (dRVVT) and activated partial thromboplastin time (APTT) because no single test is sensitive to all LAs. The anticoagulant drugs prescribed for the prevention and treatment of thrombosis disorders can interfere with the assays, and it is important to know the effects of these drugs in the assays. Especially, new generation anticoagulant drugs, called direct oral anticoagulants (DOACs), affect the results. In this review, the following points are discussed: i) LA detection flow and data interpretation, ii) the principles of coagulation assays proposed and their characteristics, and iii) the effects of anticoagulant drugs in LA detection.

[Names] => Osamu Kumano ... Jean Amiral [Doi] => 10.37349/ei.2023.00110 [Published] => October 08, 2023 [Viewed] => 669 [Downloaded] => 24 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00110 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 112 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:416–432 [Recommend] => 0 [Keywords] => Lupus anticoagulant, thrombosis, antiphospholipid syndrome, antiphospholipid antibodies, activated partial thromboplastin time, dilute Russell’s viper venom time [DetailTitle] => Autoantibodies Associated to Thrombosis and Hemostasis [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/112 [Id] => 1003110 [ris] => https://www.explorationpub.com/uploads/Article/A1003110/9feda9c6225036de4c011d95f966fc4c.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003110/78cfb077674bee4178b0bb2882772df6.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-25 [CitethisArticle] => Kumano O, Peyrafitte M, Amiral J. Update on laboratory practice for the diagnosis of lupus anticoagulant and the antiphospholipid syndrome. Explor Immunol. 2023;3:416–32. https://doi.org/10.37349/ei.2023.00110 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-09-22 05:47:06 [Bib_Time] => 2023-09-22 05:47:06 [KeysWordContens] => Update on laboratory practice for the diagnosis of lupus anticoagulant and the antiphospholipid syndrome, Lupus anticoagulant, thrombosis, antiphospholipid syndrome, antiphospholipid antibodies, activated partial thromboplastin time, dilute Russell’s viper venom time, Antiphospholipid syndrome (APS) is defined as an autoimmune and prothrombotic disorder in patients with the persistent presence of antiphospholipid antibodies (aPLs). In the classification criteria, aPL expresses lupus anticoagulant (LA) activity, which is detected by prolongation of coagulation assays. The LA detection algorithm is a sequential flow including screening tests, mixing tests, and confirmatory tests to differentiate between LA-positive and other anticoagulant abnormalities. Two types of assays are used, like dilute Russell’s viper venom time (dRVVT) and activated partial thromboplastin time (APTT) because no single test is sensitive to all LAs. The anticoagulant drugs prescribed for the prevention and treatment of thrombosis disorders can interfere with the assays, and it is important to know the effects of these drugs in the assays. Especially, new generation anticoagulant drugs, called direct oral anticoagulants (DOACs), affect the results. In this review, the following points are discussed: i) LA detection flow and data interpretation, ii) the principles of coagulation assays proposed and their characteristics, and iii) the effects of anticoagulant drugs in LA detection. ,Osamu Kumano ... Jean Amiral [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 ) [111] => Array ( [ArticleId] => 840 [Create_Time] => 2023-10-16 [zipUrl] => https://www.explorationpub.com/uploads/zip/202310/20231027025100.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003115/1003115.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003115/1003115.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003115/1003115_cover.png [JournalsId] => 5 [Title] => Loss of regulation of T helper 17 cells: a definitive factor for critical cases of coronavirus disease 2019 [Abstract] => One of the greatest challenges in the study of coronavirus disease 2019 (COVID-19) has been to establish the determining factors in the severity of the disease. Through extensive research efforts, a [AbstractComplete] =>

One of the greatest challenges in the study of coronavirus disease 2019 (COVID-19) has been to establish the determining factors in the severity of the disease. Through extensive research efforts, a crucial factor responsible for disease control or exacerbation in COVID-19 has been identified—the regulation of the immune response. The abnormal release of interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-α) has been extensively studied in the context of the altered immune response observed in severe cases of COVID-19. However, recent attention has turned towards the excessive release of IL-17 and the increased presence of T helper 17 (Th17) cells, the main secretory cells of this cytokine. These factors have garnered interest due to their potential involvement in the cytokine storm observed in severe cases of COVID-19. In this review, it will be delved into the intricate mechanisms by which IL-6 contributes to the differentiation of Th17 cells, resulting in an increase in the population of Th17 cells. Moreover, it will be explored the proportional relationship between the increase of these lymphocytes and the release of IL-17 and other chemokines, which all together play a key role in promoting the chemotaxis and activation of neutrophils. Ultimately, this cascade of events culminates in the generation of tissue damage by neutrophils. Additionally, therapeutic options targeting these lymphocytes and cytokines are explored, providing insights into potential avenues for intervention.

[Names] => Miguel Angel Pardiño-Vega, Norma Estela Herrera-González [Doi] => 10.37349/ei.2023.00115 [Published] => October 16, 2023 [Viewed] => 587 [Downloaded] => 21 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00115 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:490–499 [Recommend] => 0 [Keywords] => Coronavirus disease 2019, severe acute respiratory syndrome coronavirus 2, T helper 17, interleukin-17, cytokine storm [DetailTitle] => [DetailUrl] => [Id] => 1003115 [ris] => https://www.explorationpub.com/uploads/Article/A1003115/f7f5a09bfc52ebc42683f2850accff44.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003115/c40c5c08f7e4a1aa2f880ba384ce899a.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Pardiño-Vega MA, Herrera-González NE. Loss of regulation of T helper 17 cells: a definitive factor for critical cases of coronavirus disease 2019. Explor Immunol. 2023;3:490–9. https://doi.org/10.37349/ei.2023.00115 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-10-13 03:49:02 [Bib_Time] => 2023-10-13 03:49:02 [KeysWordContens] => Loss of regulation of T helper 17 cells: a definitive factor for critical cases of coronavirus disease 2019, Coronavirus disease 2019, severe acute respiratory syndrome coronavirus 2, T helper 17, interleukin-17, cytokine storm, One of the greatest challenges in the study of coronavirus disease 2019 (COVID-19) has been to establish the determining factors in the severity of the disease. Through extensive research efforts, a crucial factor responsible for disease control or exacerbation in COVID-19 has been identified—the regulation of the immune response. The abnormal release of interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-α) has been extensively studied in the context of the altered immune response observed in severe cases of COVID-19. However, recent attention has turned towards the excessive release of IL-17 and the increased presence of T helper 17 (Th17) cells, the main secretory cells of this cytokine. These factors have garnered interest due to their potential involvement in the cytokine storm observed in severe cases of COVID-19. In this review, it will be delved into the intricate mechanisms by which IL-6 contributes to the differentiation of Th17 cells, resulting in an increase in the population of Th17 cells. Moreover, it will be explored the proportional relationship between the increase of these lymphocytes and the release of IL-17 and other chemokines, which all together play a key role in promoting the chemotaxis and activation of neutrophils. Ultimately, this cascade of events culminates in the generation of tissue damage by neutrophils. Additionally, therapeutic options targeting these lymphocytes and cytokines are explored, providing insights into potential avenues for intervention. ,Miguel Angel Pardiño-Vega, Norma Estela Herrera-González [PublishedText] => Published [IsEdit] => 0 [AccountId] => 55 [Zh] => 1 ) [112] => Array ( [ArticleId] => 833 [Create_Time] => 2023-10-11 [zipUrl] => https://www.explorationpub.com/uploads/zip/202310/20231011011423.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003111/1003111.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003111/1003111.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003111/1003111_cover.png [JournalsId] => 5 [Title] => Effect of coronavirus disease 2019 on the vaccine development paradigm [Abstract] => Vaccines are prophylactic medical products effectively used against infectious diseases. Although a high amount of vaccine studies are conducted at the preclinical stage, the number of approved vacc [AbstractComplete] =>

Vaccines are prophylactic medical products effectively used against infectious diseases. Although a high amount of vaccine studies are conducted at the preclinical stage, the number of approved vaccines is less than 10%. Development of vaccines from the research stage to the approval of administrative institutions takes about 5 years to 10 years conventionally. However, this period of time for vaccine development is not convenient during public health emergencies because an effective vaccine is required in a short time to restrict the speed of high mortality and morbidity. The pandemic of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), had its catastrophic effects worldwide quickly. Therefore, an atypical process was followed for the development of COVID-19 vaccines. Great effort was spent in terms of cooperation among the governmental institutions, academia, and medical companies as well as a high amount of budget was allocated to develop effective vaccines against COVID-19. As of March 2023, the numbers of COVID-19 vaccines in clinical and preclinical development were 183 and 199, respectively. An emergency use authorization (EUA) process was applied to accelerate the approval of the vaccines. Consequently, vaccinations could be started in less than a year, which decelerated the speed of the pandemic. Although EUA caused hesitancy among some people questioning the safety and efficacy of the vaccines, the vast majority of the population was vaccinated. Currently, more than 5.5 billion people (about 70% of the world population) have received 13.38 billion doses of 11 different COVID-19 vaccines, and 73% of the doses were Comirnaty manufactured by Pfizer/BioNTech.

[Names] => Sezer Okay [Doi] => 10.37349/ei.2023.00111 [Published] => October 10, 2023 [Viewed] => 556 [Downloaded] => 14 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00111 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 63 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:433–441 [Recommend] => 0 [Keywords] => Coronavirus disease 2019, emergency use authorization, vaccine development, vaccine hesitancy [DetailTitle] => Old and New Paradigms in Viral Vaccinology [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/63 [Id] => 1003111 [ris] => https://www.explorationpub.com/uploads/Article/A1003111/7aba1cb219f6c8518cd59b6e72c656bc.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003111/ae2631a0cf72a9b01a78b850d852924e.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Okay S. Effect of coronavirus disease 2019 on the vaccine development paradigm. Explor Immunol. 2023;3:433–41. https://doi.org/10.37349/ei.2023.00111 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-10-11 01:01:49 [Bib_Time] => 2023-10-11 01:01:49 [KeysWordContens] => Effect of coronavirus disease 2019 on the vaccine development paradigm, Coronavirus disease 2019, emergency use authorization, vaccine development, vaccine hesitancy, Vaccines are prophylactic medical products effectively used against infectious diseases. Although a high amount of vaccine studies are conducted at the preclinical stage, the number of approved vaccines is less than 10%. Development of vaccines from the research stage to the approval of administrative institutions takes about 5 years to 10 years conventionally. However, this period of time for vaccine development is not convenient during public health emergencies because an effective vaccine is required in a short time to restrict the speed of high mortality and morbidity. The pandemic of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), had its catastrophic effects worldwide quickly. Therefore, an atypical process was followed for the development of COVID-19 vaccines. Great effort was spent in terms of cooperation among the governmental institutions, academia, and medical companies as well as a high amount of budget was allocated to develop effective vaccines against COVID-19. As of March 2023, the numbers of COVID-19 vaccines in clinical and preclinical development were 183 and 199, respectively. An emergency use authorization (EUA) process was applied to accelerate the approval of the vaccines. Consequently, vaccinations could be started in less than a year, which decelerated the speed of the pandemic. Although EUA caused hesitancy among some people questioning the safety and efficacy of the vaccines, the vast majority of the population was vaccinated. Currently, more than 5.5 billion people (about 70% of the world population) have received 13.38 billion doses of 11 different COVID-19 vaccines, and 73% of the doses were Comirnaty manufactured by Pfizer/BioNTech. ,Sezer Okay [PublishedText] => Published [IsEdit] => 0 [AccountId] => 86 [Zh] => 1 ) [113] => Array ( [ArticleId] => 834 [Create_Time] => 2023-10-11 [zipUrl] => https://www.explorationpub.com/uploads/zip/202310/20231030084907.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003112/1003112.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003112/1003112.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003112/1003112_cover.png [JournalsId] => 5 [Title] => Mitochondrial dysfunction at the cornerstone of inflammatory exacerbation in aged macrophages [Abstract] => Immunosenescence encompasses multiple age-related adaptations that result in increased susceptibility to infections, chronic inflammatory disorders, and higher mortality risk. Macrophages are key in [AbstractComplete] =>

Immunosenescence encompasses multiple age-related adaptations that result in increased susceptibility to infections, chronic inflammatory disorders, and higher mortality risk. Macrophages are key innate cells implicated in inflammatory responses and tissue homeostasis, functions progressively compromised by aging. This process coincides with declining mitochondrial physiology, whose integrity is required to sustain and orchestrate immune responses. Indeed, multiple insults observed in aged macrophages have been implied as drivers of mitochondrial dysfunction, but how this translates into impaired immune function remains sparsely explored. This review provides a perspective on recent studies elucidating the underlying mechanisms linking dysregulated mitochondria homeostasis to immune function in aged macrophages. Genomic stress alongside defective mitochondrial turnover accounted for the progressive accumulation of damaged mitochondria in aged macrophages, thus resulting in a higher susceptibility to excessive mitochondrial DNA (mtDNA) leakage and reactive oxygen species (ROS) production. Increased levels of these mitochondrial products following infection were demonstrated to contribute to exacerbated inflammatory responses mediated by overstimulation of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and cyclic GMP-ATP synthase (cGAS)-stimulator of interferon genes (STING) pathways. While these mechanisms are not fully elucidated, the present evidence provides a promising area to be explored and a renewed perspective of potential therapeutic targets for immunological dysfunction.

[Names] => Rafael Moura Maurmann ... Brandt D. Pence [Doi] => 10.37349/ei.2023.00112 [Published] => October 11, 2023 [Viewed] => 521 [Downloaded] => 18 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00112 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 111 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:442–452 [Recommend] => 0 [Keywords] => Immunometabolism, senescence, mtDNA, cGAS-STING, NAD [DetailTitle] => Immunosenescence: Mechanisms and Its Impact [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/111 [Id] => 1003112 [ris] => https://www.explorationpub.com/uploads/Article/A1003112/d562e975b29e25d6341120d87e55e891.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003112/d1dce0bdae2dfcc7d7bf7f5778cb5c32.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Maurmann RM, Schmitt BL, Mosalmanzadeh N, Pence BD. Mitochondrial dysfunction at the cornerstone of inflammatory exacerbation in aged macrophages. Explor Immunol. 2023;3:442–52. https://doi.org/10.37349/ei.2023.00112 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-10-10 01:38:52 [Bib_Time] => 2023-10-10 01:38:52 [KeysWordContens] => Mitochondrial dysfunction at the cornerstone of inflammatory exacerbation in aged macrophages, Immunometabolism, senescence, mtDNA, cGAS-STING, NAD, Immunosenescence encompasses multiple age-related adaptations that result in increased susceptibility to infections, chronic inflammatory disorders, and higher mortality risk. Macrophages are key innate cells implicated in inflammatory responses and tissue homeostasis, functions progressively compromised by aging. This process coincides with declining mitochondrial physiology, whose integrity is required to sustain and orchestrate immune responses. Indeed, multiple insults observed in aged macrophages have been implied as drivers of mitochondrial dysfunction, but how this translates into impaired immune function remains sparsely explored. This review provides a perspective on recent studies elucidating the underlying mechanisms linking dysregulated mitochondria homeostasis to immune function in aged macrophages. Genomic stress alongside defective mitochondrial turnover accounted for the progressive accumulation of damaged mitochondria in aged macrophages, thus resulting in a higher susceptibility to excessive mitochondrial DNA (mtDNA) leakage and reactive oxygen species (ROS) production. Increased levels of these mitochondrial products following infection were demonstrated to contribute to exacerbated inflammatory responses mediated by overstimulation of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and cyclic GMP-ATP synthase (cGAS)-stimulator of interferon genes (STING) pathways. While these mechanisms are not fully elucidated, the present evidence provides a promising area to be explored and a renewed perspective of potential therapeutic targets for immunological dysfunction. ,Rafael Moura Maurmann ... Brandt D. Pence [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 ) [114] => Array ( [ArticleId] => 836 [Create_Time] => 2023-10-12 [zipUrl] => https://www.explorationpub.com/uploads/zip/202310/20231030085550.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003113/1003113.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003113/1003113.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003113/1003113_cover.png [JournalsId] => 5 [Title] => Research progress of immune balance and genetic polymorphism in unexplained recurrent abortion [Abstract] => The etiology of recurrent spontaneous abortion (RSA) is extremely complex, as there are 40–50% of patients with unexplained miscarriages, known as unexplained RSA (URSA). URSA affects approximatel [AbstractComplete] =>

The etiology of recurrent spontaneous abortion (RSA) is extremely complex, as there are 40–50% of patients with unexplained miscarriages, known as unexplained RSA (URSA). URSA affects approximately 1–2% of females of childbearing age and has a massive impact on the physical and mental conditions of both patients and their families. The pathogenesis of the disease remains unclear, making its treatment complicated. In recent years, considerable progress has been made in the exploration of the URSA immune balance mechanism and it has been universally acknowledged that a balanced immune response (as abnormal immunity) may be the root cause of poor pregnancy outcomes. This review discussed and summarized the effects of immune cells and blocking antibodies (BAs) on URSA based on the current state of knowledge in this area. Additionally, molecular genetics also plays an essential role in the incidence rate of URSA since the role of genetic polymorphism in the pathogenesis of URSA has been thoroughly studied. Nonetheless, the outcomes of these studies are inconsistent, particularly across populations. This paper reviewed previous studies on URSA and maternal genetic polymorphism, focusing on and synthesizing the most important findings to date, and providing diagnostic recommendation for URSA patients with clinical symptoms.

