A dominant insulin-specific and islet-destructive T-cell response is sufficient to activate CD8 T cells directed against the fatty-acid receptor GPR40  

作　　者：Andreas Spyrantis Jana Krieger Katja Stifter Bernhard Otto Boehm Reinhold Schirmbeck 

机构地区：[1]Department of Internal Medicine I,Ulm University Hospital/Albert Einstein Allee 23,89081 Ulm,Germany [2]Lee Kong Chian School of Medicine,Nanyang Technological University,Singapore,Singapore [3]Imperial College London,London,UK

出　　处：《Cellular & Molecular Immunology》2020年第6期659-661,共3页中国免疫学杂志（英文版）

基　　金：supported by a grant from the Deutsche Forschungsgemeinschaft(DFG SCHI-505/6–1)to R.S.B.O.B;supported by Lee Kong Chian School of Medicine,Nanyang Technological University Start Up Grant,MOE AcRF Tier 1(2015-T1-001-258);MOE Tier 1(MOE2015-T1-001-258);MOE Tier 2(MOE2018-T2-1-085);supported by an Ong Tiong Tat professorship.

摘　　要：Type 1 diabetes mellitus(T1D)is an autoimmune disease that is characterized by a progressive infiltration of autoreactive T cells into the pancreatic islets and the destruction of insulin-producing beta cells.1 It is generally assumed that T1D is initiated by yet unidentified T cells that escape from thymic negative selection2 and trigger an initial destruction of beta cells.3 These initial hits could generate suitable conditions in beta cells and/or in islets that favor the coactivation and amplification of autoreactive T cells directed against a broad spectrum of beta cell-specific antigens,such as GAD65,IGRP,and IA-2.

关 键 词：GPR40 ISLET directed 

分 类 号：R392[医药卫生—免疫学]