Failure in immune regulation begets IDDM in NOD mice

Diabetes Metab Rev. 1998 Jun;14(2):177-85. doi: 10.1002/(sici)1099-0895(199806)14:2<177::aid-dmr209>;2-t.


The nonobese diabetic (NOD) mouse model of insulin-dependent diabetes mellitus (IDDM) has provided evidence which suggests that an important mechanism of the induction of this T-cell-mediated autoimmune disease is a failure in immune regulation. The role of T-cell immune dysregulation in the initiation of diabetes is the focus of this review. Immunological mechanisms such as T-cell anergy and deficient T-cell-mediated suppression are discussed as mediators of IDDM susceptibility. In particular, T helper (Th) 2 cell anergy may be responsible for defective regulation of autoreactive effector T-cells. Therapies designed to overcome these T-cell-mediated deficiencies may prevent IDDM onset.

Publication types

  • Review

MeSH terms

  • Animals
  • Autoantigens / immunology
  • Diabetes Mellitus, Type 1 / immunology*
  • Major Histocompatibility Complex / immunology
  • Mice
  • Mice, Inbred NOD / immunology*
  • T-Lymphocytes / immunology
  • Th1 Cells / immunology
  • Th2 Cells / immunology


  • Autoantigens