[Names] => Yafei Kang ... Donghui Huang [Doi] => 10.37349/ei.2023.00113 [Published] => October 12, 2023 [Viewed] => 629 [Downloaded] => 15 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00113 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:453–474 [Recommend] => 0 [Keywords] => Unexplained recurrent spontaneous abortion, immune cells, gene polymorphism [DetailTitle] => [DetailUrl] => [Id] => 1003113 [ris] => https://www.explorationpub.com/uploads/Article/A1003113/9fd56df9558b27e252d767326118c708.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003113/949d83ea8d99dac5acb1f3f5e8c63907.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Kang Y, Xie Q, Chen S, Li Q, Dong X, Zhang T, et al. Research progress of immune balance and genetic polymorphism in unexplained recurrent abortion. Explor Immunol. 2023;3:453–74. https://doi.org/10.37349/ei.2023.00113 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-10-10 03:41:43 [Bib_Time] => 2023-10-10 03:41:43 [KeysWordContens] => Research progress of immune balance and genetic polymorphism in unexplained recurrent abortion, Unexplained recurrent spontaneous abortion, immune cells, gene polymorphism, The etiology of recurrent spontaneous abortion (RSA) is extremely complex, as there are 40–50% of patients with unexplained miscarriages, known as unexplained RSA (URSA). URSA affects approximately 1–2% of females of childbearing age and has a massive impact on the physical and mental conditions of both patients and their families. The pathogenesis of the disease remains unclear, making its treatment complicated. In recent years, considerable progress has been made in the exploration of the URSA immune balance mechanism and it has been universally acknowledged that a balanced immune response (as abnormal immunity) may be the root cause of poor pregnancy outcomes. This review discussed and summarized the effects of immune cells and blocking antibodies (BAs) on URSA based on the current state of knowledge in this area. Additionally, molecular genetics also plays an essential role in the incidence rate of URSA since the role of genetic polymorphism in the pathogenesis of URSA has been thoroughly studied. Nonetheless, the outcomes of these studies are inconsistent, particularly across populations. This paper reviewed previous studies on URSA and maternal genetic polymorphism, focusing on and synthesizing the most important findings to date, and providing diagnostic recommendation for URSA patients with clinical symptoms. ,Yafei Kang ... Donghui Huang [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 ) [115] => Array ( [ArticleId] => 837 [Create_Time] => 2023-10-13 [zipUrl] => https://www.explorationpub.com/uploads/zip/202310/20231030084630.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003114/1003114.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003114/1003114.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003114/1003114_cover.png [JournalsId] => 5 [Title] => Risk factors and recurrent thrombosis in primary antiphospholipid syndrome [Abstract] => Aim: The study aims to evaluate the incidence of recurrent thromboses in patients with primary antiphospholipid syndrome (PAPS) and its association with the presence of different antiphospholipid [AbstractComplete] =>

Aim:

The study aims to evaluate the incidence of recurrent thromboses in patients with primary antiphospholipid syndrome (PAPS) and its association with the presence of different antiphospholipid antibodies (aPLs) and known thrombogenic risk factors.

Methods:

This retrospective study included 52 patients. The median age of the patients was 38.5 years [31.5; 43.5], and the duration of the disease was 9.0 years [3.1; 13.0]. aPLs, including IgG/IgM/IgA antibodies to cardiolipin (aCLs), IgG/IgM/IgA anti-beta2-glycoprotein I (anti-β2-GPI), IgG anti-domain I-β2-GPI (anti-β2-GPIDI) antibodies, IgG/IgM antibodies to the phosphatidylserine/prothrombin complex (aPS/PT), and other thrombosis risk factors were included for analysis.

Results:

Recurrent thrombosis was reported in 34 (65%) out of 52 patients and 18 (35%) did not have it. The main reason for the recurrence of thrombosis was the lack of anticoagulant therapy: in 18 (52.9%) out of 34 patients with recurrent thrombosis. Three patients were taking warfarin at the time of thrombosis recurrence, but target international normalized ratio (INR) levels were not achieved. Other patients with recurrent thrombosis were taking direct oral anticoagulants (DOACs). The risk of recurrent thrombotic events with positive IgG aCL was 10.33 (P = 0.002) and 21 (P = 0.007) times higher were examined in enzyme-linked immunoassay (ELISA) and chemiluminescent assay (CLA), respectively. The risk of thrombosis was 4.58 times higher in patients who were IgA aCL-positive (P = 0.01). Compared with other antibodies, with positive IgG values of anti-β2-GPI and IgG aPS/PT by ELISA, a lower probability of thrombosis recurrence was observed: 7.56 and 7.25, respectively. A high risk of recurrent thrombosis [odds ratio (OR) = 32.0] was observed in IgG anti-β2-GPI (CLA). The combination of IgG aCL with IgG anti-β2-GPI and with IgG anti-β2-GPIDI is more informative with respect to the risks of thrombosis recurrence compared to double positivity for aCL with anti-β2-GPI (OR = 20.71 vs. OR = 10.18). Triple positivity for IgG aCL with IgG anti-β2-GPI and with IgG aPS/PT also shows better results compared to positivity for aCL with anti-β2-GPI (OR = 6.06 vs. OR = 5.79). Among other risk factors, arterial hypertension (AH) and obesity were significant in relation to the recurrence of thrombosis. AH occurred in 22 (42%) of 52 patients with PAPS. AH was associated with recurrent thrombosis in PAPS patients: 18 (53%) out of 34 with recurrent thrombosis had AH versus 4 out of 18 without recurrent thrombosis (P = 0.003).

Conclusions:

Recurrent thrombosis in antiphospholipid syndrome (APS) is largely associated with IgG aCL, IgG anti-β2-GPI, IgG anti-β2-GPIDI, IgG aPS/PT, and IgA aCL positivity. AH was a significant risk factor for recurrent thrombosis.

[Names] => Fariza A. Cheldieva ... Tatiana M. Reshetnyak [Doi] => 10.37349/ei.2023.00114 [Published] => October 12, 2023 [Viewed] => 578 [Downloaded] => 24 [Subject] => Original Article [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00114 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 112 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:475–489 [Recommend] => 0 [Keywords] => Antiphospholipid antibodies, antiphospholipid syndrome, thrombosis, thrombosis risk factors [DetailTitle] => Autoantibodies Associated to Thrombosis and Hemostasis [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/112 [Id] => 1003114 [ris] => https://www.explorationpub.com/uploads/Article/A1003114/2712cc436a5158825cb18384480e3a61.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003114/dd74952891650999b84678014f3b36be.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Cheldieva FA, Shumilova AA, Cherkasova MV, Glukhova SI, Lila AM, Nasonov EL, et al. Risk factors and recurrent thrombosis in primary antiphospholipid syndrome. Explor Immunol. 2023;3:475–89. https://doi.org/10.37349/ei.2023.00114 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-10-31 01:21:58 [Bib_Time] => 2023-10-31 01:21:58 [KeysWordContens] => Risk factors and recurrent thrombosis in primary antiphospholipid syndrome, Antiphospholipid antibodies, antiphospholipid syndrome, thrombosis, thrombosis risk factors, Aim: The study aims to evaluate the incidence of recurrent thromboses in patients with primary antiphospholipid syndrome (PAPS) and its association with the presence of different antiphospholipid antibodies (aPLs) and known thrombogenic risk factors. Methods: This retrospective study included 52 patients. The median age of the patients was 38.5 years [31.5; 43.5], and the duration of the disease was 9.0 years [3.1; 13.0]. aPLs, including IgG/IgM/IgA antibodies to cardiolipin (aCLs), IgG/IgM/IgA anti-beta2-glycoprotein I (anti-β2-GPI), IgG anti-domain I-β2-GPI (anti-β2-GPIDI) antibodies, IgG/IgM antibodies to the phosphatidylserine/prothrombin complex (aPS/PT), and other thrombosis risk factors were included for analysis. Results: Recurrent thrombosis was reported in 34 (65%) out of 52 patients and 18 (35%) did not have it. The main reason for the recurrence of thrombosis was the lack of anticoagulant therapy: in 18 (52.9%) out of 34 patients with recurrent thrombosis. Three patients were taking warfarin at the time of thrombosis recurrence, but target international normalized ratio (INR) levels were not achieved. Other patients with recurrent thrombosis were taking direct oral anticoagulants (DOACs). The risk of recurrent thrombotic events with positive IgG aCL was 10.33 (P = 0.002) and 21 (P = 0.007) times higher were examined in enzyme-linked immunoassay (ELISA) and chemiluminescent assay (CLA), respectively. The risk of thrombosis was 4.58 times higher in patients who were IgA aCL-positive (P = 0.01). Compared with other antibodies, with positive IgG values of anti-β2-GPI and IgG aPS/PT by ELISA, a lower probability of thrombosis recurrence was observed: 7.56 and 7.25, respectively. A high risk of recurrent thrombosis [odds ratio (OR) = 32.0] was observed in IgG anti-β2-GPI (CLA). The combination of IgG aCL with IgG anti-β2-GPI and with IgG anti-β2-GPIDI is more informative with respect to the risks of thrombosis recurrence compared to double positivity for aCL with anti-β2-GPI (OR = 20.71 vs. OR = 10.18). Triple positivity for IgG aCL with IgG anti-β2-GPI and with IgG aPS/PT also shows better results compared to positivity for aCL with anti-β2-GPI (OR = 6.06 vs. OR = 5.79). Among other risk factors, arterial hypertension (AH) and obesity were significant in relation to the recurrence of thrombosis. AH occurred in 22 (42%) of 52 patients with PAPS. AH was associated with recurrent thrombosis in PAPS patients: 18 (53%) out of 34 with recurrent thrombosis had AH versus 4 out of 18 without recurrent thrombosis (P = 0.003). Conclusions: Recurrent thrombosis in antiphospholipid syndrome (APS) is largely associated with IgG aCL, IgG anti-β2-GPI, IgG anti-β2-GPIDI, IgG aPS/PT, and IgA aCL positivity. AH was a significant risk factor for recurrent thrombosis. ,Fariza A. Cheldieva ... Tatiana M. Reshetnyak [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 ) [116] => Array ( [ArticleId] => 880 [Create_Time] => 2023-10-27 [zipUrl] => https://www.explorationpub.com/uploads/zip/202311/20231101035252.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003116/1003116.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003116/1003116.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003116/1003116_cover.png [JournalsId] => 5 [Title] => The concept and assessment of immune fitness [Abstract] => [AbstractComplete] => [Names] => Joris C. Verster ... Johan Garssen [Doi] => 10.37349/ei.2023.00116 [Published] => October 27, 2023 [Viewed] => 542 [Downloaded] => 19 [Subject] => Editorial [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00116 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 235 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:500–505 [Recommend] => 0 [Keywords] => [DetailTitle] => Immune Fitness in Health, Disease, and Longevity [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/235 [Id] => 1003116 [ris] => https://www.explorationpub.com/uploads/Article/A1003116/2bc39583fbab60ed94f3c5410fbaff5b.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003116/2fdffe11fd7086762f35979461979bc0.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-25 [CitethisArticle] => Verster JC, Išerić E, Garssen J. The concept and assessment of immune fitness. Explor Immunol. 2023;3:500–5. https://doi.org/10.37349/ei.2023.00116 [Jindex] => 0 [CName] => Joris C.Verster, [CEmail] => j.c.verster@uu.nl, [Ris_Time] => 2023-11-01 03:52:52 [Bib_Time] => 2023-11-01 03:52:52 [KeysWordContens] => The concept and assessment of immune fitness,,,Joris C. Verster ... Johan Garssen [PublishedText] => Published [IsEdit] => 0 [AccountId] => 86 [Zh] => 1 ) [117] => Array ( [ArticleId] => 908 [Create_Time] => 2023-10-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202310/20231030080447.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003117/1003117.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003117/1003117.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003117/1003117_cover.png [JournalsId] => 5 [Title] => Immune-based, multifaceted inactivation of pathogenic T lymphocytes in treating autoimmune diseases [Abstract] => Immunotherapeutic treatment of autoimmune diseases should aim to inactivate autoaggressive memory T-cells and restore immune tolerance. It is envisaged that three approaches could be used to achieve [AbstractComplete] =>

Immunotherapeutic treatment of autoimmune diseases should aim to inactivate autoaggressive memory T-cells and restore immune tolerance. It is envisaged that three approaches could be used to achieve this goal: stimulation of anti-idiotypic immune responses by vaccination with pathogenic T-cells; administration of suboptimal doses of antibodies (Abs) against two or more surface T-cell markers to provide selective Ab-mediated destruction of activated pathogenic memory T-cells; and induction of oral immune tolerance. The proposal entails the use of T-cell vaccination (TCV) or Ab-based therapy as an initial approach to reduce autoantigenic T-cell sensitization. Subsequently, the implementation of oral immunotherapy (OIT) is recommended to reinstate a consistent immune tolerance.

