In the immune synapse, ZAP-70 controls T cell polarization and recruitment of signaling proteins but not formation of the synaptic pattern

被引:107
作者
Blanchard, N
Di Bartolo, V
Hivroz, C
机构
[1] Inst Curie, INSERM, U520, F-75005 Paris, France
[2] Inst Pasteur, Mol Immunol Unit, F-75724 Paris 15, France
基金
澳大利亚研究理事会;
关键词
D O I
10.1016/S1074-7613(02)00421-1
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Recognition by T cells of their ligands at the surface of antigen-presenting cells (APCs) leads to T cell activation, polarization of the T cell toward the APC, and formation of an immune synapse. Using ZAP-70-deficient T cells expressing zeta-GFP, we show that ZAP-70 signaling drives the TCR-dependent reorientation of the microtubule-organizing center thus leading to relocation of a zeta-GFP(+) intracellular compartment close to the APC. ZAP-70 is also necessary to supply the synapse with the signaling molecules PKC-theta and LAT. In contrast, ZAP-70 is not required for clustering of zeta-GFP and CD2 or exclusion of CD45 and CD43 from the synapse. These data show that ZAP-70-dependent signaling is required for formation of a functional immune synapse.
引用
收藏
页码:389 / 399
页数:11
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