糖基磷脂酰肌醇连接的CD48的参与有助于T细胞受体信号传导和细胞骨架重组：脂筏在T细胞活化中的作用。

Engagement of GPI-linked CD48 contributes to TCR signals and cytoskeletal reorganization: a role for lipid rafts in T cell activation.

作者信息

Moran M, Miceli M C

机构信息

Department of Microbiology, Immunology, and Molecular Genetics, UCLA School of Medicine, Los Angeles, California 90095-1570, USA.

出版信息

Immunity. 1998 Dec;9(6):787-96. doi: 10.1016/s1074-7613(00)80644-5.

DOI:10.1016/s1074-7613(00)80644-5

PMID:9881969

Abstract

GPI-linked proteins coassociate with intracellular tyrosine kinases in "lipid rafts" proposed to function as platforms for signal transduction and cytoskeletal reorganization. TCR activation requires both tyrosine kinase signals and cytoskeletal reorganization. How receptor engagement initiates cytoskeletal changes remains poorly understood. We investigated the consequences of recruiting GPI-linked CD48 and associated rafts to the site of T cell:APC contact by stimulating T cells with APCs that express the CD48 ligand CD2. We demonstrate that CD2:CD48 interactions enhance TCR-mediated functions. CD48/TCR coengagement qualitatively and quantitatively enhances lipid raft-dependent zeta association with the actin cytoskeleton and zeta tyrosine phosphorylation. This implicates lipid rafts as sites where receptor-induced signals and cytoskeletal reorganization are integrated and reveals a novel component of accessory molecule function.

摘要

糖基磷脂酰肌醇（GPI）连接的蛋白质与细胞内酪氨酸激酶在“脂筏”中共同缔合，这些脂筏被认为是信号转导和细胞骨架重组的平台。T细胞受体（TCR）激活既需要酪氨酸激酶信号，也需要细胞骨架重组。受体结合如何引发细胞骨架变化仍知之甚少。我们通过用表达CD48配体CD2的抗原呈递细胞（APC）刺激T细胞，研究了将GPI连接的CD48和相关脂筏募集到T细胞与APC接触位点的后果。我们证明CD2:CD48相互作用增强了TCR介导的功能。CD48/TCR共同结合在定性和定量上增强了脂筏依赖性的ζ链与肌动蛋白细胞骨架的缔合以及ζ链酪氨酸磷酸化。这表明脂筏是整合受体诱导信号和细胞骨架重组的位点，并揭示了辅助分子功能的一个新组分。