[Names] => Victor Ivanovich Seledtsov ... Alexei A. von Delwig [Doi] => 10.37349/ei.2023.00117 [Published] => October 30, 2023 [Viewed] => 632 [Downloaded] => 27 [Subject] => Perspective [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00117 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 146 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:506–512 [Recommend] => 0 [Keywords] => Autoimmune disease, memory T-cell, T-cell vaccination, therapeutic antibody, oral immunotherapy [DetailTitle] => [DetailUrl] => [Id] => 1003117 [ris] => https://www.explorationpub.com/uploads/Article/A1003117/8274bb09c43dc9f00c91395a990d9576.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003117/56cab52f9c58224855a7f061bccd0d86.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Seledtsov VI, Seledtsova GV, von Delwig AA. Immune-based, multifaceted inactivation of pathogenic T lymphocytes in treating autoimmune diseases. Explor Immunol. 2023;3:506–12. https://doi.org/10.37349/ei.2023.00117 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-10-30 08:04:47 [Bib_Time] => 2023-10-30 08:04:47 [KeysWordContens] => Immune-based, multifaceted inactivation of pathogenic T lymphocytes in treating autoimmune diseases, Autoimmune disease, memory T-cell, T-cell vaccination, therapeutic antibody, oral immunotherapy, Immunotherapeutic treatment of autoimmune diseases should aim to inactivate autoaggressive memory T-cells and restore immune tolerance. It is envisaged that three approaches could be used to achieve this goal: stimulation of anti-idiotypic immune responses by vaccination with pathogenic T-cells; administration of suboptimal doses of antibodies (Abs) against two or more surface T-cell markers to provide selective Ab-mediated destruction of activated pathogenic memory T-cells; and induction of oral immune tolerance. The proposal entails the use of T-cell vaccination (TCV) or Ab-based therapy as an initial approach to reduce autoantigenic T-cell sensitization. Subsequently, the implementation of oral immunotherapy (OIT) is recommended to reinstate a consistent immune tolerance. ,Victor Ivanovich Seledtsov ... Alexei A. von Delwig [PublishedText] => Published [IsEdit] => 0 [AccountId] => 83 [Zh] => 1 ) [118] => Array ( [ArticleId] => 932 [Create_Time] => 2023-11-10 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231227060121.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003118/1003118.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003118/1003118.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003118/1003118_cover.png [JournalsId] => 5 [Title] => Anti-factor H autoantibody-associated hemolytic uremic syndrome in an Argentine pediatric cohort [Abstract] => Aim: To describe the clinical characteristics and frequency of anti-factor H (FH) autoantibody-associated atypical hemolytic uremic syndrome (aHUS) in the first cohort of Argentine patients. [AbstractComplete] =>

Aim:

To describe the clinical characteristics and frequency of anti-factor H (FH) autoantibody-associated atypical hemolytic uremic syndrome (aHUS) in the first cohort of Argentine patients.

Methods:

The presence of anti-FH autoantibodies in 70 pediatric patients with suspected aHUS was investigated between 2013 and 2022. Clinical and laboratory parameters were collected and compared between patients who were positive and negative for anti-FH antibodies.

Results:

The 70 patients screened for anti-FH autoantibodies presented clinical features of non-immune microangiopathic hemolytic anemia, thrombocytopenia and renal injury. Positive titers were found in 14 children [mean: 1,938 arbitrary units per mL (AU/mL), range 179–8,500]. Due to missing clinical data, two patients who tested positive for anti-FH and 20 patients who tested negative for anti-FH were excluded from the data analysis. The laboratory features and clinical manifestations of anti-FH-positive aHUS cases (n = 12) were very similar to those of subjects with no autoantibodies detected (n = 36). Treatment administration was heterogeneous among the 12 patients analyzed. Dialysis was performed in six patients in total. Five children received plasmapheresis, while three patients were treated with plasma exchange followed by administration of eculizumab. Two patients received eculizumab only and one showed significant improvement solely through supportive care. Eight patients in total received immunosuppressive therapy. Follow-up of three patients showed a significant decrease of anti-FH autoantibody titers in 2/3 after treatment and during clinical remission.

Conclusions:

The cohort of 70 pediatric patients in this study demonstrated that the frequency of anti-FH autoantibody-associated aHUS in Argentina is 20%. The implementation of anti-FH testing in the country can potentially contribute to improved treatment and follow-up for patients with autoimmune aHUS.

[Names] => Célia Dos Santos ... Analía Sánchez-Luceros [Doi] => 10.37349/ei.2023.00118 [Published] => November 10, 2023 [Viewed] => 544 [Downloaded] => 23 [Subject] => Original Article [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00118 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 123 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:513–524 [Recommend] => 0 [Keywords] => Atypical hemolytic uremic syndrome, complement, factor H, autoantibody, children [DetailTitle] => The Complement System in Health and Disease [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/123 [Id] => 1003118 [ris] => https://www.explorationpub.com/uploads/Article/A1003118/21ab122c51c7de1eab6489b7960b3b76.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003118/df5b83f777c6a821c30c50bf24d1b0a0.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Dos Santos C, Trinidad J, Castera S, Alconcher L, Coccia PA, Manni FJ, et al. Anti-factor H autoantibody-associated hemolytic uremic syndrome in an Argentine pediatric cohort. Explor Immunol. 2023;3:513–24. https://doi.org/10.37349/ei.2023.00118 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-11-07 03:01:32 [Bib_Time] => 2023-11-07 03:01:32 [KeysWordContens] => Anti-factor H autoantibody-associated hemolytic uremic syndrome in an Argentine pediatric cohort, Atypical hemolytic uremic syndrome, complement, factor H, autoantibody, children, Aim: To describe the clinical characteristics and frequency of anti-factor H (FH) autoantibody-associated atypical hemolytic uremic syndrome (aHUS) in the first cohort of Argentine patients. Methods: The presence of anti-FH autoantibodies in 70 pediatric patients with suspected aHUS was investigated between 2013 and 2022. Clinical and laboratory parameters were collected and compared between patients who were positive and negative for anti-FH antibodies. Results: The 70 patients screened for anti-FH autoantibodies presented clinical features of non-immune microangiopathic hemolytic anemia, thrombocytopenia and renal injury. Positive titers were found in 14 children [mean: 1,938 arbitrary units per mL (AU/mL), range 179–8,500]. Due to missing clinical data, two patients who tested positive for anti-FH and 20 patients who tested negative for anti-FH were excluded from the data analysis. The laboratory features and clinical manifestations of anti-FH-positive aHUS cases (n = 12) were very similar to those of subjects with no autoantibodies detected (n = 36). Treatment administration was heterogeneous among the 12 patients analyzed. Dialysis was performed in six patients in total. Five children received plasmapheresis, while three patients were treated with plasma exchange followed by administration of eculizumab. Two patients received eculizumab only and one showed significant improvement solely through supportive care. Eight patients in total received immunosuppressive therapy. Follow-up of three patients showed a significant decrease of anti-FH autoantibody titers in 2/3 after treatment and during clinical remission. Conclusions: The cohort of 70 pediatric patients in this study demonstrated that the frequency of anti-FH autoantibody-associated aHUS in Argentina is 20%. The implementation of anti-FH testing in the country can potentially contribute to improved treatment and follow-up for patients with autoimmune aHUS. ,Célia Dos Santos ... Analía Sánchez-Luceros [PublishedText] => Published [IsEdit] => 0 [AccountId] => 87 [Zh] => 1 ) [119] => Array ( [ArticleId] => 941 [Create_Time] => 2023-11-22 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231227075235.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003119/1003119.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003119/1003119.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003119/1003119_cover.png [JournalsId] => 5 [Title] => Immunopathogenesis of Orthopoxviridae: insights into immunology from smallpox to monkeypox (mpox) [Abstract] => Since 2019, notable global viral outbreaks have occurred necessitating further research and healthcare system investigations. Following the coronavirus disease 2019 (COVID-19) pandemic, in 2022, whi [AbstractComplete] =>

Since 2019, notable global viral outbreaks have occurred necessitating further research and healthcare system investigations. Following the coronavirus disease 2019 (COVID-19) pandemic, in 2022, whilst severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strains evolved, monkeypox virus (MPXV) infections became more evident. MPXV is of the Orthopoxviridae genus, belonging to the family Poxviridae. Zoonotic transmission (animal-to-human transmission) may occur. The Orthopoxviridae genus includes other orthopoxviruses (OPXVs) present in animal host reservoirs that include cowpox viruses (CPXVs), vaccinia virus (VACV), and variola virus (VARV), with the latter being a causal agent of smallpox and excessive mortality. This review aims to present facts about MPXV-specific pathogenesis, epidemiology, and immunology alongside historical perspectives. MPXV was rarely reported outside Africa before April 2000. Early research since 1796 contributed towards the eradication of VARV leading to immunisation strategies. The World Health Organisation (WHO) announcement that VARV had been eradicated was confirmed in 1980. On the 23rd of July 2022, the WHO announced MPXV as a health emergency. Therefore, concern due to the propagation of MPXV causing monkeypox (mpox) disease requires clarity. Infected hosts display symptoms like extensive cellular-initiated rashes and lesions. Infection with MPXV makes it difficult to differentiate from other diseases or skin conditions. Antiviral therapeutic drugs were typically prescribed for smallpox and mpox disease; however, the molecular and immunological mechanisms with cellular changes remain of interest. Furthermore, no official authorized treatment exists for mpox disease. Some humans across the globe may be considered at risk. Historically, presenting symptoms of mpox resemble other viral diseases. Symptoms include rashes or lesions like Streptococcus, but also human herpes viruses (HHVs), including Varicella zoster virus (VZV).

[Names] => Brent Brown ... Enrique Chacon-Cruz [Doi] => 10.37349/ei.2023.00119 [Published] => November 21, 2023 [Viewed] => 1818 [Downloaded] => 43 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00119 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 63 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:525–553 [Recommend] => 0 [Keywords] => Adaptive, innate, immunology orthopoxvirus, cellular, monkeypox, smallpox [DetailTitle] => Old and New Paradigms in Viral Vaccinology [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/63 [Id] => 1003119 [ris] => https://www.explorationpub.com/uploads/Article/A1003119/f99956a91d7eca17a2a731b8624d6b0d.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003119/84c5adec2d3485a451c2fa9475fc3c1b.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Brown B, Fricke I, Imarogbe C, Padrón González AA, Batista OA, Mensah P, et al. Immunopathogenesis of Orthopoxviridae: insights into immunology from smallpox to monkeypox (mpox). Explor Immunol. 2023;3:525–53. https://doi.org/10.37349/ei.2023.00119 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-11-22 02:49:12 [Bib_Time] => 2023-11-22 02:49:12 [KeysWordContens] => Immunopathogenesis of Orthopoxviridae: insights into immunology from smallpox to monkeypox (mpox), Adaptive, innate, immunology orthopoxvirus, cellular, monkeypox, smallpox, Since 2019, notable global viral outbreaks have occurred necessitating further research and healthcare system investigations. Following the coronavirus disease 2019 (COVID-19) pandemic, in 2022, whilst severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strains evolved, monkeypox virus (MPXV) infections became more evident. MPXV is of the Orthopoxviridae genus, belonging to the family Poxviridae. Zoonotic transmission (animal-to-human transmission) may occur. The Orthopoxviridae genus includes other orthopoxviruses (OPXVs) present in animal host reservoirs that include cowpox viruses (CPXVs), vaccinia virus (VACV), and variola virus (VARV), with the latter being a causal agent of smallpox and excessive mortality. This review aims to present facts about MPXV-specific pathogenesis, epidemiology, and immunology alongside historical perspectives. MPXV was rarely reported outside Africa before April 2000. Early research since 1796 contributed towards the eradication of VARV leading to immunisation strategies. The World Health Organisation (WHO) announcement that VARV had been eradicated was confirmed in 1980. On the 23rd of July 2022, the WHO announced MPXV as a health emergency. Therefore, concern due to the propagation of MPXV causing monkeypox (mpox) disease requires clarity. Infected hosts display symptoms like extensive cellular-initiated rashes and lesions. Infection with MPXV makes it difficult to differentiate from other diseases or skin conditions. Antiviral therapeutic drugs were typically prescribed for smallpox and mpox disease; however, the molecular and immunological mechanisms with cellular changes remain of interest. Furthermore, no official authorized treatment exists for mpox disease. Some humans across the globe may be considered at risk. Historically, presenting symptoms of mpox resemble other viral diseases. Symptoms include rashes or lesions like Streptococcus, but also human herpes viruses (HHVs), including Varicella zoster virus (VZV). ,Brent Brown ... Enrique Chacon-Cruz [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 ) [120] => Array ( [ArticleId] => 967 [Create_Time] => 2023-12-06 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231227081459.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003120/1003120.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003120/1003120.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003120/1003120_cover.png [JournalsId] => 5 [Title] => An update on anti-protein Z antibodies [Abstract] => Protein Z (PZ) is a vitamin K-dependent protein that acts as a cofactor for the inhibition of activated factor X by the PZ-dependent protease inhibitor, an anticoagulant protein of the serpin superf [AbstractComplete] =>

Protein Z (PZ) is a vitamin K-dependent protein that acts as a cofactor for the inhibition of activated factor X by the PZ-dependent protease inhibitor, an anticoagulant protein of the serpin superfamily. The presence of antibodies against PZ (aPZ-Abs) was first described in women with unexplained recurrent embryo loss, pre-eclampsia, or foetal death, independently from habitual antiphospholipid/anti-cofactor antibodies. Other studies suggested that aPZ-Ab could be associated with a small birthweight for the gestational age. The mechanism of action of these antibodies is not yet understood. At this time, even aPZ-Abs are frequently observed in patients with lupus anticoagulant or anticardiolipin antibodies, there is no evidence that aPZ-Abs increase systemic venous or arterial thrombotic risk. The comparison of the various published studies shows that the threshold suggesting an obstetric risk is not clearly defined. At present, it is not known whether one isotype of immunoglobulin (G or M, or both) is particularly involved in certain obstetric manifestations, or these antibodies persist during time, or can be induced by infectious diseases. Consequently, detection of these antibodies is not routinely warranted and should only be performed in randomized clinical trials.

[Names] => Tiffany Pascreau ... Marc Vasse [Doi] => 10.37349/ei.2023.00120 [Published] => December 05, 2023 [Viewed] => 475 [Downloaded] => 14 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00120 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 112 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:554–564 [Recommend] => 0 [Keywords] => Anti-protein Z antibodies, obstetrical complications, antiphospholipids [DetailTitle] => Autoantibodies Associated to Thrombosis and Hemostasis [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/112 [Id] => 1003120 [ris] => https://www.explorationpub.com/uploads/Article/A1003120/d470009b343aebefade61b5c71eb5b4a.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003120/cb9eda5342dc311ccbe6b698f59b5ff0.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Pascreau T, Zia-Chahabi S, Andriamandimbisoa TH, Vasse M. An update on anti-protein Z antibodies. Explor Immunol. 2023;3:554–64. https://doi.org/10.37349/ei.2023.00120 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-11-30 06:11:10 [Bib_Time] => 2023-11-30 06:11:10 [KeysWordContens] => An update on anti-protein Z antibodies, Anti-protein Z antibodies, obstetrical complications, antiphospholipids, Protein Z (PZ) is a vitamin K-dependent protein that acts as a cofactor for the inhibition of activated factor X by the PZ-dependent protease inhibitor, an anticoagulant protein of the serpin superfamily. The presence of antibodies against PZ (aPZ-Abs) was first described in women with unexplained recurrent embryo loss, pre-eclampsia, or foetal death, independently from habitual antiphospholipid/anti-cofactor antibodies. Other studies suggested that aPZ-Ab could be associated with a small birthweight for the gestational age. The mechanism of action of these antibodies is not yet understood. At this time, even aPZ-Abs are frequently observed in patients with lupus anticoagulant or anticardiolipin antibodies, there is no evidence that aPZ-Abs increase systemic venous or arterial thrombotic risk. The comparison of the various published studies shows that the threshold suggesting an obstetric risk is not clearly defined. At present, it is not known whether one isotype of immunoglobulin (G or M, or both) is particularly involved in certain obstetric manifestations, or these antibodies persist during time, or can be induced by infectious diseases. Consequently, detection of these antibodies is not routinely warranted and should only be performed in randomized clinical trials. ,Tiffany Pascreau ... Marc Vasse [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 ) [121] => Array ( [ArticleId] => 968 [Create_Time] => 2023-12-08 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231208064512.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003121/1003121.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003121/1003121.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003121/1003121_cover.png [JournalsId] => 5 [Title] => Treatment of a non-healing oral wound in diabetic-induced rats [Abstract] => Aim: Non-healing wounds are one of the most substantial and difficult problems to treat. Wound healing involves a sequence of complex biological processes, but often the oral cavity microbiota ad [AbstractComplete] =>

Aim:

Non-healing wounds are one of the most substantial and difficult problems to treat. Wound healing involves a sequence of complex biological processes, but often the oral cavity microbiota adversely affects healing and forms a chronic non-healing wound.

