t-cell tolerance following bacterial glutamic acid decarboxylase (gad) feeding in streptozotocin-induced diabetes

background: autoimmune type 1 diabetes mellitus is caused by t-cell mediated immune 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. objective: to determine whether glutamic acid decarboxylase (gad) feeding would induce oral tolerance of   either t-cell or b-cell compartment in streptozotocin (stz) diabetic rats. methods: 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. results: 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. conclusion: gad feeding induces systemic t-cell tolerance in stz-induced diabetes.