Coordination of T cell activation and migration through formation of the immunological synapse

被引:34
作者
Dustin, ML
机构
[1] NYU, Sch Med, Skirball Inst Biomol Med, Program Mol Pathogenesis, New York, NY 10016 USA
[2] NYU, Sch Med, Dept Pathol, New York, NY 10016 USA
来源
IMMUNE MECHANISMS AND DISEASE | 2003年 / 987卷
关键词
adhesion; migration; activation; antigen; receptors; kinases; phosphorylation; signaling; EXTRACELLULAR-MATRIX; ANTIGEN PRESENTATION; ACTIN CYTOSKELETON; DOWN-REGULATION; RECEPTOR; LYMPHOCYTES; VAV; REQUIREMENT; RECOGNITION; MOLECULES;
D O I
10.1111/j.1749-6632.2003.tb06032.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
T cell activation is based on interactions of T cell antigen receptors with NMC-peptide complexes in a specialized cell-cell junction between the T cell and antigen-presenting cell-the immunological synapse. The immunological synapse coordinates naive T cell activation and migration by stopping T cell migration with antigen-presenting cells bearing appropriate major histocompatibility complex (MHC) peptide complexes. At the same time, the immunological synapse allows full T cell activation through sustained signaling over a period of several hours. The immunological synapse supports activation in the absence of continued T cell migration, which is required for T cell activation through serial encounters. Src and Syk family kinases are activated early in immunological synapse formation, but this signaling process returns to the basal level after 30 min; at the same time, the interactions between T cell receptors (TCRs) and MHC peptides are stabilized within the immunological synapse. The molecular pattern of the mature synapse in helper T cells is a selfstabilized structure that is correlated with cytokine production and proliferation. I propose that this molecular pattern and its specific biochemical constituents are necessary to amplify signals from the partially desensitized TCR.
引用
收藏
页码:51 / 59
页数:9
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