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Abstract
Pemphigus vulgaris (PV) is an autoimmune bullous skin disease where tolerance to the desmosomal protein desmoglein 3 (Dsg3), and perhaps additional epidermal targets, is lost, leading to the production of autoantibodies directed against cellular adhesion molecules. As auto-reactive T cells are involved in the induction and maintenance of antibody production, it has been hypothesized that cytokines play a crucial role in disease pathogenesis. Qualitative and quantitative alterations in cytokine profiles have been previously reported; however, despite recent advancements, the characterization of the disease supporting cytokine network in PV has yet to be fully elucidated. It is overwhelmingly suggested that PV is a TH2-mediated disease, confirmed by the majority of studies demonstrating an increase in TH2-type cytokines. Recently, a focus has been placed on the contribution of the newly discovered TH17 subset to autoimmune states, and current evidence suggests that this inflammatory pathway may play a role in PV as well. Anti-cytokine medications are on the forefront as potential therapeutic options, and the growing number of reports of clinical benefit serves to confirm the major contribution of various inflammatory mediators in the development of disease phenotype. This work aimed to comprehend the complexity of cytokine and T cell involvement in pemphigus, taking account of known information and emphasizing the areas where additional research would be of great benefit, particularly in pharmacological development and expansion of the pemphigus therapeutic armamentarium.
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
