Spontaneous diabetes in BB rats: evidence for a T cell dependent immune response defect

Diabetologia. 1982 Oct;23(4):359-64. doi: 10.1007/BF00253745.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Concanavalin A
  • Diabetes Mellitus, Experimental / immunology*
  • Interleukin-2
  • Leukocyte Count
  • Lymphocyte Activation
  • Lymphocyte Culture Test, Mixed
  • Lymphocytes
  • Rats
  • T-Lymphocytes / immunology*


  • Interleukin-2
  • Concanavalin A