Spontaneous diabetes in BB rats: evidence for a T cell dependent immune response defect.
Approximately 50% of BB rats develop insulinopenic hyperglycaemia and ketosis spontaneously in association with insulitis. Amelioration of the syndrome by immunosuppression suggests a cell mediated immune pathogenesis. Analysis of the cell-mediated immune profile of overtly diabetic and normoglycaemic diabetes prone BB rats indicates that they are lymphocytopenic relative to non-diabetes prone BB rats and that the T cell pool is particularly affected. Furthermore, lymphocytes from diabetic and diabetes prone BB rats, while producing normal responses to the T cell mitogen concanavalin A, do not respond when mixed in vitro with major histocompatibility complex incompatible lymphocytes. This anergy is not restored either by enriching the responding cell population for T cells or by adding exogenous T cell growth promoting factor. Thus BB rats have a numerical and regulatory deficit of their T cells which could be related to their propensity for diabetes.
D000818:Animals; D003208:Concanavalin A; D003921:Diabetes Mellitus, Experimental / Q000276:immunology*; D007376:Interleukin-2; D007958:Leukocyte Count; D008213:Lymphocyte Activation; D007959:Lymphocyte Culture Test, Mixed; D008214:Lymphocytes; D051381:Rats; D013601:T-Lymphocytes / Q000276:immunology*
D007376:Interleukin-2; D003208:Concanavalin A