Methods:

In this study, a biologically active membrane (BAM) is present, consisting of decellularized human amniotic membrane and bone marrow stem cells (BMSCs). The efficacy of BAM was evaluated in a model of non-healing oral wounds in rats with streptozotocin (STZ)-induced diabetes mellitus.

Results:

Studies have shown that BAM enhanced the healing of chronic oral wounds in animals with induced diabetes mellitus, reduced scarring, and reduced risk of infection. Paracrine freeze-dried BMSCs stimulated angiogenesis and improved wound conditions.

Conclusions:

BMSCs may lower glucose levels in rats with STZ-induced diabetes mellitus and improve the healing process of chronic diseases. However, more studies are needed to study the paracrine factors of BMSCs and their role in the treatment of non-healing wounds.

[Names] => Lia Karalashvili ... Zurab Kakabadze [Doi] => 10.37349/ei.2023.00121 [Published] => December 08, 2023 [Viewed] => 539 [Downloaded] => 9 [Subject] => Original Article [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00121 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 140 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:565–573 [Recommend] => 0 [Keywords] => Chronic non-healing wounds, stem cells, amniotic membrane, oral cavity, diabetes mellitus [DetailTitle] => Immunoregulatory Function of Mesenchymal Stem Cells in Tissue Repair and Regeneration [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/140 [Id] => 1003121 [ris] => https://www.explorationpub.com/uploads/Article/A1003121/4a928f09d13bcc583793680c1a5f970f.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003121/abe16255153aba9bfef806eb3ba48147.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Karalashvili L, Chakhunashvili D, Kakabadze M, Paresishvili T, Kakabadze Z. Treatment of a non-healing oral wound in diabetic-induced rats. Explor Immunol. 2023;3:565–73. https://doi.org/10.37349/ei.2023.00121 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-11-30 06:19:36 [Bib_Time] => 2023-11-30 06:19:36 [KeysWordContens] => Treatment of a non-healing oral wound in diabetic-induced rats, Chronic non-healing wounds, stem cells, amniotic membrane, oral cavity, diabetes mellitus, Aim: Non-healing wounds are one of the most substantial and difficult problems to treat. Wound healing involves a sequence of complex biological processes, but often the oral cavity microbiota adversely affects healing and forms a chronic non-healing wound. Methods: In this study, a biologically active membrane (BAM) is present, consisting of decellularized human amniotic membrane and bone marrow stem cells (BMSCs). The efficacy of BAM was evaluated in a model of non-healing oral wounds in rats with streptozotocin (STZ)-induced diabetes mellitus. Results: Studies have shown that BAM enhanced the healing of chronic oral wounds in animals with induced diabetes mellitus, reduced scarring, and reduced risk of infection. Paracrine freeze-dried BMSCs stimulated angiogenesis and improved wound conditions. Conclusions: BMSCs may lower glucose levels in rats with STZ-induced diabetes mellitus and improve the healing process of chronic diseases. However, more studies are needed to study the paracrine factors of BMSCs and their role in the treatment of non-healing wounds. ,Lia Karalashvili ... Zurab Kakabadze [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 ) [122] => Array ( [ArticleId] => 989 [Create_Time] => 2023-12-15 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231228023708.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003122/1003122.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003122/1003122.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003122/1003122_cover.png [JournalsId] => 5 [Title] => The role of complement component C1q in angiogenesis [Abstract] => The complement component C1q plays a role as a pro-angiogenic factor in different contexts, acting in a complement-independent way. For example, this molecule is able to foster the remodeling of the [AbstractComplete] =>

The complement component C1q plays a role as a pro-angiogenic factor in different contexts, acting in a complement-independent way. For example, this molecule is able to foster the remodeling of the spiral arteries for a physiological pregnancy and to promote the wound healing process. It is also involved in angiogenesis after post-stroke ischemia. Furthermore, it has a role in supporting the tumor vessel growth. Given its role in promoting angiogenesis both under physiological and pathological situations, other studies are needed to understand its potential therapeutic implications.

[Names] => Mariagiulia Spazzapan ... Roberta Bulla [Doi] => 10.37349/ei.2023.00122 [Published] => December 14, 2023 [Viewed] => 512 [Downloaded] => 27 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00122 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 123 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:574–589 [Recommend] => 0 [Keywords] => Angiogenesis, C1q, endothelial cells, angiogenic factors [DetailTitle] => The Complement System in Health and Disease [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/123 [Id] => 1003122 [ris] => https://www.explorationpub.com/uploads/Article/A1003122/359da268f79c19547368d0a1cef9839a.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003122/886186abd0ec58be43225246184fe387.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Spazzapan M, Pegoraro S, Agostinis C, Bulla R. The role of complement component C1q in angiogenesis. Explor Immunol. 2023;3:574–89. https://doi.org/10.37349/ei.2023.00122 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-12-27 08:20:20 [Bib_Time] => 2023-12-27 08:20:20 [KeysWordContens] => The role of complement component C1q in angiogenesis, Angiogenesis, C1q, endothelial cells, angiogenic factors, The complement component C1q plays a role as a pro-angiogenic factor in different contexts, acting in a complement-independent way. For example, this molecule is able to foster the remodeling of the spiral arteries for a physiological pregnancy and to promote the wound healing process. It is also involved in angiogenesis after post-stroke ischemia. Furthermore, it has a role in supporting the tumor vessel growth. Given its role in promoting angiogenesis both under physiological and pathological situations, other studies are needed to understand its potential therapeutic implications. ,Mariagiulia Spazzapan ... Roberta Bulla [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 ) [123] => Array ( [ArticleId] => 1002 [Create_Time] => 2023-12-15 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231215020712.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003123/1003123.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003123/1003123.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003123/1003123_cover.png [JournalsId] => 5 [Title] => Ningmitai capsule improves the semen quality of male infertile with chronic prostatitis by antioxidant and anti-inflammatory [Abstract] => Aim: To observe the effects of Ningmitai capsule on semen parameters of infertile patients with chronic prostatitis (CP) and explore the mechanisms. Methods: A total of 43 patients diagnose [AbstractComplete] =>

Aim:

To observe the effects of Ningmitai capsule on semen parameters of infertile patients with chronic prostatitis (CP) and explore the mechanisms.

Methods:

A total of 43 patients diagnosed with CP were included in the study and administered Ningmitai capsules (4 capsules per dose) for a duration of 6 weeks. Subsequently, assessments were conducted on parameters including sperm concentration, forward progressive motility, total motility, oxidative and anti-oxidative indicators, as well as the concentration of interleukin-8 (IL-8) in seminal plasma before and after the treatment period.

Results:

Compared to pre-treatment, forward progressive motility and total motility of the semen increased significantly (37.15% ± 18.77% vs. 45.44% ± 19.08%, P < 0.05 and 42.56% ± 21.22% vs. 51.64% ± 19.48%, P < 0.05). And the expression of superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) increased significantly after treatment as well (11.36 μmol/L ± 3.28 μmol/L vs. 12.79 μmol/L ± 2.87 μmol/L, P < 0.05 and 9.34 U/mL ± 3.22 U/mL vs. 11.21 U/mL ± 4.87 U/mL, P < 0.05). In addition, the expression of malondialdehyde (MDA) and IL-8 decreased significantly after treatment (41.06 μmol/L ± 24.39 μmol/L vs. 32.17 μmol/L ± 15.04 μmol/L, P < 0.05 and 79.69 ng/L ± 26.24 ng/L vs. 61.35 ng/L ± 23.41 ng/L, P < 0.05). No significant difference in sperm concentration and sperm DNA fragmentation index was observed after the treatment (P > 0.05).

Conclusions:

Ningmitai capsule can enhance the antioxidant capacity and down-regulate the expression of cytokines in the semen, thereby improving the semen parameters of infertile patients with CP.

[Names] => Xiaoyu Wu ... Xinzong Zhang [Doi] => 10.37349/ei.2023.00123 [Published] => December 14, 2023 [Viewed] => 605 [Downloaded] => 14 [Subject] => Original Article [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00123 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 87 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:590–597 [Recommend] => 0 [Keywords] => Ningmitai, infertile patients, prostatitis [DetailTitle] => Immunobiology and Inflammation in the Male Reproductive System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/87 [Id] => 1003123 [ris] => https://www.explorationpub.com/uploads/Article/A1003123/c1cdc10bf2cc99cf7051c2796efa4892.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003123/1b3e3ca57e4e2baf78c4f9a160a27237.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Wu X, Ye Z, Li L, Zhang H, Huang X, Chai J, et al. Ningmitai capsule improves the semen quality of male infertile with chronic prostatitis by antioxidant and anti-inflammatory. Explor Immunol. 2023;3:590–7. https://doi.org/10.37349/ei.2023.00123 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-12-15 02:07:12 [Bib_Time] => 2023-12-15 02:07:12 [KeysWordContens] => Ningmitai capsule improves the semen quality of male infertile with chronic prostatitis by antioxidant and anti-inflammatory, Ningmitai, infertile patients, prostatitis, Aim: To observe the effects of Ningmitai capsule on semen parameters of infertile patients with chronic prostatitis (CP) and explore the mechanisms. Methods: A total of 43 patients diagnosed with CP were included in the study and administered Ningmitai capsules (4 capsules per dose) for a duration of 6 weeks. Subsequently, assessments were conducted on parameters including sperm concentration, forward progressive motility, total motility, oxidative and anti-oxidative indicators, as well as the concentration of interleukin-8 (IL-8) in seminal plasma before and after the treatment period. Results: Compared to pre-treatment, forward progressive motility and total motility of the semen increased significantly (37.15% ± 18.77% vs. 45.44% ± 19.08%, P < 0.05 and 42.56% ± 21.22% vs. 51.64% ± 19.48%, P < 0.05). And the expression of superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) increased significantly after treatment as well (11.36 μmol/L ± 3.28 μmol/L vs. 12.79 μmol/L ± 2.87 μmol/L, P < 0.05 and 9.34 U/mL ± 3.22 U/mL vs. 11.21 U/mL ± 4.87 U/mL, P < 0.05). In addition, the expression of malondialdehyde (MDA) and IL-8 decreased significantly after treatment (41.06 μmol/L ± 24.39 μmol/L vs. 32.17 μmol/L ± 15.04 μmol/L, P < 0.05 and 79.69 ng/L ± 26.24 ng/L vs. 61.35 ng/L ± 23.41 ng/L, P < 0.05). No significant difference in sperm concentration and sperm DNA fragmentation index was observed after the treatment (P > 0.05). Conclusions: Ningmitai capsule can enhance the antioxidant capacity and down-regulate the expression of cytokines in the semen, thereby improving the semen parameters of infertile patients with CP. ,Xiaoyu Wu ... Xinzong Zhang [PublishedText] => Published [IsEdit] => 0 [AccountId] => 86 [Zh] => 1 ) [124] => Array ( [ArticleId] => 1022 [Create_Time] => 2023-12-22 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231227073321.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003124/1003124.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003124/1003124.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003124/1003124_cover.png [JournalsId] => 5 [Title] => High percentage of blood-based T-cell receptor gamma V9-JP recombinations associated with amyotrophic lateral sclerosis: extensive retention of the JP KKIK amino acid motif [Abstract] => Exome and RNAseq files prepared from blood samples can be mined for adaptive immune receptor recombinations and thus for the complementarity determining region-3 (CDR3) amino acid (AA) sequences, im [AbstractComplete] =>

Exome and RNAseq files prepared from blood samples can be mined for adaptive immune receptor recombinations and thus for the complementarity determining region-3 (CDR3) amino acid (AA) sequences, important for antigen binding. In this report, the T-cell receptor gamma (TRG) recombinations were mined from amyotrophic lateral sclerosis (ALS) blood sample exome and RNAseq files, mainly inspired by: (i) a high level of gamma-delta T-cells in Parkinson’s disease and (ii) TRG CDR3 AA features associated with a higher Braak stage in Alzheimer’s disease. Results indicated a high percentage of V9-JP recombinations from ALS blood sample genomics files, in comparison to TRG recombinations obtained from a large number of blood and other tissue samples not representing ALS. This result is discussed in the context of potential phospholipid sponging by adaptive immune receptors and potential impacts on membrane rigidity and amyloid development.

[Names] => George Blanck ... Joanna J. Song [Doi] => 10.37349/ei.2023.00124 [Published] => December 22, 2023 [Viewed] => 439 [Downloaded] => 18 [Subject] => Commentary [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00124 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:598–603 [Recommend] => 0 [Keywords] => Amyotrophic lateral sclerosis, T-cell receptor gamma, phospholipids, amyloid development [DetailTitle] => [DetailUrl] => [Id] => 1003124 [ris] => https://www.explorationpub.com/uploads/Article/A1003124/ad79b5644c6718bf8355bee6b5bfcaf2.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003124/f45d0118259e4cc7d3db87b9580131c6.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Blanck G, Huda TI, Cios KJ, Angelakakis G, Song JJ. High percentage of blood-based T-cell receptor gamma V9-JP recombinations associated with amyotrophic lateral sclerosis: extensive retention of the JP KKIK amino acid motif. Explor Immunol. 2023;3:598–603. https://doi.org/10.37349/ei.2023.00124 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-12-21 03:22:33 [Bib_Time] => 2023-12-21 03:22:33 [KeysWordContens] => High percentage of blood-based T-cell receptor gamma V9-JP recombinations associated with amyotrophic lateral sclerosis: extensive retention of the JP KKIK amino acid motif, Amyotrophic lateral sclerosis, T-cell receptor gamma, phospholipids, amyloid development, Exome and RNAseq files prepared from blood samples can be mined for adaptive immune receptor recombinations and thus for the complementarity determining region-3 (CDR3) amino acid (AA) sequences, important for antigen binding. In this report, the T-cell receptor gamma (TRG) recombinations were mined from amyotrophic lateral sclerosis (ALS) blood sample exome and RNAseq files, mainly inspired by: (i) a high level of gamma-delta T-cells in Parkinson’s disease and (ii) TRG CDR3 AA features associated with a higher Braak stage in Alzheimer’s disease. Results indicated a high percentage of V9-JP recombinations from ALS blood sample genomics files, in comparison to TRG recombinations obtained from a large number of blood and other tissue samples not representing ALS. This result is discussed in the context of potential phospholipid sponging by adaptive immune receptors and potential impacts on membrane rigidity and amyloid development. ,George Blanck ... Joanna J. Song [PublishedText] => Published [IsEdit] => 0 [AccountId] => 86 [Zh] => 1 ) [125] => Array ( [ArticleId] => 1054 [Create_Time] => 2023-12-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231227062409.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003125/1003125.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003125/1003125.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003125/1003125_cover.png [JournalsId] => 5 [Title] => Potential therapeutic applications of targeting signal-transducing adaptor protein-2 in autoimmune diseases [Abstract] => Adaptor proteins are involved in various immune responses via the modulation of many signaling pathways. Signal-transducing adaptor protein-2 (STAP-2) is an adaptor protein that contains typical dom [AbstractComplete] =>

Adaptor proteins are involved in various immune responses via the modulation of many signaling pathways. Signal-transducing adaptor protein-2 (STAP-2) is an adaptor protein that contains typical domains such as the pleckstrin homology (PH) domain, Src homology domain, and a proline-rich region from the N-terminal region. In T cells, STAP-2 positively regulates T cell receptor (TCR)-mediated signaling by associating with CD3ζ immunoreceptor tyrosine-based activation motifs (ITAMs) and lymphocyte-specific protein tyrosine kinase (LCK). Therefore, a peptide that inhibits the interaction between STAP-2 and CD3ζ ITAMs is likely to suppress TCR-mediated T cell activation, as well as T cell-mediated diseases. As expected, the peptide successfully inhibited the STAP-2/CD3ζ ITAM interaction and suppressed TCR-mediated signaling, cell proliferation, and interleukin (IL)-2 production in human/murine T cells. Furthermore, this inhibitor suppressed the pathogenesis of experimental autoimmune encephalomyelitis (EAE), which is widely recognized as a mouse model of multiple sclerosis, via the downregulation of T cell activation and infiltration of T helper (Th) 1/Th17 cells. These results suggest a new strategy for the treatment of multiple sclerosis and other immune diseases.

