Numerical and functional abnormaLity of T suppressor cells in diabetic rats.
Insulin-dependent diabetic patients have been reported to have abnormal suppressor T cell function. However, the importance of this abnormality in the etiology of the disease is difficult to evaluate, since the abnormality could be a result of hyperglycemia rather than a predisposing factor. A genetic condition in rats that closely resembles type I (insulin-dependent) diabetes mellitus made it possible to study their suppressor T cell status before they displayed the disease. Thus, monoclonal antibodies and a fluorescence-activated cell sorter were used to define lymphocyte subpopulations in these animals. In prediabetic rats the number of suppressor T cells was reduced strikingly. In vitro assays showed that lymphocytes from predisposed rats were also functionally deficient in regard to suppression. Susceptible rats inoculated with bone marrow cells from normal donors were protected from diabetes. Moreover, the numbers and functions of suppressor T cells in these marrow recipients were almost restored to normal. These observations indicate that a suppressor T cell abnormality is responsible for the hyperglycemia of diabetic rats and raises the possibility that the human disease has a similar etiology.
D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D001854:Bone Marrow Cells; D002452:Cell Count; D003208:Concanavalin A / Q000494:pharmacology; D003920:Diabetes Mellitus / Q000276:immunology* / Q000517:prevention & control; D005455:Fluorescent Antibody Technique; D066298:In Vitro Techniques; D008198:Lymph Nodes / Q000166:cytology; D008213:Lymphocyte Activation; D008934:Mitogens / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000473:pathology
D000911:Antibodies, Monoclonal; D008934:Mitogens; D003208:Concanavalin A