T cell costimulation by chemokine receptors
T cell costimulation by chemokine receptors
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DOI：
10.1038/ni1191
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发表时间：
2005-05-01
影响因子：
30.5
通讯作者：
Viola, A
中科院分区：
文献类型：
--
作者：
Molon, B;Gri, G;Viola, A
趋化因子受体介导的信号可能与T细胞受体停止信号竞争，并决定T细胞抗原呈递细胞相互作用的持续时间。本研究表明，在抗原提呈细胞刺激T细胞时，T细胞趋化因子受体偶联G(q)和/或G（11）蛋白通过G(i)不依赖的机制被募集到免疫突触。当趋化因子受体被隔离在免疫突触时，T细胞对趋化梯度变得不敏感，形成更稳定的偶联物，最终以增强增殖和细胞因子产生作出反应。我们认为，趋化因子受体在免疫突触的捕获通过改善T细胞-抗原呈递细胞的吸引力和阻止其他趋化因子来源成功接合的T细胞的“分心”来增强T细胞的激活。
Signals mediated by chemokine receptors may compete with T cell receptor stop signals and determine the duration of T cell antigen-presenting cell interactions. Here we show that during T cell stimulation by antigen-presenting cells, T cell chemokine receptors coupled to G(q) and/or G(11) protein were recruited to the immunological synapse by a G(i)-independent mechanism. When chemokine receptors were sequestered at the immunological synapse, T cells became insensitive to chemotactic gradients, formed more stable conjugates and finally responded with enhanced proliferation and cytokine production. We suggest that chemokine receptor trapping at the immunological synapse enhances T cell activation by improving T cell-antigen-presenting cell attraction and impeding the 'distraction' of successfully engaged T cells by other chemokine sources.