We are studying the cellular and molecular basis of autoimmune diseases with two purposes. First, we want to establish the pathogenic role and antigen-specificity of T cells that cause autoimmune diseases such as multiple sclerosis, myasthenia gravis, insulin-dependent diabetes, among others. Second, we would like to determine the feasibility of specific antigen- induced apoptosis as a means of treating such autoimmune diseases. To these ends, we have made progress in the following areas: 1) we have successfully established the marmoset model of experimental allergic encephalomyelitis at the NIH; 2) we found that an important component of the marmoset disease is the formation of a pathogenic antibody against a protein component of the insulating sheath (myelin) of nerves in the central nervous system; 3) we are taking the first steps towards a clinical trial of antigen-induced apoptosis in multiple sclerosis, and 4) we are creating a transgenic mouse model of myasthenia gravis in order to test the efficacy of antigen-induced apoptosis. As part of these studies we are also trying to understand the regulation of antigen-induced death by T cell receptor stimulation. These studies should yield important new insights into the pathogenesis and treatment of autoimmune diseases which is a widespread health problem in the U.S. particularly among working women.
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