title: Insulin as an autoantigen in NOD/human diabetes.
abstract: Although multiple islet autoantigens are recognized by T lymphocytes and autoantibodies before the development of type 1A (immune-mediated diabetes), there is increasing evidence that autoimmunity to insulin may be central to disease pathogenesis. Evidence is strongest for the NOD mouse model where blocking immune responses to insulin prevents diabetes, and insulin peptides can be utilized to induce diabetes. In man insulin gene polymorphisms are associated with disease risk, and autoantibodies and T cells reacting with multiple insulin/proinsulin epitopes are present. It is not currently clear why insulin autoimmunity is so prominent and frequent, and though insulin can be used to immunologically prevent diabetes of NOD mice, insulin-based preventive immunoregulation of diabetes in man is not yet possible.
authors.affiliation: Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Box B140, Building M20, 1775 N. Ursula St., P.O. Box 6511, Aurora, CO 80045-6511, USA. Li.Zhang@uchsc.edu
authors.forename: Li
authors.initials: L
authors.lastname: Zhang
authors.forename: Maki
authors.initials: M
authors.lastname: Nakayama
authors.forename: George S
authors.initials: GS
authors.lastname: Eisenbarth
mesh_terms: D000818:Animals; D001323:Autoantibodies / Q000096:biosynthesis; D001324:Autoantigens / Q000276:immunology*; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology* / Q000517:prevention & control; D006801:Humans; D007328:Insulin / Q000276:immunology*; D051379:Mice; D016688:Mice, Inbred NOD; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D001323:Autoantibodies; D001324:Autoantigens; D007328:Insulin