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

作     者：Ji Eon Kim Eunmi Kim Jung Weon Lee 

作者机构：Department of PharmacyResearch Institute of Pharmaceutical SciencesCollege of PharmacySeoul National UniversitySeoul08826Republic of Korea 

出 版 物：《Cellular & Molecular Immunology》 (中国免疫学杂志（英文版）)

年 卷 期：2023年第20卷第1期

页      面：1-2页

核心收录：

学科分类：1001[医学-基础医学(可授医学、理学学位)] 100102[医学-免疫学] 10[医学] 

主　　题：thereby traffic weakly 

摘      要：In a recent issue of Nature Immunology,Kennedy et *** 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 ***,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(pH6)and recycling of CTLA-4 to the plasma membrane for further CD86 ***,CD86 targeting by CTLA-4 regulates T-cell function in autoimmunity[1]and presumably immune surveillance of cancer cells(Fig.1).