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Integration of the movement of signaling microclusters with cellular motility in immunological synapses

机译：免疫突触中信号微团运动与细胞运动的整合

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摘要

Immune synapses form between T cells and antigen-presenting cells (APCs). Increasing evidence suggests synapses must form flexibly to accommodate ongoing motility and displacement of the synapse. Here, time-lapse total internal reflection fluorescence (TIRF) microscopy showed that signaling via the T cell antigen receptor (TCR) occurred during synapse translation. TCR microclusters in motile synapses did not flow directly into supramolecular activating complexes (SMACs) but were directed, independently of myosin II contractility, toward an F-actin-poor 'sink' region. Inward microcluster flow often followed collapse of the leading edge, which suggested that actin depolymerization regulated microcluster flow and the formation of SMACs. The coordination of TCR movement with the translocation of this 'sink' shows how T cells coordinate TCR signaling and microcluster flow in dynamic physiological synapses.
机译：免疫突触在T细胞和抗原呈递细胞（APC）之间形成。越来越多的证据表明，突触必须灵活地形成，以适应突触的持续运动和移位。在这里，延时全内反射荧光（TIRF）显微镜显示在突触翻译过程中发生了通过T细胞抗原受体（TCR）发出的信号。运动性突触中的TCR微簇不直接流入超分子激活复合物（SMAC），而是独立于肌球蛋白II的收缩性而指向贫F-肌动蛋白的“沉陷”区域。内向微团流动经常跟随前缘的崩溃，这表明肌动蛋白解聚调节微团流动和SMAC的形成。 TCR运动与该“水槽”易位的协调显示了T细胞如何在动态生理突触中协调TCR信号传导和微簇流动。

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