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.

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.

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.