Prospective Analysis of the Th17 Cellular Response in Pemphigus Vulgaris Patients

Summary

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Description

Pemphigus is an autoimmune disease characterized by production of autoantibodies against desmogleins 1 and 3, which are part of the epidermis desmosomes. The first line of treatment are corticosteroids with or without the use of adjuvants (e.g. azathioprine, mycophenolate or rituximab). T lymphocyte...

Pemphigus is an autoimmune disease characterized by production of autoantibodies against desmogleins 1 and 3, which are part of the epidermis desmosomes. The first line of treatment are corticosteroids with or without the use of adjuvants (e.g. azathioprine, mycophenolate or rituximab). T lymphocytes are responsible for the initiation and maturation of the humoral response and the B cell activation required for the production of autoantibodies. In the last decade, the Th17 immune response has been implicated in the pathogenesis of pemphigus. Recently, the existence of tertiary lymphoid organ-like structures within the skin lesions was suggested. This structures contain T lymphocytes, B lymphocytes and plasma cells; these cells interact and create a local microenvironment for the production of autoantibodies. Most of the T cells in this structures are T helper CD4+ and express IL-21, and half of them produce IL-17. In this study the investigators aim to evaluate prospectively the Th17 and T regulatory immune response in the lesional skin and serum of active pemphigus subjects that are treated with corticosteroids with or without adjuvants. The investigators will study skin and serum due to the difference of lymphocytes and cytokines in both tissues. The primary hypothesis is: "the subjects who receive corticosteroids with or without adjuvants and who reach a 75% of improvement (measured by the pemphigus disease area index) in comparison to the enrollment visit will have a decrease in Th17 immune response (IL-23). The investigators will use descriptive statistics, association and correlation test of hypothesis.

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