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T细胞/抗原呈递细胞界面肌动蛋白动力学的变化:对T细胞无能的影响?

Changes in actin dynamics at the T-cell/APC interface: implications for T-cell anergy?

作者信息

Sechi Antonio S, Buer Jan, Wehland Jürgen, Probst-Kepper Michael

机构信息

Department of Cell Biology, Gesellschaft für Biotechnologische Forschung, Braunschweig, Germany.

出版信息

Immunol Rev. 2002 Nov;189:98-110. doi: 10.1034/j.1600-065x.2002.18909.x.

Abstract

Over the past 20 years the role of the actin cytoskeleton in the formation of the immunological synapse and in T-cell activation has been the subject of intense scrutiny. T-cell receptor (TCR) signaling leads to tyrosine phosphorylation of numerous adapter proteins whose function is to relay signals to downstream components of the TCR signaling pathway and, in particular, to molecules implicated in remodeling the actin cytoskeleton. Here, we discuss how signals from the TCR converge on two key regulators of the actin cytoskeleton, Ena/vasodilator-stimulated phosphoproteins (VASPs) and the actin-related protein (ARP2/3) complex. We also discuss the implications of TCR signaling in the process of T-cell anergy with particular emphasis on the actin remodeling and molecules involved in the control of T-cell proliferation.

摘要

在过去20年里,肌动蛋白细胞骨架在免疫突触形成和T细胞活化中的作用一直是深入研究的主题。T细胞受体(TCR)信号传导导致众多衔接蛋白的酪氨酸磷酸化,这些衔接蛋白的功能是将信号传递至TCR信号通路的下游成分,特别是传递至与肌动蛋白细胞骨架重塑相关的分子。在此,我们讨论来自TCR的信号如何汇聚于肌动蛋白细胞骨架的两个关键调节因子,即Ena/血管舒张刺激磷蛋白(VASPs)和肌动蛋白相关蛋白(ARP2/3)复合体。我们还讨论了TCR信号传导在T细胞无能过程中的意义,特别强调了肌动蛋白重塑以及参与控制T细胞增殖的分子。

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