[Names] => Yuto Sasaki ... Tadashi Matsuda [Doi] => 10.37349/ei.2023.00125 [Published] => December 28, 2023 [Viewed] => 586 [Downloaded] => 25 [Subject] => Perspective [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00125 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 136 [TitleAbbr] => Explor Immunol. [Pages] => 2023;3:604–612 [Recommend] => 0 [Keywords] => Signal-transducing adaptor protein, adaptor protein, signal transduction, T cell receptor, immune response, autoimmunity, multiple sclerosis, peptides [DetailTitle] => Chronic Inflammation and Autoimmunity [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/136 [Id] => 1003125 [ris] => https://www.explorationpub.com/uploads/Article/A1003125/59a88c0f79c166678c56347947218320.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003125/3acaaaf25d45f897423bd50376679438.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Sasaki Y, Kawahara S, Sekine Y, Kashiwakura JI, Oritani K, Matsuda T. Potential therapeutic applications of targeting signal-transducing adaptor protein-2 in autoimmune diseases. Explor Immunol. 2023;3:604–12. https://doi.org/10.37349/ei.2023.00125 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-12-27 07:01:33 [Bib_Time] => 2023-12-27 07:01:33 [KeysWordContens] => Potential therapeutic applications of targeting signal-transducing adaptor protein-2 in autoimmune diseases, Signal-transducing adaptor protein, adaptor protein, signal transduction, T cell receptor, immune response, autoimmunity, multiple sclerosis, peptides, Adaptor proteins are involved in various immune responses via the modulation of many signaling pathways. Signal-transducing adaptor protein-2 (STAP-2) is an adaptor protein that contains typical domains such as the pleckstrin homology (PH) domain, Src homology domain, and a proline-rich region from the N-terminal region. In T cells, STAP-2 positively regulates T cell receptor (TCR)-mediated signaling by associating with CD3ζ immunoreceptor tyrosine-based activation motifs (ITAMs) and lymphocyte-specific protein tyrosine kinase (LCK). Therefore, a peptide that inhibits the interaction between STAP-2 and CD3ζ ITAMs is likely to suppress TCR-mediated T cell activation, as well as T cell-mediated diseases. As expected, the peptide successfully inhibited the STAP-2/CD3ζ ITAM interaction and suppressed TCR-mediated signaling, cell proliferation, and interleukin (IL)-2 production in human/murine T cells. Furthermore, this inhibitor suppressed the pathogenesis of experimental autoimmune encephalomyelitis (EAE), which is widely recognized as a mouse model of multiple sclerosis, via the downregulation of T cell activation and infiltration of T helper (Th) 1/Th17 cells. These results suggest a new strategy for the treatment of multiple sclerosis and other immune diseases. ,Yuto Sasaki ... Tadashi Matsuda [PublishedText] => Published [IsEdit] => 0 [AccountId] => 80 [Zh] => 1 ) [126] => Array ( [ArticleId] => 1082 [Create_Time] => 2024-01-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240226032951.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003126/1003126.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003126/1003126.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003126/1003126_cover.png [JournalsId] => 5 [Title] => Paradigm of immune dysregulation in coronavirus disease-2019 infection [Abstract] => The coronavirus disease 2019 (COVID-19) pandemic cost 7–8 million deaths worldwide, creating an unprecedented health and economic crisis. Affecting 700 million people globally, the magnitude of th [AbstractComplete] =>

The coronavirus disease 2019 (COVID-19) pandemic cost 7–8 million deaths worldwide, creating an unprecedented health and economic crisis. Affecting 700 million people globally, the magnitude of this pandemic is far from anything that humanity has encountered in recent times. A detailed investigation revealed that more than the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, the hyperactive immune system mediated injury as the real cause of mortality. Cytokine storm following viral infection leads to the surge of proinflammatory cytokines resulting in acute respiratory distress syndrome (ARDS) and lung injury. Anti-inflammatory intervention with anti-interleukin-6 (anti-IL-6) receptor monoclonal antibodies (mAbs; e.g., sarilumab and tocilizumab) and anti-IL-6 mAbs (i.e., siltuximab) and/or steroid-based approach leads to substantial protection and prevent death thereby implying the role of inflammation in COVID-19. In this review, the authors have summarized the dysregulated immune system in COVID-19 infection, investigating in detail the virus-host immune cross talks and presenting the possibilities of therapeutic intervention.

[Names] => Om Saswat Sahoo ... Subhradip Karmakar [Doi] => 10.37349/ei.2024.00126 [Published] => January 31, 2024 [Viewed] => 493 [Downloaded] => 16 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2024.00126 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 63 [TitleAbbr] => Explor Immunol. [Pages] => 2024;4:1–33 [Recommend] => 0 [Keywords] => Coronavirus disease 2019, SARS-CoV-2, cytokine storm, PANoptosis, inflammation, host response [DetailTitle] => Old and New Paradigms in Viral Vaccinology [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/63 [Id] => 1003126 [ris] => https://www.explorationpub.com/uploads/Article/A1003126/053d0e26dafea78be4a7e6803800b33c.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003126/0a180001dab6d958b8f81e7ca7540ae8.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Sahoo OS, Pethusamy K, Nayek A, Minocha R, Dhar R, Karmakar S. Paradigm of immune dysregulation in coronavirus disease-2019 infection. Explor Immunol. 2024;4:1–33. https://doi.org/10.37349/ei.2024.00126 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-01-22 06:45:16 [Bib_Time] => 2024-01-22 06:45:16 [KeysWordContens] => Paradigm of immune dysregulation in coronavirus disease-2019 infection, Coronavirus disease 2019, SARS-CoV-2, cytokine storm, PANoptosis, inflammation, host response, The coronavirus disease 2019 (COVID-19) pandemic cost 7–8 million deaths worldwide, creating an unprecedented health and economic crisis. Affecting 700 million people globally, the magnitude of this pandemic is far from anything that humanity has encountered in recent times. A detailed investigation revealed that more than the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, the hyperactive immune system mediated injury as the real cause of mortality. Cytokine storm following viral infection leads to the surge of proinflammatory cytokines resulting in acute respiratory distress syndrome (ARDS) and lung injury. Anti-inflammatory intervention with anti-interleukin-6 (anti-IL-6) receptor monoclonal antibodies (mAbs; e.g., sarilumab and tocilizumab) and anti-IL-6 mAbs (i.e., siltuximab) and/or steroid-based approach leads to substantial protection and prevent death thereby implying the role of inflammation in COVID-19. In this review, the authors have summarized the dysregulated immune system in COVID-19 infection, investigating in detail the virus-host immune cross talks and presenting the possibilities of therapeutic intervention. ,Om Saswat Sahoo ... Subhradip Karmakar [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 ) [127] => Array ( [ArticleId] => 1102 [Create_Time] => 2024-02-05 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240223084615.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003127/1003127.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003127/1003127.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003127/1003127_cover.png [JournalsId] => 5 [Title] => Generation and pathogenicity of autoantibodies associated to thrombosis and hemostasis [Abstract] => Many acquired bleeding and thrombotic complications are provoked by autoantibodies to blood coagulation factors, or to hemostasis inhibitors and regulatory proteins. If occurrence of those antibodie [AbstractComplete] =>

Many acquired bleeding and thrombotic complications are provoked by autoantibodies to blood coagulation factors, or to hemostasis inhibitors and regulatory proteins. If occurrence of those antibodies remains rare or ultra-rare, affected patients are not always well-identified and associated pathologies are not always understood. Today, autoantigens tend to be better characterized. New available methods allow investigating structural changes of body components, responsible for auto-immunization. This renders it possible to develop laboratory assays for detecting autoantibodies and estimating their blood concentration. This review analyzes the major autoantibodies reported to be associated with hemorrhagic or thrombotic pathologies and their possible inducing causes when known. Pathogenicity is strongly patient- and context-dependent and is related to autoantibodies’ concentration, avidity, and capacity to bind to autoantigen structures in-vivo, misdirecting the immune system to the own body’s cells or organs. Identification of autoantigens allows for developing laboratory methods for testing autoantibodies and following their evolution kinetics. In-vitro investigations concern functional assays, to evaluate autoantibody’s capacity to inhibit physiological activities, or autoantigen-capture-based assays to detect autoantibodies, like with enzyme-linked immuno-sorbent assay (ELISA) methods. Exploring patients with autoimmune complications remains difficult as few specific assays are available. They mainly concern diseases with the highest incidence, like anti-phospholipid antibodies, lupus anticoagulants, or heparin-dependent antibodies. The present understanding suggests that antibodies to ubiquitous components, like phospholipids or polysaccharides, are actually targeted to proteins with a strong affinity binding to those components: Autoantibodies are not directed to phospholipids, but to phospholipid-binding proteins, and heparin-dependent antibodies are not directed to anticoagulant polysaccharides, but to platelet factor 4. Most pathogenic autoantibodies are of immunoglobulin G (IgG) isotype, but in some cases, IgM or IgA isotypes can be involved. Identification and characterization of autoantibodies associated to hemorrhagic or thrombotic pathologies remains complex at the laboratory level, although they are of high relevance for the right management of concerned patients.

[Names] => Jean Amiral [Doi] => 10.37349/ei.2024.00127 [Published] => February 05, 2024 [Viewed] => 418 [Downloaded] => 21 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2024.00127 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 112 [TitleAbbr] => Explor Immunol. [Pages] => 2024;4:34–58 [Recommend] => 0 [Keywords] => Autoantibodies, thrombosis, bleeding, pathogenicity, autoantigen, immunogenicity, pathogenicity, laboratory methods [DetailTitle] => Autoantibodies Associated to Thrombosis and Hemostasis [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/112 [Id] => 1003127 [ris] => https://www.explorationpub.com/uploads/Article/A1003127/1866a0bedcb16a9d181d455da9278288.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003127/683cd42594addeae1e79388b99ad07ad.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Amiral J. Generation and pathogenicity of autoantibodies associated to thrombosis and hemostasis. Explor Immunol. 2024;4:34–58. https://doi.org/10.37349/ei.2024.00127 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-02-04 04:56:40 [Bib_Time] => 2024-02-04 04:56:40 [KeysWordContens] => Generation and pathogenicity of autoantibodies associated to thrombosis and hemostasis, Autoantibodies, thrombosis, bleeding, pathogenicity, autoantigen, immunogenicity, pathogenicity, laboratory methods, Many acquired bleeding and thrombotic complications are provoked by autoantibodies to blood coagulation factors, or to hemostasis inhibitors and regulatory proteins. If occurrence of those antibodies remains rare or ultra-rare, affected patients are not always well-identified and associated pathologies are not always understood. Today, autoantigens tend to be better characterized. New available methods allow investigating structural changes of body components, responsible for auto-immunization. This renders it possible to develop laboratory assays for detecting autoantibodies and estimating their blood concentration. This review analyzes the major autoantibodies reported to be associated with hemorrhagic or thrombotic pathologies and their possible inducing causes when known. Pathogenicity is strongly patient- and context-dependent and is related to autoantibodies’ concentration, avidity, and capacity to bind to autoantigen structures in-vivo, misdirecting the immune system to the own body’s cells or organs. Identification of autoantigens allows for developing laboratory methods for testing autoantibodies and following their evolution kinetics. In-vitro investigations concern functional assays, to evaluate autoantibody’s capacity to inhibit physiological activities, or autoantigen-capture-based assays to detect autoantibodies, like with enzyme-linked immuno-sorbent assay (ELISA) methods. Exploring patients with autoimmune complications remains difficult as few specific assays are available. They mainly concern diseases with the highest incidence, like anti-phospholipid antibodies, lupus anticoagulants, or heparin-dependent antibodies. The present understanding suggests that antibodies to ubiquitous components, like phospholipids or polysaccharides, are actually targeted to proteins with a strong affinity binding to those components: Autoantibodies are not directed to phospholipids, but to phospholipid-binding proteins, and heparin-dependent antibodies are not directed to anticoagulant polysaccharides, but to platelet factor 4. Most pathogenic autoantibodies are of immunoglobulin G (IgG) isotype, but in some cases, IgM or IgA isotypes can be involved. Identification and characterization of autoantibodies associated to hemorrhagic or thrombotic pathologies remains complex at the laboratory level, although they are of high relevance for the right management of concerned patients. ,Jean Amiral [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 ) [128] => Array ( [ArticleId] => 1106 [Create_Time] => 2024-02-06 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240206084909.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003128/1003128.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003128/1003128.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003128/1003128_cover.png [JournalsId] => 5 [Title] => The mammary gland is intolerant to bacterial intrusion [Abstract] => Mammals depend on the secretion of milk to rear their offspring, which exposes the organ in charge of the function, the mammary gland (MG), to bacterial threat. The essential driving force that cond [AbstractComplete] =>

Mammals depend on the secretion of milk to rear their offspring, which exposes the organ in charge of the function, the mammary gland (MG), to bacterial threat. The essential driving force that conditions the interactions of bacteria with the MG is the abundant secretion of milk, a nutritious fluid which endows the common mastitis-causing pathogens with a doubling time of less than 30 min. From this angle, mammals rely on a potential bacterial bioreactor for the survival of their offspring. The MG is lined with a two-layered epithelium devoid of protective mucus. This means that the mammary epithelium is exposed directly to bacteria once they have passed through the opening lactiferous canal. To cope with the threat, the MG resorts to neutrophilic inflammation to check bacterial proliferation in its lumen and at its epithelial lining. Promptness of neutrophil recruitment is a necessity, which requires a low threshold of activation on the part of the mammary epithelium. Constrained by natural selection, the MG has evolved an innate and adaptive immunity intolerant to bacteria regardless of their level of virulence. The evolutionary issue has been to find a compromise between the deleterious tissue-damaging side effects of inflammation and the maintenance of the secretory function indispensable for the offspring’s survival. It appears that the MG relies mainly on neutrophilic inflammation for its protection and is regulated by type 3 immunity. Advances in knowledge of type 3 immunity in the MG will be necessary to induce immune protection adapted to the physiology of this peculiar organ.

