1Department of Immunology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran
2Department of Immunology and
3Autoimmune Disease Research Centre, Faculty of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
4Institute of Biochemistry and Biophysics, Tehran University, Tehran, Iran, and
5Department of Pathology, Faculty of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
Background: 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. 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.