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

BACKGROUND
Autoimmune type 1 diabetes mellitus is caused by the T-cell mediated immune destruction of the insulin-producing beta-cell in pancreatic islets of Langerhans. The specificity of the auto-antibodies and of the auto-reactive T cells has been investigated, in which several auto-antigens were proposed.


OBJECTIVE
The purpose of this study was to determine whether glutamic acid decarboxylase (GAD) feeding would induce oral tolerance of either the T cell or B cell compartment in streptozotocin (STZ) diabetic rats.


METHODS
Experimental rats were fed 2 mg/kg of GAD (extracted from Escherichia coli) 14 days before being given intra-peritoneal injections of streptozotocin (STZ, 30 mg/kg body weight for 5 consecutive days). Of the two control groups, one was the diabetic control, which underwent STZ injections without being given the GAD; and the second was the normal control group. Systemic responses were compared between the three groups. T cell responses were assessed by a proliferation assay of spleen cells, and those of the B cell, by enzyme-linked immunosorbent assay ELISA for anti-GAD specific Abs 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
We concluded that GAD feeding induces systemic T cell tolerance in STZ-induced diabetes.