Kuhné Michelle R, Lin Joseph, Yablonski Deborah, Mollenauer Marianne N, Ehrlich Lauren I Richie, Huppa Johannes, Davis Mark M, Weiss Arthur
Department of Medicine, Howard Hughes Medical Institute, Rosalind Russell Center for Medical Research in Arthritis, University of California, San Francisco, CA 94143, USA.
J Immunol. 2003 Jul 15;171(2):860-6. doi: 10.4049/jimmunol.171.2.860.
Engagement of the T cell with Ag on an APC results in a series of immediate signaling events emanating from the stimulation of the TCR. These events include the induced phosphorylation of a number of cellular proteins with a subsequent increase in intracellular calcium and the restructuring of the microtubule and actin cytoskeleton within the T cell. This restructuring of the cytoskeleton culminates in the polarization of the T cell's secretory apparatus toward the engaging APC, allowing the T cell to direct secretion of cytokines toward the appropriate APC. This polarization can be monitored by analyzing the position of the microtubule-organizing center (MTOC), as it moves toward the interface of the T cell and APC. The requirements for MTOC polarization were examined at a single-cell level by studying the interaction of a Jurkat cell line expressing a fluorescently labeled MTOC with Staphylococcal enterotoxin superantigen-bound Raji B cell line, which served as the APC. We found that repolarization of the MTOC substantially followed fluxes in calcium. We also used immobilized anti-TCR mAb and Jurkat signaling mutants, defective in TCR-induced calcium increases, to determine whether signaling components that are necessary for a calcium response also play a role in MTOC polarization. We found that zeta-associated protein-70 as well as its substrate adaptor proteins linker for activation of T cells and Src homology 2 domain-containing leukocyte protein-76 are required for MTOC polarization. Moreover, our studies revealed that a calcium-dependent event not requiring calcineurin or calcium/calmodulin-dependent kinase is required for TCR-induced polarization of the MTOC.
T细胞与抗原呈递细胞(APC)上的抗原结合会引发一系列由T细胞受体(TCR)刺激产生的即时信号事件。这些事件包括多种细胞蛋白的诱导磷酸化,随后细胞内钙增加,以及T细胞内微管和肌动蛋白细胞骨架的重组。细胞骨架的这种重组最终导致T细胞分泌装置向与之结合的APC极化,使T细胞能够将细胞因子分泌导向合适的APC。这种极化可以通过分析微管组织中心(MTOC)的位置来监测,因为它会向T细胞与APC的界面移动。通过研究表达荧光标记MTOC的Jurkat细胞系与作为APC的结合葡萄球菌肠毒素超抗原的Raji B细胞系之间的相互作用,在单细胞水平上研究了MTOC极化的要求。我们发现MTOC的重新极化基本上跟随钙的流动。我们还使用固定化抗TCR单克隆抗体和TCR诱导钙增加有缺陷的Jurkat信号突变体,来确定钙反应所需的信号成分是否也在MTOC极化中起作用。我们发现ζ相关蛋白70及其底物衔接蛋白T细胞活化连接蛋白和含Src同源2结构域的白细胞蛋白76是MTOC极化所必需的。此外,我们的研究表明,TCR诱导的MTOC极化需要一个不依赖钙调神经磷酸酶或钙/钙调蛋白依赖性激酶的钙依赖性事件。