[Names] => Pascal Rainard [Doi] => 10.37349/ei.2024.00128 [Published] => February 06, 2024 [Viewed] => 417 [Downloaded] => 25 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2024.00128 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2024;4:59–72 [Recommend] => 0 [Keywords] => Mammary gland, mastitis, innate immunity, adaptive immunity, neutrophilic inflammation [DetailTitle] => [DetailUrl] => [Id] => 1003128 [ris] => https://www.explorationpub.com/uploads/Article/A1003128/86c460a3bba4024e839d9518795fac54.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003128/39442308c902a6c5a31aed10bb0e9d3e.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Rainard P. The mammary gland is intolerant to bacterial intrusion. Explor Immunol. 2024;4:59–72. https://doi.org/10.37349/ei.2024.00128 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-02-04 08:29:30 [Bib_Time] => 2024-02-04 08:29:30 [KeysWordContens] => The mammary gland is intolerant to bacterial intrusion, Mammary gland, mastitis, innate immunity, adaptive immunity, neutrophilic inflammation, Mammals depend on the secretion of milk to rear their offspring, which exposes the organ in charge of the function, the mammary gland (MG), to bacterial threat. The essential driving force that conditions the interactions of bacteria with the MG is the abundant secretion of milk, a nutritious fluid which endows the common mastitis-causing pathogens with a doubling time of less than 30 min. From this angle, mammals rely on a potential bacterial bioreactor for the survival of their offspring. The MG is lined with a two-layered epithelium devoid of protective mucus. This means that the mammary epithelium is exposed directly to bacteria once they have passed through the opening lactiferous canal. To cope with the threat, the MG resorts to neutrophilic inflammation to check bacterial proliferation in its lumen and at its epithelial lining. Promptness of neutrophil recruitment is a necessity, which requires a low threshold of activation on the part of the mammary epithelium. Constrained by natural selection, the MG has evolved an innate and adaptive immunity intolerant to bacteria regardless of their level of virulence. The evolutionary issue has been to find a compromise between the deleterious tissue-damaging side effects of inflammation and the maintenance of the secretory function indispensable for the offspring’s survival. It appears that the MG relies mainly on neutrophilic inflammation for its protection and is regulated by type 3 immunity. Advances in knowledge of type 3 immunity in the MG will be necessary to induce immune protection adapted to the physiology of this peculiar organ. ,Pascal Rainard [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 ) [129] => Array ( [ArticleId] => 1121 [Create_Time] => 2024-02-23 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240229082234.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003129/1003129.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003129/1003129.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003129/1003129_cover.png [JournalsId] => 5 [Title] => Decoding the impact of autoinflammatory/autoimmune diseases on inner ear harmony and hearing loss [Abstract] => Autoimmune and autoinflammatory diseases affecting the inner ear can cause symptoms such as hearing loss, imbalance, vertigo, and tinnitus, presenting demanding and often underdiagnosed conditions. [AbstractComplete] =>

Autoimmune and autoinflammatory diseases affecting the inner ear can cause symptoms such as hearing loss, imbalance, vertigo, and tinnitus, presenting demanding and often underdiagnosed conditions. Diagnostic challenges arise due to their diverse manifestations, potential long-term consequences, and the absence of specific serological markers, necessitating a multidisciplinary approach combining clinical evaluation, audiological assessments, and imaging techniques. Various autoimmune disorders, including systemic lupus erythematosus, rheumatoid arthritis, and Sjogren’s syndrome, have been implicated in immune-mediated damage to auditory structures, resulting in inner ear dysfunction. Inflammatory processes in autoinflammatory diseases like Cogan’s syndrome and relapsing polychondritis can also affect the inner ear. While the exact mechanisms of inner ear involvement in these conditions are still being studied, immune-mediated inflammation, damage to auditory structures, and vascular involvement play significant roles in auditory impairments. Treatment strategies primarily focus on immunomodulation and inflammation control using corticosteroids, immunosuppressants, and targeted biologic agents to ameliorate symptoms and preserve hearing function. Hearing aids and cochlear implants may be also considered for severe hearing loss. Individualized approaches are necessary due to patient response heterogeneity. This review provides a concise overview of key autoimmune and autoinflammatory diseases impacting the inner ear, highlighting clinical manifestations, diagnostics, pathophysiology, and treatment options. Early recognition and appropriate management are crucial for optimizing patient outcomes. Further research is needed to understand underlying mechanisms and identify novel therapeutic targets. Collaboration between otolaryngologists, rheumatologists, and immunologists is crucial for improving the quality of life in these complex conditions.

[Names] => Michail Athanasopoulos ... Ioannis Athanasopoulos [Doi] => 10.37349/ei.2024.00129 [Published] => February 22, 2024 [Viewed] => 423 [Downloaded] => 15 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2024.00129 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 146 [TitleAbbr] => Explor Immunol. [Pages] => 2024;4:73–89 [Recommend] => 0 [Keywords] => Autoimmune, autoinflammatory, inner ear disease, hearing loss, imbalance, corticosteroids, cochlear implants [DetailTitle] => [DetailUrl] => [Id] => 1003129 [ris] => https://www.explorationpub.com/uploads/Article/A1003129/3b7691cbfcc0b2c5cbe856d24d90ffb3.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003129/810c4300d1f11160be72bc4b443a6ea4.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Athanasopoulos M, Samara P, Athanasopoulos I. Decoding the impact of autoinflammatory/autoimmune diseases on inner ear harmony and hearing loss. Explor Immunol. 2024;4:73–89. https://doi.org/10.37349/ei.2024.00129 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-02-29 08:22:35 [Bib_Time] => 2024-02-29 08:22:35 [KeysWordContens] => Decoding the impact of autoinflammatory/autoimmune diseases on inner ear harmony and hearing loss, Autoimmune, autoinflammatory, inner ear disease, hearing loss, imbalance, corticosteroids, cochlear implants, Autoimmune and autoinflammatory diseases affecting the inner ear can cause symptoms such as hearing loss, imbalance, vertigo, and tinnitus, presenting demanding and often underdiagnosed conditions. Diagnostic challenges arise due to their diverse manifestations, potential long-term consequences, and the absence of specific serological markers, necessitating a multidisciplinary approach combining clinical evaluation, audiological assessments, and imaging techniques. Various autoimmune disorders, including systemic lupus erythematosus, rheumatoid arthritis, and Sjogren’s syndrome, have been implicated in immune-mediated damage to auditory structures, resulting in inner ear dysfunction. Inflammatory processes in autoinflammatory diseases like Cogan’s syndrome and relapsing polychondritis can also affect the inner ear. While the exact mechanisms of inner ear involvement in these conditions are still being studied, immune-mediated inflammation, damage to auditory structures, and vascular involvement play significant roles in auditory impairments. Treatment strategies primarily focus on immunomodulation and inflammation control using corticosteroids, immunosuppressants, and targeted biologic agents to ameliorate symptoms and preserve hearing function. Hearing aids and cochlear implants may be also considered for severe hearing loss. Individualized approaches are necessary due to patient response heterogeneity. This review provides a concise overview of key autoimmune and autoinflammatory diseases impacting the inner ear, highlighting clinical manifestations, diagnostics, pathophysiology, and treatment options. Early recognition and appropriate management are crucial for optimizing patient outcomes. Further research is needed to understand underlying mechanisms and identify novel therapeutic targets. Collaboration between otolaryngologists, rheumatologists, and immunologists is crucial for improving the quality of life in these complex conditions. ,Michail Athanasopoulos ... Ioannis Athanasopoulos [PublishedText] => Published [IsEdit] => 0 [AccountId] => 83 [Zh] => 1 ) [130] => Array ( [ArticleId] => 1127 [Create_Time] => 2024-02-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240228015951.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003130/1003130.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003130/1003130.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003130/1003130_cover.png [JournalsId] => 5 [Title] => Nutritional effects on mucosal integrity and immune function [Abstract] => The intestinal mucosal barrier plays a critical role in maintaining the integrity of the gastrointestinal (GI) tract and protecting the body from harmful toxins and pathogens. Nutrition additionally [AbstractComplete] =>

The intestinal mucosal barrier plays a critical role in maintaining the integrity of the gastrointestinal (GI) tract and protecting the body from harmful toxins and pathogens. Nutrition additionally serves as a vital component in maintaining bodily homeostasis. Macronutrients, micronutrients, and specific dietary habits exert profound effects on the immune system. The complex interactions of the immune system reflect a multifaceted, integrated epithelial and immune cell-mediated regulatory system. While several factors can influence the intestinal mucosal barrier and its pro- and anti-inflammatory processes, such as myeloid cell, regulatory T cell (Treg), or intraepithelial lymphocyte populations, there is growing evidence that macronutrients play an essential role in regulating its function. Herein this is a review of the peer-reviewed literature pertaining to dietary effects on mucosal integrity, including intraepithelial lymphocyte populations and immune function. This review is intended to explore the underlying mechanisms by which macronutrients impact and modulate the mucosal immune system.

[Names] => Lindsey B. Cundra ... David A. Johnson [Doi] => 10.37349/ei.2024.00130 [Published] => February 28, 2024 [Viewed] => 398 [Downloaded] => 13 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2024.00130 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 159 [TitleAbbr] => Explor Immunol. [Pages] => 2024;4:90–105 [Recommend] => 0 [Keywords] => Inflammatory bowel disease, diet, microbiota, immunity, intestinal barrier [DetailTitle] => Mucosal Immune Cells - Border Protection or Entrance Gate? [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/159 [Id] => 1003130 [ris] => https://www.explorationpub.com/uploads/Article/A1003130/b204727d22d14e3dd8d93254d637853e.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003130/c179b60e22062a3c4aeb8d175b038d51.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Cundra LB, Vallabhaneni M, Houston K, Saadeh M, Vargas A, D’Souza SM, et al. Nutritional effects on mucosal integrity and immune function. Explor Immunol. 2024;4:90–105. https://doi.org/10.37349/ei.2024.00130 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-02-22 06:44:14 [Bib_Time] => 2024-02-22 06:44:14 [KeysWordContens] => Nutritional effects on mucosal integrity and immune function, Inflammatory bowel disease, diet, microbiota, immunity, intestinal barrier, The intestinal mucosal barrier plays a critical role in maintaining the integrity of the gastrointestinal (GI) tract and protecting the body from harmful toxins and pathogens. Nutrition additionally serves as a vital component in maintaining bodily homeostasis. Macronutrients, micronutrients, and specific dietary habits exert profound effects on the immune system. The complex interactions of the immune system reflect a multifaceted, integrated epithelial and immune cell-mediated regulatory system. While several factors can influence the intestinal mucosal barrier and its pro- and anti-inflammatory processes, such as myeloid cell, regulatory T cell (Treg), or intraepithelial lymphocyte populations, there is growing evidence that macronutrients play an essential role in regulating its function. Herein this is a review of the peer-reviewed literature pertaining to dietary effects on mucosal integrity, including intraepithelial lymphocyte populations and immune function. This review is intended to explore the underlying mechanisms by which macronutrients impact and modulate the mucosal immune system. ,Lindsey B. Cundra ... David A. Johnson [PublishedText] => Published [IsEdit] => 0 [AccountId] => 72 [Zh] => 1 ) [131] => Array ( [ArticleId] => 1145 [Create_Time] => 2024-02-29 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240229090112.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003132/1003132.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003132/1003132.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003132/1003132_cover.png [JournalsId] => 5 [Title] => Myelitis associated with COVID-19: clinical, radiological, and laboratory characteristics [Abstract] => Aim: The current study aimed to describe various types of myelitis associated with a novel coronavirus infection [coronavirus disease 2019 (COVID-19)] as well as to analyze cytokine profiles and cerebrospinal fluid (CSF) parameters in affected patients and to compare them to patients with other immune-mediated disorders—multiple sclerosis (MS), in order to identify possible common pathogenetic pathways and consequently treatment targets. Methods: Clinical, radiological, and laboratory characteristics were studied based on patients’ history. CSF from patients with myelitis associated with COVID-19 (11 patients) was compared with CSF of healthy controls (HC) (7 patients) and patients with MS (37 patients) from the non-COVID era. CSF cytological examination, protein levels and oligoclonal bands (OCBs) evaluation, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus detection and cytokine profiling using Bio-Plex Pro Human Inflammation Panel 1, 37-Plex were performed. [AbstractComplete] =>

Aim:

The current study aimed to describe various types of myelitis associated with a novel coronavirus infection [coronavirus disease 2019 (COVID-19)] as well as to analyze cytokine profiles and cerebrospinal fluid (CSF) parameters in affected patients and to compare them to patients with other immune-mediated disorders—multiple sclerosis (MS), in order to identify possible common pathogenetic pathways and consequently treatment targets.

Methods:

Clinical, radiological, and laboratory characteristics were studied based on patients’ history. CSF from patients with myelitis associated with COVID-19 (11 patients) was compared with CSF of healthy controls (HC) (7 patients) and patients with MS (37 patients) from the non-COVID era. CSF cytological examination, protein levels and oligoclonal bands (OCBs) evaluation, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus detection and cytokine profiling using Bio-Plex Pro Human Inflammation Panel 1, 37-Plex were performed.

Results:

In total 11 patients with different types of myelitis developed up to 3 months after COVID-19 were enrolled in the study. Radiological findings were diverse: short transverse myelitis (lesion of fewer than 3 segments) (n = 6), longitudinal extensive transverse myelitis (LETM) (n = 2), multifocal spinal cord lesions (n = 1), and myelitis involving dorsal and lateral columns (n = 2). The most pronounced response to treatment was observed in patients with partial transverse myelitis and patients with anti-myelin oligodendrocyte glycoprotein (MOG) antibodies (MOG Abs). Multiple comparisons have demonstrated decreased levels of interleukin-10 (IL-10), interferon-α2 (IFN-α2), IFN-β, and thymic stromal lymphopoietin (TSLP), and increased IL-19 and B cell activating factor (BAFF) in patients with COVID-19 myelitis (CM) compared to the MS group. The highest BAFF and a proliferation-inducing ligand (APRIL) concentrations were found in patients with the most profound neurological disability.

Conclusions:

Myelitis associated with COVID-19 is clinically and radiologically heterogeneous. Evaluation of cytokine profiles in patients with myelitis associated with COVID-19 revealed their relative similarity with ones of MS patients, except for a few cytokines. BAFF/APRIL system as well as IL-10 is well-known for the role in the development and progression of autoimmune diseases, however, their links with COVID-19 and effects on the development of immune-mediated central nervous system (CNS) disorders after SARS-CoV-2 remain to be further studied.

