T Cell Tolerance Following Bacterial Glutamic Acid Decarboxylase (GAD) Feeding in Streptozotocin- Induced Diabetes

Autoimmune type 1 diabetes mellitus is caused by T-cell mediatedimmune destruction of the insulin-producing β-cell in pancreatic islets of Langerhans. Specificity of the auto-antibodies and of the auto-reactive T-cells has been investigated, in which several auto-antigens were proposed. To determinewhether glutamic acid decarboxylase (GAD) feeding would induce oral tolerance of either T-cell or B-cell compartment in streptozotocin (STZ) diabetic rats. Rats in the experimental group were fed 2 mg/kg of GAD (extracted from Escherichia coli) 14 days before intra-peritoneal injections of streptozotocin (30 mg/kg body weight for 5 consecutive days). Two control groups were considered diabetic control group, which underwent STZ injections without receiving GAD, and normal control group. Systemic response was compared between the three groups. T-cells response was assessed by a proliferation assay of spleen cells and those of the B-cells by enzyme-linked immunosorbent assay (ELISA) for anti-GAD specific antibodies in serum. Compared with the diabetic control group, a significant reduction was observed only in the proliferative response of spleen cells, but not in the level of anti-GAD antibody. GAD feeding induces systemic T-cell tolerance in STZ-induced diabetes.