@article { author = {Fani, Fereshteh and kamali-Sarvestani, Eskandar and Yazdanparast, Razieh and Monabati, Ahmad and Rafiei, Shahnaz}, title = {T-cell Tolerance Following Bacterial Glutamic Acid Decarboxylase (GAD) Feeding in Streptozotocin-induced Diabetes}, journal = {Iranian Journal of Immunology}, volume = {3}, number = {4}, pages = {169-175}, year = {2006}, publisher = {Shiraz Institute for Cancer Research}, issn = {1735-1383}, eissn = {1735-367X}, doi = {}, abstract = {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.}, keywords = {Escherichia coli,Glutamic Acid Decarboxylase,Streptozotocin,Oral Tolerance}, url = {https://iji.sums.ac.ir/article_16999.html}, eprint = {https://iji.sums.ac.ir/article_16999_e5df23476e3a8b4f4c85eacd769c4e34.pdf} }