THE IMMUNOLOGICAL STUDY OF GULUTAMIC ACID DECARBOXYLASE SPECIFIC T LYMPHOCYTES IN THE ETIOLOGY OF JUBENILE DIABETES

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Type I diabetes is thought to be an autoimmune disease mediated by T lymphocytes against pancreatic beta cells. Recently, glutamic acid decarboxylase (GAD) was identified as a major autoanitigen of antibody existing in Type 1 diabetes patients. In this study, we focused on the T lymphocytes against GAD in Japanese Type 1 diabetes.Tlymphocytes isolated from peripheral blood were cultured with insulin, rat insulinoma cell (RIN) homogenate, or GAD in 10% AB type human serum contained RPMI medium for 7 days. At 7days, ^3H-Thymidine uptake was measured. T lymphocyte response against GAD in Type 1 diabetes patients was significantly stronger than that in healthy controls. The significant response against insulin was not observed. The response against RIN showed higher tendency in the patients but not significant. The secretion of cytokines in the supernatant during the response against GAD were measured by ELISA.In results, the lymphocytes secreted gamma-interferon but interleukin 4.We tried to make the GAD specific T cell clones but failed at the present time, but succeeded to make the GAD specific T cell lines. The flow cytometry analysis revealed that these cell lines were composed of CD4^+ Tlymphocytes and CD8^+ Tlymphocytes.These results indicated that GAD specific CD4^+ and CD8^+ T lymphocytes exist in the peripheral blood of Type diabetes I patients. The cellular immunity against GAD may play a role in the pathogenesis of Type 1 diabetes.