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Fani, Fereshteh, kamali-Sarvestani, Eskandar, Yazdanparast, Razieh, Monabati, Ahmad, Rafiei, Shahnaz. (1385). T-cell Tolerance Following Bacterial Glutamic Acid Decarboxylase (GAD) Feeding in Streptozotocin-induced Diabetes. سامانه مدیریت نشریات علمی, 3(4), 169-175.
Fereshteh Fani; Eskandar kamali-Sarvestani; Razieh Yazdanparast; Ahmad Monabati; Shahnaz Rafiei. "T-cell Tolerance Following Bacterial Glutamic Acid Decarboxylase (GAD) Feeding in Streptozotocin-induced Diabetes". سامانه مدیریت نشریات علمی, 3, 4, 1385, 169-175.
Fani, Fereshteh, kamali-Sarvestani, Eskandar, Yazdanparast, Razieh, Monabati, Ahmad, Rafiei, Shahnaz. (1385). 'T-cell Tolerance Following Bacterial Glutamic Acid Decarboxylase (GAD) Feeding in Streptozotocin-induced Diabetes', سامانه مدیریت نشریات علمی, 3(4), pp. 169-175.
Fani, Fereshteh, kamali-Sarvestani, Eskandar, Yazdanparast, Razieh, Monabati, Ahmad, Rafiei, Shahnaz. T-cell Tolerance Following Bacterial Glutamic Acid Decarboxylase (GAD) Feeding in Streptozotocin-induced Diabetes. سامانه مدیریت نشریات علمی, 1385; 3(4): 169-175.

T-cell Tolerance Following Bacterial Glutamic Acid Decarboxylase (GAD) Feeding in Streptozotocin-induced Diabetes

Iranian Journal of Immunology
مقاله 4، دوره 3، شماره 4 - شماره پیاپی 11، اسفند 2006، صفحه 169-175    اصل مقاله (94.44 K)
نوع مقاله: Original Article
نویسندگان
Fereshteh Fani* 1؛ Eskandar kamali-Sarvestani2، 3؛ Razieh Yazdanparast4؛ Ahmad Monabati5؛ Shahnaz Rafiei1
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
چکیده
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.
کلیدواژه‌ها
Escherichia coli؛ Glutamic Acid Decarboxylase؛ Streptozotocin؛ Oral Tolerance
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