[Names] => Aleksandra Kozlova ... Maria Zakharova [Doi] => 10.37349/ei.2024.00132 [Published] => February 29, 2024 [Viewed] => 649 [Downloaded] => 16 [Subject] => Original Article [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2024.00132 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 136 [TitleAbbr] => Explor Immunol. [Pages] => 2024;4:115–128 [Recommend] => 0 [Keywords] => Novel coronavirus infection, cytokine profile, myelitis, immune-mediated diseases, multiple sclerosis [DetailTitle] => Chronic Inflammation and Autoimmunity [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/136 [Id] => 1003132 [ris] => https://www.explorationpub.com/uploads/Article/A1003132/bba77e1b1eb0107c261df65035f354fe.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003132/910fece76c7e240025283aa3fd71eecb.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Kozlova A, Dzharullaeva A, Tukhvatulin A, Zakroyshchikova I, Simaniv T, Askarova L, et al. Myelitis associated with COVID-19: clinical, radiological, and laboratory characteristics. Explor Immunol. 2024;4:115–28. https://doi.org/10.37349/ei.2024.00132 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-02-29 02:59:59 [Bib_Time] => 2024-02-29 02:59:59 [KeysWordContens] => Myelitis associated with COVID-19: clinical, radiological, and laboratory characteristics, Novel coronavirus infection, cytokine profile, myelitis, immune-mediated diseases, multiple sclerosis, Aim: The current study aimed to describe various types of myelitis associated with a novel coronavirus infection [coronavirus disease 2019 (COVID-19)] as well as to analyze cytokine profiles and cerebrospinal fluid (CSF) parameters in affected patients and to compare them to patients with other immune-mediated disorders—multiple sclerosis (MS), in order to identify possible common pathogenetic pathways and consequently treatment targets. Methods: Clinical, radiological, and laboratory characteristics were studied based on patients’ history. CSF from patients with myelitis associated with COVID-19 (11 patients) was compared with CSF of healthy controls (HC) (7 patients) and patients with MS (37 patients) from the non-COVID era. CSF cytological examination, protein levels and oligoclonal bands (OCBs) evaluation, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus detection and cytokine profiling using Bio-Plex Pro Human Inflammation Panel 1, 37-Plex were performed. Results: In total 11 patients with different types of myelitis developed up to 3 months after COVID-19 were enrolled in the study. Radiological findings were diverse: short transverse myelitis (lesion of fewer than 3 segments) (n = 6), longitudinal extensive transverse myelitis (LETM) (n = 2), multifocal spinal cord lesions (n = 1), and myelitis involving dorsal and lateral columns (n = 2). The most pronounced response to treatment was observed in patients with partial transverse myelitis and patients with anti-myelin oligodendrocyte glycoprotein (MOG) antibodies (MOG Abs). Multiple comparisons have demonstrated decreased levels of interleukin-10 (IL-10), interferon-α2 (IFN-α2), IFN-β, and thymic stromal lymphopoietin (TSLP), and increased IL-19 and B cell activating factor (BAFF) in patients with COVID-19 myelitis (CM) compared to the MS group. The highest BAFF and a proliferation-inducing ligand (APRIL) concentrations were found in patients with the most profound neurological disability. Conclusions: Myelitis associated with COVID-19 is clinically and radiologically heterogeneous. Evaluation of cytokine profiles in patients with myelitis associated with COVID-19 revealed their relative similarity with ones of MS patients, except for a few cytokines. BAFF/APRIL system as well as IL-10 is well-known for the role in the development and progression of autoimmune diseases, however, their links with COVID-19 and effects on the development of immune-mediated central nervous system (CNS) disorders after SARS-CoV-2 remain to be further studied. ,Aleksandra Kozlova ... Maria Zakharova [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 ) [132] => Array ( [ArticleId] => 1144 [Create_Time] => 2024-02-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240229021539.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003131/1003131.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003131/1003131.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003131/1003131_cover.png [JournalsId] => 5 [Title] => Immune cell dynamics in male reproductive health: orchestrating immune privilege and inflammatory responses [Abstract] => Epididymitis or epididymo-orchitis is a common urological condition in males characterized by scrotal pain, swelling, and potential urinary symptoms. Although antibiotics can eliminate the causative [AbstractComplete] =>

Epididymitis or epididymo-orchitis is a common urological condition in males characterized by scrotal pain, swelling, and potential urinary symptoms. Although antibiotics can eliminate the causative pathogens, persistent inflammation may compromise spermatogenesis and steroidogenesis. The testis, an immune-privileged organ, possesses a specialized immune microenvironment that shields germ cells (GCs) from autoimmune attacks and orchestrates immune defenses against pathogens. This review focuses on the complex interplay between immune cells, including macrophages, dendritic cells (DCs), mast cells (MCs), and T cell subsets, in the testis. The roles of these immune cells in infection-induced orchitis were deliberated upon, emphasizing their involvement in inflammation and immune tolerance. Furthermore, the implications of testicular fibrosis and its effect on male infertility are discussed, emphasizing the role of MCs in tissue remodeling. The objective of this review is to expand comprehension of male reproductive health and foster the identification of potential therapeutic targets for epididymo-orchitis.

[Names] => Yiming Zhang ... Ming Wang [Doi] => 10.37349/ei.2024.00131 [Published] => February 28, 2024 [Viewed] => 500 [Downloaded] => 11 [Subject] => Mini Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2024.00131 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 87 [TitleAbbr] => Explor Immunol. [Pages] => 2024;4:106–114 [Recommend] => 0 [Keywords] => Orchitis, immune cells, inflammation [DetailTitle] => Immunobiology and Inflammation in the Male Reproductive System [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/87 [Id] => 1003131 [ris] => https://www.explorationpub.com/uploads/Article/A1003131/0ca64b4ceccfa4dfc6d4c621d6c40865.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003131/df91d9b2724568bb46738361af407154.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Zhang Y, Zhu J, Wang M. Immune cell dynamics in male reproductive health: orchestrating immune privilege and inflammatory responses. Explor Immunol. 2024;4:106–14. https://doi.org/10.37349/ei.2024.00131 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-02-23 07:23:19 [Bib_Time] => 2024-02-23 07:23:19 [KeysWordContens] => Immune cell dynamics in male reproductive health: orchestrating immune privilege and inflammatory responses, Orchitis, immune cells, inflammation, Epididymitis or epididymo-orchitis is a common urological condition in males characterized by scrotal pain, swelling, and potential urinary symptoms. Although antibiotics can eliminate the causative pathogens, persistent inflammation may compromise spermatogenesis and steroidogenesis. The testis, an immune-privileged organ, possesses a specialized immune microenvironment that shields germ cells (GCs) from autoimmune attacks and orchestrates immune defenses against pathogens. This review focuses on the complex interplay between immune cells, including macrophages, dendritic cells (DCs), mast cells (MCs), and T cell subsets, in the testis. The roles of these immune cells in infection-induced orchitis were deliberated upon, emphasizing their involvement in inflammation and immune tolerance. Furthermore, the implications of testicular fibrosis and its effect on male infertility are discussed, emphasizing the role of MCs in tissue remodeling. The objective of this review is to expand comprehension of male reproductive health and foster the identification of potential therapeutic targets for epididymo-orchitis. ,Yiming Zhang ... Ming Wang [PublishedText] => Published [IsEdit] => 0 [AccountId] => 72 [Zh] => 1 ) [133] => Array ( [ArticleId] => 1161 [Create_Time] => 2024-02-29 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240423082832.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003133/1003133.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003133/1003133.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003133/1003133_cover.png [JournalsId] => 5 [Title] => Periodontitis and lipopolysaccharides: How far have we understood? [Abstract] => Periodontitis is a ubiquitous chronic inflammatory worldwide disease. The multiplicity of gram-negative microbiomes and their endotoxins, such as lipopolysaccharides (LPS), play a crucial role in it [AbstractComplete] =>

Periodontitis is a ubiquitous chronic inflammatory worldwide disease. The multiplicity of gram-negative microbiomes and their endotoxins, such as lipopolysaccharides (LPS), play a crucial role in its pathogenesis. The detection and consequent effects of LPS occur either via membrane-based cluster of differentiation 14 (CD14)/myeloid differentiation factor 2 (MD2)/Toll-like receptor (TLR)-4 complex activation or through intracellular cytosolic LPS detection that further cascades its effects, resulting in a variety of cell death processes, including apoptosis, pyroptosis, necroptosis, NETosis, and their crosstalk. Irrespective of the detection of LPS, the cellular response is for protecting and resolving the inflammation. However, chronic and exaggerated responses in periodontitis result in the destruction of periodontal structures. This review summarizes the extracellular and cytosolic detection of LPS and its further consequences. Then, it sheds light on methods reported to mitigate the adverse effects of LPS.

[Names] => Spoorthi Ravi Banavar ... Suan Phaik Khoo [Doi] => 10.37349/ei.2024.00133 [Published] => February 29, 2024 [Viewed] => 384 [Downloaded] => 24 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2024.00133 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 140 [TitleAbbr] => Explor Immunol. [Pages] => 2024;4:129–151 [Recommend] => 0 [Keywords] => Periodontitis, lipopolysaccharides, periodontal stem cells [DetailTitle] => Immunoregulatory Function of Mesenchymal Stem Cells in Tissue Repair and Regeneration [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/140 [Id] => 1003133 [ris] => https://www.explorationpub.com/uploads/Article/A1003133/40ea90ba8049c71e85149738db4b5786.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003133/f042172b67112466f81d08a28a6eec69.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Banavar SR, Tan EL, Davamani F, Khoo SP. Periodontitis and lipopolysaccharides: How far have we understood? Explor Immunol. 2024;4:129–51. https://doi.org/10.37349/ei.2024.00133 [Jindex] => 0 [CName] => Spoorthi RaviBanavar, [CEmail] => spoorthiravi@imu.edu.my, [Ris_Time] => 2024-02-27 02:44:34 [Bib_Time] => 2024-02-27 02:44:34 [KeysWordContens] => Periodontitis and lipopolysaccharides: How far have we understood?, Periodontitis, lipopolysaccharides, periodontal stem cells, Periodontitis is a ubiquitous chronic inflammatory worldwide disease. The multiplicity of gram-negative microbiomes and their endotoxins, such as lipopolysaccharides (LPS), play a crucial role in its pathogenesis. The detection and consequent effects of LPS occur either via membrane-based cluster of differentiation 14 (CD14)/myeloid differentiation factor 2 (MD2)/Toll-like receptor (TLR)-4 complex activation or through intracellular cytosolic LPS detection that further cascades its effects, resulting in a variety of cell death processes, including apoptosis, pyroptosis, necroptosis, NETosis, and their crosstalk. Irrespective of the detection of LPS, the cellular response is for protecting and resolving the inflammation. However, chronic and exaggerated responses in periodontitis result in the destruction of periodontal structures. This review summarizes the extracellular and cytosolic detection of LPS and its further consequences. Then, it sheds light on methods reported to mitigate the adverse effects of LPS. ,Spoorthi Ravi Banavar ... Suan Phaik Khoo [PublishedText] => Published [IsEdit] => 0 [AccountId] => 80 [Zh] => 1 ) [134] => Array ( [ArticleId] => 1170 [Create_Time] => 2024-03-06 [zipUrl] => https://www.explorationpub.com/uploads/zip/202403/20240313015136.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003134/1003134.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003134/1003134.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003134/1003134_cover.png [JournalsId] => 5 [Title] => Entrance to the multifaceted world of CD4+ T cell subsets [Abstract] => This review provides a detailed examination of CD4+ T lymphocyte subsets, crucial components of the immune system originating from the thymus. This study explores the distinct roles and mechanisms o [AbstractComplete] =>

This review provides a detailed examination of CD4+ T lymphocyte subsets, crucial components of the immune system originating from the thymus. This study explores the distinct roles and mechanisms of various T helper (Th) cell subsets, including Th1, Th2, Th17, Th22, regulatory T cells (Tregs), Th9, and T follicular helper (Tfh) cells, focusing on their induction by specific cytokines, regulation by transcription factors, and the production of post-induction cytokines. The study traces the historical origins of Th lymphocyte research, emphasizing the unique cytokine profiles and functional implications of each subset in immune regulation and pathology, including autoimmune diseases, allergies, and cancer. Key findings include the delineation of cytokine-mediated induction processes, highlighting factors like interferon-gamma (IFN-γ), interleukin-4 (IL-4), transforming growth factor-beta (TGF-β), and IL-6. The review delves into transcription factors such as T-box transcription factor 21 (T-bet), GATA binding protein 3 (GATA3), and forkhead box P3 (Foxp3), underlying the lineage-specific development of these cells, and discusses the significant roles of post-induction cytokines. The research underscores the clinical relevance of CD4+ T cell subset dysregulation in various diseases, advocating for a nuanced understanding of these subsets for potential therapeutic advancements in immune-related disorders.

[Names] => Murilo Porfírio de Aguiar, Julia Hailer Vieira [Doi] => 10.37349/ei.2024.00134 [Published] => March 05, 2024 [Viewed] => 377 [Downloaded] => 28 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2024.00134 [Inline] => 1 [Type] => 0 [Issue] => [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2024;4:152–168 [Recommend] => 0 [Keywords] => Helper lymphocyte, regulatory lymphocyte, T helper cell, regulatory T cell, CD4+, subsets [DetailTitle] => [DetailUrl] => [Id] => 1003134 [ris] => https://www.explorationpub.com/uploads/Article/A1003134/f4d3199e3540b0ec69634d0e684e21c8.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003134/1df67af4eae07cc67dc27a61105a0262.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Aguiar MPd, Vieira JH. Entrance to the multifaceted world of CD4+ T cell subsets. Explor Immunol. 2024;4:152–68. https://doi.org/10.37349/ei.2024.00134 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-03-01 07:52:42 [Bib_Time] => 2024-03-01 07:52:42 [KeysWordContens] => Entrance to the multifaceted world of CD4+ T cell subsets, Helper lymphocyte, regulatory lymphocyte, T helper cell, regulatory T cell, CD4+, subsets, This review provides a detailed examination of CD4+ T lymphocyte subsets, crucial components of the immune system originating from the thymus. This study explores the distinct roles and mechanisms of various T helper (Th) cell subsets, including Th1, Th2, Th17, Th22, regulatory T cells (Tregs), Th9, and T follicular helper (Tfh) cells, focusing on their induction by specific cytokines, regulation by transcription factors, and the production of post-induction cytokines. The study traces the historical origins of Th lymphocyte research, emphasizing the unique cytokine profiles and functional implications of each subset in immune regulation and pathology, including autoimmune diseases, allergies, and cancer. Key findings include the delineation of cytokine-mediated induction processes, highlighting factors like interferon-gamma (IFN-γ), interleukin-4 (IL-4), transforming growth factor-beta (TGF-β), and IL-6. The review delves into transcription factors such as T-box transcription factor 21 (T-bet), GATA binding protein 3 (GATA3), and forkhead box P3 (Foxp3), underlying the lineage-specific development of these cells, and discusses the significant roles of post-induction cytokines. The research underscores the clinical relevance of CD4+ T cell subset dysregulation in various diseases, advocating for a nuanced understanding of these subsets for potential therapeutic advancements in immune-related disorders. ,Murilo Porfírio de Aguiar, Julia Hailer Vieira [PublishedText] => Published [IsEdit] => 0 [AccountId] => 38 [Zh] => 1 ) [135] => Array ( [ArticleId] => 1196 [Create_Time] => 2024-04-02 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240421062531.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003135/1003135.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003135/1003135.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003135/1003135_cover.png [JournalsId] => 5 [Title] => Cancer stem cell, chromosomal instability, and cancer immunity [Abstract] => Cancer stem cells (CSCs) are a unique population of tumor cells with stem cell-like properties. They are believed to be involved in drug resistance, potential therapy failure, tumor relapse after tr [AbstractComplete] =>

Cancer stem cells (CSCs) are a unique population of tumor cells with stem cell-like properties. They are believed to be involved in drug resistance, potential therapy failure, tumor relapse after treatment, and ultimately reduced overall survival of cancer patients. One of the causal factors that may lead to CSC formation is chromosomal instability (CIN), a dynamic event leading to numerical and structural changes in the chromosomes. The CIN is also proposed to aid the maintenance of CSCs, contribute towards their heterogeneity, and facilitate their immune escape. However, the role of CIN in the modulation of the immune system in tumors remains contradictory. Studies have revealed that it can lead to both activation and suppression of the immune system. Previous literature suggests that the CIN, CSCs, and cancer immunity (3Cs), interact with and complement each other to create a pro-tumor environment. However, the mechanisms underlying such an interaction are poorly understood. So, in this review article, an attempt has been made to understand the nature of the interaction between the triad of CIN, CSC, and the immune response in tumors and some of the pathways governing the same. Understanding the above may be a positive step towards the complete cure for malignant diseases.

