趋化因子受体介导的T细胞共刺激
T cell costimulation by chemokine receptors.
作者信息
Molon Barbara, Gri Giorgia, Bettella Monica, Gómez-Moutón Concepción, Lanzavecchia Antonio, Martínez-A Carlos, Mañes Santos, Viola Antonella
机构信息
Venetian Institute of Molecular Medicine and Department of Biomedical Science, University of Padua, 35100 Padua, Italy.
出版信息
Nat Immunol. 2005 May;6(5):465-71. doi: 10.1038/ni1191. Epub 2005 Apr 10.
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.
趋化因子受体介导的信号可能与T细胞受体终止信号相互竞争,并决定T细胞与抗原呈递细胞相互作用的持续时间。我们在此表明,在抗原呈递细胞刺激T细胞的过程中,与G(q)和/或G(11)蛋白偶联的T细胞趋化因子受体通过一种不依赖G(i)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,形成更稳定的结合物,并最终以增强的增殖和细胞因子产生做出反应。我们认为,免疫突触处趋化因子受体的捕获通过改善T细胞与抗原呈递细胞的相互吸引,并阻止成功结合的T细胞被其他趋化因子来源“分散注意力”,从而增强T细胞活化。