title: NOD mice and autoimmunity.
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-A(g7) 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.
authors.affiliation: Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis School of Medicine, Davis, CA 95616, USA.
authors.forename: Christopher A
authors.initials: CA
authors.lastname: Aoki
authors.forename: Andrea T
authors.initials: AT
authors.lastname: Borchers
authors.forename: William M
authors.initials: WM
authors.lastname: Ridgway
authors.forename: Carl L
authors.initials: CL
authors.lastname: Keen
authors.forename: Aftab A
authors.initials: AA
authors.lastname: Ansari
authors.forename: M Eric
authors.initials: ME
authors.lastname: Gershwin
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000235:genetics / Q000276:immunology; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics* / Q000276:immunology* / Q000473:pathology; D020022:Genetic Predisposition to Disease; D051379:Mice; D016688:Mice, Inbred NOD