title: A "hotspot" for autoimmune T cells in type 1 diabetes.
abstract: The ability of a single T cell antigen receptor (TCR) to cross-react with multiple antigens allows the finite number of T cells within an organism to respond to the compendium of pathogen challenges faced during a lifetime. Effective immune surveillance, however, comes at a price. TCR cross-reactivity can allow molecular mimics to spuriously activate autoimmune T cells; it also underlies T cell rejection of organ transplants and drives graft-versus-host disease. In this issue of the JCI, Cole and colleagues provide insight into how an insulin-reactive T cell cross-reacts with pathogen-derived antigens by focusing on a limited portion of the peptides to provide a hotspot for binding. These findings dovetail with recent studies of alloreactive and autoimmune TCRs and suggest that the biochemical principles that govern conventional protein-protein interactions may allow the specificity and cross-reactivity profiles of T cells to be predicted.
authors.forename: Brian D
authors.initials: BD
authors.lastname: Stadinski
authors.forename: Reinhard
authors.initials: R
authors.lastname: Obst
authors.forename: Eric S
authors.initials: ES
authors.lastname: Huseby
mesh_terms: D003922:Diabetes Mellitus, Type 1; D006086:Graft vs Host Disease / Q000276:immunology; D006801:Humans; D010455:Peptides / Q000737:chemistry; D011948:Receptors, Antigen, T-Cell / Q000737:chemistry; D013601:T-Lymphocytes / Q000166:cytology*
chemical_list: D010455:Peptides; D011948:Receptors, Antigen, T-Cell