Immunology: Insulin auto-antigenicity in type 1 diabetes.
Spontaneous type 1 diabetes occurs when the autoimmune destruction of pancreatic beta-islet cells prevents production of the hormone insulin. This causes an inability to regulate glucose metabolism, which results in dangerously raised blood glucose concentrations. It is generally accepted that thymus-derived lymphocytes (T cells) are critically involved in the onset and progression of type 1 diabetes, but the antigens that initiate and drive this destructive process remain poorly characterized--although several candidates have been considered. Nakayama et al. and Kent et al. claim that insulin itself is the primary autoantigen that initiates spontaneous type 1 diabetes in mice and humans, respectively, a result that could have implications for more effective prevention and therapy. However, I believe that this proposed immunological role of insulin may be undermined by the atypical responses of T cells to the human insulin fragment that are described by Kent et al..
Wilson
Darcy B
DB
Torrey Pines Institute for Molecular Studies, San Diego, California 92121-1122, USA. dbwilson@tpims.org
D000818:Animals; D001324:Autoantigens / Q000737:chemistry / Q000276:immunology*; D015551:Autoimmunity / Q000276:immunology*; D003429:Cross Reactions; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D004195:Disease Models, Animal; D006801:Humans; D007328:Insulin / Q000737:chemistry / Q000276:immunology* / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008198:Lymph Nodes / Q000166:cytology / Q000276:immunology; D051379:Mice; D018448:Models, Immunological; D010446:Peptide Fragments / Q000737:chemistry / Q000276:immunology; D015203:Reproducibility of Results; D013601:T-Lymphocytes / Q000276:immunology*
D001324:Autoantigens; D007328:Insulin; D010446:Peptide Fragments