NOD mice and autoimmunity

Christopher A. Aoki, Andrea T. Borchers, William M. Ridgway, Carl L Keen, Aftab A. Ansari, M. Eric Gershwin

Research output: Contribution to journalArticle

68 Scopus citations

Abstract

The NOD mouse has been an important model of type 1 diabetes and autoimmune diseases for over 20 years. Experimental and genetic manipulations of the NOD mouse have demonstrated a broad susceptibility to multiple autoimmune syndromes. This predisposition to autoimmunity is due to defects in both central and peripheral tolerance. The defect of central tolerance is likely secondary to improper negative selection mediated by the unique MHC Class II molecule, I-Ag7 as well as intrinsic T cell signaling defects. The genetic basis for impaired peripheral tolerance is controlled by over 20 susceptibility loci termed insulin-dependent diabetes (idd) loci. The maintenance of peripheral tolerance is impaired by alterations in T cell signaling and apoptosis. In addition, insufficient co-stimulation from accessory cells, and defective regulatory T cells, may promote the production of autoreactive T cells.

Original languageEnglish (US)
Pages (from-to)373-379
Number of pages7
JournalAutoimmunity Reviews
Volume4
Issue number6
DOIs
StatePublished - Jul 2005

Keywords

  • Apoptosis
  • T cell signaling
  • Thymic education
  • Tolerance

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

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    Aoki, C. A., Borchers, A. T., Ridgway, W. M., Keen, C. L., Ansari, A. A., & Gershwin, M. E. (2005). NOD mice and autoimmunity. Autoimmunity Reviews, 4(6), 373-379. https://doi.org/10.1016/j.autrev.2005.02.002