Role of Fyn in the rearrangement of tubulin cytoskeleton induced through TCR
Role of Fyn in the rearrangement of tubulin cytoskeleton induced through TCR
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DOI：
10.4049/jimmunol.176.7.4201
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发表时间：
2006-04-01
影响因子：
4.4
通讯作者：
Sanchez-Madrid, Francisco
中科院分区：
文献类型：
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作者：
Martin-Cofreces, Noa B.;Sancho, David;Sanchez-Madrid, Francisco
微管组织中心（MTOC）、其相关信号复合物和分泌器的移位是最典型的早期事件，涉及T细胞或NK细胞与APC或靶细胞相互作用后的微管细胞骨架。我们的研究结果表明，Fyn激酶活性是必不可少的MTOC重定向在Ag依赖性系统。此外，来自Fyn缺陷小鼠的T细胞不能响应于抗CD 3包被的珠粒而重排其微管蛋白细胞骨架。对来自转基因OT-I小鼠的T细胞与树突状细胞的缀合物的分析揭示，拮抗剂肽诱导MTOC的易位，并且该过程在来自Fyn（-/-）OT-I小鼠的T细胞中受损。此外，Fyn缺陷显着影响MTOC搬迁介导的激动剂肽刺激。这些结果表明Fyn是T细胞中微管蛋白细胞骨架重组的关键调节因子。
The translocation of the microtubule-organizing center (MTOC), its associated signaling complex, and the secretory apparatus is the most characteristic early event that involves the tubulin cytoskeleton of T or NK cells after their interaction with APC or target cells. Our results show that Fyn kinase activity is essential for MTOC reorientation in an Ag-dependent system. Moreover, T cells from Fyn-deficient mice are unable to rearrange their tubulin cytoskeleton in response to anti-CD3-coated beads. Analysis of conjugates of T cells from transgenic OT-I mice with dendritic cells revealed that an antagonist peptide induces translocation of the MTOC, and that this process is impaired in T cells from Fyn(-/-) OT-I mice. In addition, Fyn deficiency significantly affects the MTOC relocation mediated by agonist peptide stimulation. These results reveal Fyn to be a key regulator of tubulin cytoskeleton reorganization in T cells.