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This study will evaluate the pattern of Th17 immune response throughout pemphigus treatment. Skin and serum samples will be taken at the moment of enrollment and at the moment the subject reaches a 75% improvement on disease activity.
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.
Hospital General de Mexico
Instituto Nacional de Ciencias Medicas y Nutricion Salvador Zubiran
Published on BioPortfolio: 2019-09-25T06:13:35-0400
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Separation of the prickle cells of the stratum spinosum of the epidermis, resulting in atrophy of the prickle cell layer. It is seen in diseases such as pemphigus vulgaris (see PEMPHIGUS) and DARIER DISEASE.
A desmosomal cadherin that is an autoantigen in the acquired skin disorder PEMPHIGUS VULGARIS.
An autosomal dominantly inherited skin disorder characterized by recurrent eruptions of vesicles and BULLAE mainly on the neck, axillae, and groin. Mutations in the ATP2C1 gene (encoding the secretory pathway Ca2++/Mn2++ ATPase 1 (SPCA1)) cause this disease. It is clinically and histologically similar to DARIER DISEASE - both have abnormal, unstable DESMOSOMES between KERATINOCYTES and defective CALCIUM-TRANSPORTING ATPASES. It is unrelated to PEMPHIGUS VULGARIS though it closely resembles that disease.
A group of D-related human leukocyte antigens that are polymorphic glycoproteins found on lymphoid cells. They consist of alpha and beta chains and their inheritance differs from that of the DQ and DP antigens; their presence seems to be associated with certain skin diseases like pemphigus vulgaris, dermatitis herpetiformis, and type I diabetes.
A desmosomal cadherin that is an autoantigen in the acquired skin disorder PEMPHIGUS FOLIACEUS.
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