Affiliations: [a] Department of Neurology, Xiangya Hospital, Research Laboratory for Immunology | [b] Hunan Medical University, Changsha, Hunan, China
Correspondence:
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Correspondence and reprint requests to: Dr Jian Zhang, Autoimmunity/Diabetes Group, The John P. Robarts Research Institute, 1400 Western Road, London, Ontario N6G 2V4, Canada.
Abstract: Myasthenia gravis is an autoimmune disease mediated by antibodies to acetylcholine receptors (AChR) of skeletal muscle. The production of anti-AChR antibodies has been shown to be T cell dependent. To elucidate the mechanism(s) of anti-AChR antibody production in myasthenic patients, we studied the effects of regulatory T cells and/or IL-2 on the differentiation of AChR-primed B cells, with use of AChR stimulation for the induction of anti-AChR antibodies in vitro. Our data suggest that CD8+ T cells possess some complicated functions. CD8+ T cells could not only provide help for B cells to secrete anti-AChR antibody, but also possibly inhibit response of CD4+ T cells or kill B cells, then repress anti-AChR antibody production in MG patients. There might be some defect either in the number or function of CD8+ T cell in MG patients. Exogenous IL-2 could completely restore the suppression activity of CD8+ T cells in anti-AChR antibody production in vitro.
Keywords: Myasthenia gravis, anti-A ChR antibody, IL-2, B cell differentiation, T cell subpopulation
