Strategies employed by pathogenic enteric bacteria, such as Shigella, to subvert the host adaptive immunity are not well defined. Impairment of T lymphocyte chemotaxis by blockage of polarised edge formation has been reported upon Shigella infection. However, the functional impact of Shigella on T lymphocytes remains to be determined. Here, we show that Shigella modulates CD4+ T cell F-actin dynamics and increases cell cortical stiffness. The scanning ability of T lymphocytes when encountering antigen-presenting cells (APC) is subsequently impaired resulting in decreased cell-cell contacts (or conjugates) between the two cell types, as compared with non-infected T cells. In addition, the few conjugates established between the invaded T cells and APCs display no polarised delivery and accumulation of the T cell receptor to the contact zone characterising canonical immunological synapses. This is most likely due to the targeting of intracellular vesicular trafficking by the bacterial type III secretion system (T3SS) effectors IpaJ and VirA. The collective impact of these cellular reshapings by Shigella eventually results in T cell activation dampening. Altogether, these results highlight the combined action of T3SS effectors leading to T cell defects upon Shigella infection.

中文翻译：

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志贺氏菌通过劫持肌动蛋白的细胞骨架动力学和T细胞受体水泡运输，削弱了人类T淋巴细胞的反应能力。

致病性肠细菌（例如志贺氏菌）用来破坏宿主适应性免疫的策略尚未明确定义。在志贺氏菌感染后，已经报道了由于极化边缘形成受阻而使T淋巴细胞趋化性受损。然而，志贺氏菌对T淋巴细胞的功能影响尚待确定。在这里，我们显示志贺氏菌可调节CD4 + T细胞F-肌动蛋白的动力学，并增加细胞皮质的硬度。与未感染的T细胞相比，当遇到抗原呈递细胞（APC）时，T淋巴细胞的扫描能力随后受到损害，导致两种细胞类型之间的细胞间接触（或结合物）减少。此外，在入侵的T细胞和APC之间建立的少数结合物没有显示出T细胞受体极化传输和积累到特征性典型免疫突触的接触区。这很可能是由于细菌III型分泌系统（T3SS）效应子IpaJ和VirA靶向了细胞内囊泡运输。志贺氏菌对这些细胞重塑的集体影响最终导致T细胞活化减弱。总之，这些结果突出了志贺氏菌感染后导致T细胞缺陷的T3SS效应子的联合作用。志贺氏菌对这些细胞重塑的共同影响最终导致T细胞活化减弱。总之，这些结果突出了志贺氏菌感染后导致T细胞缺陷的T3SS效应子的联合作用。志贺氏菌对这些细胞重塑的共同影响最终导致T细胞活化减弱。总之，这些结果突出了志贺氏菌感染后导致T细胞缺陷的T3SS效应子的联合作用。