Differential ligand binding/trafficking for distinct CTLA-4 fates: is it an expandable mechanism?  

作　　者：Ji Eon Kim Eunmi Kim Jung Weon Lee 

机构地区：[1]Department of Pharmacy,Research Institute of Pharmaceutical Sciences,College of Pharmacy,Seoul National University,Seoul,08826,Republic of Korea

出　　处：《Cellular & Molecular Immunology》2023年第1期1-2,共2页中国免疫学杂志（英文版）

摘　　要：In a recent issue of Nature Immunology,Kennedy et al.reported that CTLA-4(CD152)differentially targets two distinct ligands,CD80 and CD86,on antigen-presenting cells(APCs)for destruction or recycling following transendocytosis(TE),resulting in separate fates for CTLA-4 on T_(reg) cells and thereby regulating autoimmunity.Mechanistically,whereas CTLA-4 tightly binds CD80 for TE and causes ubiquitination and trafficking to late endosomes and lysosomes for degradation,CTLA-4 weakly binds CD86 for TE,resulting in dissociation under acidic conditions(pH<6)and recycling of CTLA-4 to the plasma membrane for further CD86 removal.Therefore,CD86 targeting by CTLA-4 regulates T-cell function in autoimmunity[1]and presumably immune surveillance of cancer cells(Fig.1).

关 键 词：thereby traffic WEAKLY 

分 类 号：R392[医药卫生—免疫学]