title: Molecular Interactions Governing Autoantigen Presentation in Type 1 Diabetes.
abstract: Type 1 diabetes is a chronic autoimmune disease resulting from T cell-mediated destruction of insulin-producing beta cells within pancreatic islets. Disease incidence has increased significantly in the last two decades, especially in young children. Type 1 diabetes is now predictable in humans with the measurement of serum islet autoantibodies directed against insulin and beta cell proteins. Knowledge regarding the presentation of insulin and islet antigens to T cells has increased dramatically over the last several years. Here, we review the trimolecular complex in diabetes, which consists of a major histocompatibility molecule,self-peptide, and T cell receptor, with a focus on insulin peptide presentation to T cells. With this increased understanding of how antigens are presented to T cells comes the hope for improved therapies for type 1 diabetes prevention.
authors.affiliation: Barbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, CO, USA.
authors.forename: Maki
authors.initials: M
authors.lastname: Nakayama
authors.affiliation: Barbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, CO, USA.
authors.forename: Kimberly M
authors.initials: KM
authors.lastname: Simmons
authors.affiliation: Barbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, CO, USA. Aaron.Michels@ucdenver.edu.
authors.forename: Aaron W
authors.initials: AW
authors.lastname: Michels
mesh_terms: D000818:Animals; D001324:Autoantigens / Q000276:immunology*; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D006680:HLA Antigens / Q000276:immunology; D006801:Humans; D007328:Insulin / Q000276:immunology; D011948:Receptors, Antigen, T-Cell / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D001324:Autoantigens; D006680:HLA Antigens; D007328:Insulin; D011948:Receptors, Antigen, T-Cell
keywords: Autoimmunity; Diabetes; HLA; Insulin; T cells