The effects of T cell subpopulations and recombinant interleukin (IL)-2 on peripheral B cell function in patients with myasthenia gravis

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.