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首页> 外文期刊>Nature >Toll-like receptor 3 promotes cross-priming to virus-infected cells
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Toll-like receptor 3 promotes cross-priming to virus-infected cells

机译：Toll样受体3促进交叉感染病毒的细胞

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摘要

Cross-presentation of cell-associated antigens plays an important role in regulating CD8(+) T cell responses to proteins that are not expressed by antigen-presenting cells (APCs)(1). Dendritic cells are the principal cross-presenting APCs in vivo and much progress has been made in elucidating the pathways that allow dendritic cells to capture and process cellular material(1). However, little is known about the signals that determine whether such presentation ultimately results in a cytotoxic T cell (CTL) response (cross-priming) or in CD8(+) T cell inactivation (cross-tolerance). Here we describe a mechanism that promotes cross-priming during viral infections. We show that murine CD8alpha(+) dendritic cells are activated by double-stranded (ds)RNA present in virally infected cells but absent from uninfected cells. Dendritic cell activation requires phagocytosis of infected material, followed by signalling through the dsRNA receptor, toll-like receptor 3 (TLR3). Immunization with virus-infected cells or cells containing synthetic dsRNA leads to a striking increase in CTL cross-priming against cell-associated antigens, which is largely dependent on TLR3 expression by antigen-presenting cells. Thus, TLR3 may have evolved to permit cross-priming of CTLs against viruses that do not directly infect dendritic cells.
机译：细胞相关抗原的交叉呈递在调节CD8（+）T细胞对抗原呈递细胞（APC）未表达的蛋白质的反应中起重要作用。树突状细胞是体内主要的交叉呈递APC，在阐明允许树突状细胞捕获和加工细胞物质的途径方面已取得了很大进展（1）。但是，对于确定这种表现最终导致细胞毒性T细胞（CTL）反应（交叉引发）还是导致CD8（+）T细胞失活（交叉耐受）的信号知之甚少。在这里，我们描述了一种在病毒感染过程中促进交叉引发的机制。我们显示，鼠CD8alpha（+）树突状细胞被病毒感染的细胞中存在但未感染的细胞中不存在的双链（ds）RNA激活。树突状细胞的激活需要吞噬被感染的物质，然后通过dsRNA受体，toll​​样受体3（TLR3）发出信号。用病毒感染的细胞或含有合成dsRNA的细胞进行免疫可导致针对细胞相关抗原的CTL交叉引物显着增加，这在很大程度上取决于抗原呈递细胞的TLR3表达。因此，TLR3可能进化为允许CTL对不直接感染树突状细胞的病毒进行交叉启动。

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