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    Cytokines and Skin Diseases

    Submission Deadline: November 20, 2022

    Guest Editor

    Dr. Masutaka Furue E-Mail

    Emeritus professor, Kyushu University, Fukuoka, Japan

    Research Keywords: atopic dermatitis, aryl hydrocarbon receptor, antioxidant, melanoma, skin disease, dioxin


    About the Special Issue

    The skin is the outermost organ of body. To maintain the homeostatic stability and sustainability of interface between internal and external atmosphere, the skin is equipped with specialized surface barrier and immune surveillance systems. Like other organs, cytokines are indispensable tools for communication in these skin systems. Recent advancement in skin immunology reveals that dysregulation of skin-associated cytokine-tissue interaction causes various inflammatory skin diseases. One of the clear evidence is psoriasis vs IL-23/IL-17A and TNF-α axes, which is verified by an excellent therapeutic efficacy of biologics against IL-23, IL-17A and TNF-α in psoriasis. Such pathogenic implication is now accumulating in other skin diseases, for example, atopic dermatitis and IL-4/IL-13 axis, pruritus and IL-31 axis, and hidradenitis suppurativa and TNF-α axis. In this special issue, we would like to welcome original and review articles which deal with interaction between cytokines and skin diseases.

    Keywords: cytokines, skin immunology, skin diseases

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    Published Articles

    Open Access
    Review
    Role of tyrosine kinase 2 signals during progression of 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 induce [...] Read more.

    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
    Published: December 27, 2022 Explor Immunol. 2022;2:760–770
    DOI: https://doi.org/10.37349/ei.2022.00081
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    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.

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