[Names] => Laxmi Kumari ... Alka Bhatia [Doi] => 10.37349/ei.2024.00135 [Published] => April 02, 2024 [Viewed] => 207 [Downloaded] => 11 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2023.00135 [Inline] => 1 [Type] => 0 [Issue] => 0 [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2024;4:169–188 [Recommend] => 0 [Keywords] => Cancer stem cells, chromosomal instability, stem cells, immune system, non-stem cancer cells, extracellular matrix [DetailTitle] => [DetailUrl] => [Id] => 1003135 [ris] => https://www.explorationpub.com/uploads/Article/A1003135/8ee166076b3fcef15e857dc6d302185f.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003135/456165f7651e6187b78fea3ba2109463.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Kumari L, Munjal S, Yadav R, Kumar Y, Bhatia A. Cancer stem cell, chromosomal instability, and cancer immunity. Explor Immunol. 2024;4:169–88. https://doi.org/10.37349/ei.2024.00135 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-04-01 07:22:04 [Bib_Time] => 2024-04-01 07:22:59 [KeysWordContens] => Cancer stem cell, chromosomal instability, and cancer immunity, Cancer stem cells, chromosomal instability, stem cells, immune system, non-stem cancer cells, extracellular matrix, Cancer stem cells (CSCs) are a unique population of tumor cells with stem cell-like properties. They are believed to be involved in drug resistance, potential therapy failure, tumor relapse after treatment, and ultimately reduced overall survival of cancer patients. One of the causal factors that may lead to CSC formation is chromosomal instability (CIN), a dynamic event leading to numerical and structural changes in the chromosomes. The CIN is also proposed to aid the maintenance of CSCs, contribute towards their heterogeneity, and facilitate their immune escape. However, the role of CIN in the modulation of the immune system in tumors remains contradictory. Studies have revealed that it can lead to both activation and suppression of the immune system. Previous literature suggests that the CIN, CSCs, and cancer immunity (3Cs), interact with and complement each other to create a pro-tumor environment. However, the mechanisms underlying such an interaction are poorly understood. So, in this review article, an attempt has been made to understand the nature of the interaction between the triad of CIN, CSC, and the immune response in tumors and some of the pathways governing the same. Understanding the above may be a positive step towards the complete cure for malignant diseases. ,Laxmi Kumari ... Alka Bhatia [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 ) [136] => Array ( [ArticleId] => 1202 [Create_Time] => 2024-04-02 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240418004920.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003136/1003136.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003136/1003136.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003136/1003136_cover.png [JournalsId] => 5 [Title] => Dendritic cell and co-stimulatory molecule targeted therapy for autoimmune diseases: a review of the newly implemented strategies [Abstract] => Dendritic cells (DCs) play an important role in the formation of the immune response, and they are involved in the pathogenesis of autoimmune diseases. Targeting DCs has thus emerged as a new therap [AbstractComplete] =>

Dendritic cells (DCs) play an important role in the formation of the immune response, and they are involved in the pathogenesis of autoimmune diseases. Targeting DCs has thus emerged as a new therapeutic modality in the management of inflammatory and autoimmune diseases. DCs can be manipulated ex vivo and then injected back into humans to suppress the immune response. They can also be manipulated in vivo by delivering specific molecules into the DCs. Co-stimulatory molecules that shape DCs interaction with T cells can also be targeted to suppress immunity. This review tackles the latest advances in each of the 3 presented approaches.

[Names] => Mazen El Jamal, Farah Shibli [Doi] => 10.37349/ei.2024.00136 [Published] => April 02, 2024 [Viewed] => 219 [Downloaded] => 19 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2024.00136 [Inline] => 1 [Type] => 0 [Issue] => 2 [Topic] => 164 [TitleAbbr] => Explor Immunol. [Pages] => 2024;4:189–210 [Recommend] => 0 [Keywords] => Autoimmune diseases, dendritic cells, immune tolerance, co-stimulatory molecules, immunotherapy [DetailTitle] => Immunobiology of Dendritic Cells [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/164 [Id] => 1003136 [ris] => https://www.explorationpub.com/uploads/Article/A1003136/e4db1a19da723e89c18238b15251c439.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003136/d836bc95fef9ad8bbd601dda33836b9c.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Jamal ME, Shibli F. Dendritic cell and co-stimulatory molecule targeted therapy for autoimmune diseases: a review of the newly implemented strategies. Explor Immunol. 2024;4:189–210. https://doi.org/10.37349/ei.2024.00136 [Jindex] => 0 [CName] => Mazen ElJamal, [CEmail] => mazenjamal55@gmail.com, [Ris_Time] => 2024-04-03 01:16:13 [Bib_Time] => 2024-04-18 00:49:20 [KeysWordContens] => Dendritic cell and co-stimulatory molecule targeted therapy for autoimmune diseases: a review of the newly implemented strategies, Autoimmune diseases, dendritic cells, immune tolerance, co-stimulatory molecules, immunotherapy, Dendritic cells (DCs) play an important role in the formation of the immune response, and they are involved in the pathogenesis of autoimmune diseases. Targeting DCs has thus emerged as a new therapeutic modality in the management of inflammatory and autoimmune diseases. DCs can be manipulated ex vivo and then injected back into humans to suppress the immune response. They can also be manipulated in vivo by delivering specific molecules into the DCs. Co-stimulatory molecules that shape DCs interaction with T cells can also be targeted to suppress immunity. This review tackles the latest advances in each of the 3 presented approaches. ,Mazen El Jamal, Farah Shibli [PublishedText] => Published [IsEdit] => 0 [AccountId] => 86 [Zh] => 1 ) [137] => Array ( [ArticleId] => 1246 [Create_Time] => 2024-04-18 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240418005024.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003137/1003137.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003137/1003137.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003137/1003137_cover.png [JournalsId] => 5 [Title] => Physical activity, immune system and hypertension: reflections and challenges for future pandemics based on learning from coronavirus disease 2019 [Abstract] => [AbstractComplete] => [Names] => Francisco Pitanga [Doi] => 10.37349/ei.2024.00137 [Published] => April 17, 2024 [Viewed] => 109 [Downloaded] => 9 [Subject] => Commentary [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2024.00137 [Inline] => 1 [Type] => 0 [Issue] => [Topic] => 182 [TitleAbbr] => Explor Immunol. [Pages] => 2024;4:211–217 [Recommend] => 0 [Keywords] => Physical activity, immune system, hypertension, coronavirus disease 2019, severe acute respiratory syndrome coronavirus 2 [DetailTitle] => Physical Activity and Immune System in Chronic Diseases : Mechanisms and Insights [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/182 [Id] => 1003137 [ris] => https://www.explorationpub.com/uploads/Article/A1003137/1e588d4785e79e8085022354873ae7a1.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003137/6eee521543f8e75a363f64c5e6a8bef3.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Pitanga F. Physical activity, immune system and hypertension: reflections and challenges for future pandemics based on learning from coronavirus disease 2019. Explor Immunol. 2024;4:211–7. https://doi.org/10.37349/ei.2024.00137 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-04-17 07:08:07 [Bib_Time] => 2024-04-18 00:50:24 [KeysWordContens] => Physical activity, immune system and hypertension: reflections and challenges for future pandemics based on learning from coronavirus disease 2019, Physical activity, immune system, hypertension, coronavirus disease 2019, severe acute respiratory syndrome coronavirus 2,,Francisco Pitanga [PublishedText] => Published [IsEdit] => 0 [AccountId] => 86 [Zh] => 0 ) [138] => Array ( [ArticleId] => 1256 [Create_Time] => 2024-04-23 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240423083448.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003138/1003138.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003138/1003138.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003138/1003138_cover.png [JournalsId] => 5 [Title] => Targeted treatments for immune dysregulation in inborn errors of immunity [Abstract] => Primary immune regulatory disorders (PIRDs) constitute a subset of inborn errors of immunity and are characterized by lymphoproliferation, autoimmunity, malignancy, and infection. Unlike classical p [AbstractComplete] =>

Primary immune regulatory disorders (PIRDs) constitute a subset of inborn errors of immunity and are characterized by lymphoproliferation, autoimmunity, malignancy, and infection. Unlike classical primary immune deficiencies, initial symptoms of PIRDs can manifest as autoimmunity such as cytopenias or enteropathy, which can often prove resistant to conventional treatments and occur years prior to the onset of infectious complications. Raising awareness about PIRDs among specialists and adopting a multidisciplinary approach is crucial for early diagnosis, intervention, and potential prevention of severe organ damage. Significant progress has been made in identifying several PIRDs, which has contributed to a more comprehensive comprehension of their underlying immunological mechanisms. This knowledge has paved the way for targeted therapies focusing on specific molecules, which tend to offer superior disease control compared to traditional immunosuppressants. This review, informed by the latest literature, explores prevalent PIRDs, detailing their clinical manifestations and recent advancements in treatment modalities.

[Names] => Nadia Makkoukdji ... Melissa Gans [Doi] => 10.37349/ei.2024.00138 [Published] => April 23, 2024 [Viewed] => 80 [Downloaded] => 9 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2024.00138 [Inline] => 1 [Type] => 0 [Issue] => [Topic] => 0 [TitleAbbr] => Explor Immunol. [Pages] => 2024;4:218–237 [Recommend] => 0 [Keywords] => Primary immune deficiency, targeted therapies, immune dysregulation, inborn errors of immunity [DetailTitle] => [DetailUrl] => [Id] => 1003138 [ris] => https://www.explorationpub.com/uploads/Article/A1003138/a8ece4750c855cc68513b3fce9eacf20.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003138/ef6fb192c655d73f8d18765ef0a828a5.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Makkoukdji N, Pundit V, Wyke M, Giraldo J, Satnarine T, Kleiner GI, et al. Targeted treatments for immune dysregulation in inborn errors of immunity. Explor Immunol. 2024;4:218–37. https://doi.org/10.37349/ei.2024.00138 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-04-22 02:36:28 [Bib_Time] => 2024-04-22 02:36:28 [KeysWordContens] => Targeted treatments for immune dysregulation in inborn errors of immunity, Primary immune deficiency, targeted therapies, immune dysregulation, inborn errors of immunity, Primary immune regulatory disorders (PIRDs) constitute a subset of inborn errors of immunity and are characterized by lymphoproliferation, autoimmunity, malignancy, and infection. Unlike classical primary immune deficiencies, initial symptoms of PIRDs can manifest as autoimmunity such as cytopenias or enteropathy, which can often prove resistant to conventional treatments and occur years prior to the onset of infectious complications. Raising awareness about PIRDs among specialists and adopting a multidisciplinary approach is crucial for early diagnosis, intervention, and potential prevention of severe organ damage. Significant progress has been made in identifying several PIRDs, which has contributed to a more comprehensive comprehension of their underlying immunological mechanisms. This knowledge has paved the way for targeted therapies focusing on specific molecules, which tend to offer superior disease control compared to traditional immunosuppressants. This review, informed by the latest literature, explores prevalent PIRDs, detailing their clinical manifestations and recent advancements in treatment modalities. ,Nadia Makkoukdji ... Melissa Gans [PublishedText] => Published [IsEdit] => 0 [AccountId] => 86 [Zh] => 0 ) [139] => Array ( [ArticleId] => 1259 [Create_Time] => 2024-04-26 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240426031423.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A1003140/1003140.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A1003140/1003140.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A1003140/1003140_cover.png [JournalsId] => 5 [Title] => Exploring the possible link between the spike protein immunoglobulin G4 antibodies and cancer progression [Abstract] => Repeated inoculation with messenger RNA (mRNA) vaccines elicits immunoglobulin G4 (IgG4) antibody production. Such an increase in the concentration of specific and non-specific IgG4 antibodies allow [AbstractComplete] =>

Repeated inoculation with messenger RNA (mRNA) vaccines elicits immunoglobulin G4 (IgG4) antibody production. Such an increase in the concentration of specific and non-specific IgG4 antibodies allows the growth of some types of cancer by blocking the activation of effector immune cells. This work proposes the hypothesis that cancer growth may be indirectly promoted by increased concentrations of non-specific IgG4 antibodies by the following mechanisms: 1) IgG4 antibodies can bind to anti-tumor IgG1 antibodies and block their interaction with receptors located on effector cells, thus preventing the destruction of cancer cells, 2) IgG4 can interact with fragment crystallizable gamma receptor IIb (FcγRIIB) inhibitory receptors, thus reducing effector functions of innate immune cells, and 3) targeting of specific epitopes by IgG4 could be oncogenic by inducing the production of a microenvironment that can promote cancer development. This article reviews the supporting literature and suggests several experimental protocols to evaluate this hypothesis in the context of repeated inoculation with mRNA vaccines. Additionally, this work proposes some management options aimed at reducing the unfavorable molecular consequences that could mediate cancer development when encountering high concentrations of IgG4 antibodies.

[Names] => Mikolaj Raszek ... Alberto Rubio-Casillas [Doi] => 10.37349/ei.2024.00140 [Published] => April 25, 2024 [Viewed] => 10 [Downloaded] => 2 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ei.2024.00140 [Inline] => 1 [Type] => 0 [Issue] => 2 [Topic] => 63 [TitleAbbr] => Explor Immunol. [Pages] => 2024;4:267–284 [Recommend] => 0 [Keywords] => Immunoglobulin G4 antibodies, messenger RNA vaccines, cancer, galectin-3 [DetailTitle] => Old and New Paradigms in Viral Vaccinology [DetailUrl] => https://www.explorationpub.com/Journals/ei/Special_Issues/63 [Id] => 1003140 [ris] => https://www.explorationpub.com/uploads/Article/A1003140/1868ef30ba922546b2f29b732be77e66.ris [bib] => https://www.explorationpub.com/uploads/Article/A1003140/12bdbc172adeb5fc0d28cde4c2223441.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Raszek M, Cowley D, Redwan EM, Uversky VN, Rubio-Casillas A. Exploring the possible link between the spike protein immunoglobulin G4 antibodies and cancer progression. Explor Immunol. 2024;4:267–84. https://doi.org/10.37349/ei.2024.00140 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-04-23 06:25:45 [Bib_Time] => 2024-04-23 06:25:45 [KeysWordContens] => Exploring the possible link between the spike protein immunoglobulin G4 antibodies and cancer progression, Immunoglobulin G4 antibodies, messenger RNA vaccines, cancer, galectin-3, Repeated inoculation with messenger RNA (mRNA) vaccines elicits immunoglobulin G4 (IgG4) antibody production. Such an increase in the concentration of specific and non-specific IgG4 antibodies allows the growth of some types of cancer by blocking the activation of effector immune cells. This work proposes the hypothesis that cancer growth may be indirectly promoted by increased concentrations of non-specific IgG4 antibodies by the following mechanisms: 1) IgG4 antibodies can bind to anti-tumor IgG1 antibodies and block their interaction with receptors located on effector cells, thus preventing the destruction of cancer cells, 2) IgG4 can interact with fragment crystallizable gamma receptor IIb (FcγRIIB) inhibitory receptors, thus reducing effector functions of innate immune cells, and 3) targeting of specific epitopes by IgG4 could be oncogenic by inducing the production of a microenvironment that can promote cancer development. This article reviews the supporting literature and suggests several experimental protocols to evaluate this hypothesis in the context of repeated inoculation with mRNA vaccines. Additionally, this work proposes some management options aimed at reducing the unfavorable molecular consequences that could mediate cancer development when encountering high concentrations of IgG4 antibodies. ,Mikolaj Raszek ... Alberto Rubio-Casillas [PublishedText] => Published [IsEdit] => 0 [AccountId] => 38 [Zh] => 0 ) )