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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Respiratory syncytial virus impairs T cell activation by preventing synapse assembly with dendritic cells
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Respiratory syncytial virus impairs T cell activation by preventing synapse assembly with dendritic cells

机译：呼吸道合胞病毒通过阻止与树突状细胞的突触装配来损害T细胞活化

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摘要

Respiratory syncytial virus (RSV) infection is one of the leading causes of infant hospitalization and a major health and economic burden worldwide. Infection with this virus induces an exacerbated innate proinflammatory immune response characterized by abundant immune cell infiltration into the airways and lung tissue damage. RSV also impairs the induction of an adequate adaptive T cell immune response, which favors virus pathogenesis. Unfortunately, to date there are no efficient vaccines against this virus. Recent in vitro and in vivo studies suggest that RSV infection can prevent T cell activation, a phenomenon attributed in part to cytokines and chemokines secreted by RSV-infected cells. Efficient immunity against viruses is promoted by dendritic cells (DCs), professional antigen-presenting cells, that prime antigen-specific helper and cytotoxic T cells. Therefore, it would be to the advantage of RSV to impair DC function and prevent the induction of T cell immunity. Here, we show that, although RSV infection induces maturation of murine DCs, these cells are rendered unable to activate antigen-specific T cells. Inhibition of T cell activation by RSV was observed independently of the type of TCR ligand on the DC surface and applied to cognate-, allo-, and superantigen stimulation. As a result of exposure to RSV-infected DCs, T cells became unresponsive to subsequent TCR engagement. RSV-mediated impairment in T cell activation required DC-T cell contact and involved inhibition of immunological synapse assembly among these cells. Our data suggest that impairment of immunological synapse could contribute to RSV pathogenesis by evading adaptive immunity and reducing T cell-mediated virus clearance.
机译：呼吸道合胞病毒（RSV）感染是婴儿住院的主要原因之一，也是全球主要的健康和经济负担。感染这种病毒会导致先天性促炎性免疫反应加剧，其特征是大量免疫细胞浸润到气道和肺组织中。 RSV还损害了适当的适应性T细胞免疫反应的诱导，这有利于病毒的发病机理。不幸的是，迄今为止还没有针对这种病毒的有效疫苗。最近的体外和体内研究表明，RSV感染可以阻止T细胞活化，这种现象部分归因于受RSV感染的细胞分泌的细胞因子和趋化因子。树突状细胞（DC）是一种专业的抗原呈递细胞，可启动针对抗原的辅助细胞和细胞毒性T细胞，从而提高了对病毒的有效免疫力。因此，损害DC功能并防止诱导T细胞免疫将是RSV的优势。在这里，我们显示，尽管RSV感染诱导了鼠DC的成熟，但是这些细胞无法激活抗原特异性T细胞。观察到RSV对T细胞活化的抑制作用与DC表面上TCR配体的类型无关，并应用于同源，同种异体和超抗原刺激。由于暴露于RSV感染的DC，T细胞对随后的TCR结合无反应。 RSV介导的T细胞活化损伤需要DC-T细胞接触，并抑制这些细胞之间的免疫突触组装。我们的数据表明，免疫突触的损害可能通过逃避适应性免疫和减少T细胞介导的病毒清除而促进RSV发病。

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