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IL-1R signaling in dendritic cells replaces pattern-recognition receptors in promoting CD8 + T cell responses to influenza A virus

机译:树突状细胞中的IL-1R信号取代模式识别受体,促进CD8 + T细胞对甲型流感病毒的反应

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摘要

Immune responses to vaccines require direct recognition of pathogen-associated molecular patterns (PAMPs) through pattern-recognition receptors (PRRs) on dendritic cells (DCs). Unlike vaccination, infection by a live pathogen often impairs DC function and inflicts additional damage on the host. Here we found that after infection with live influenza A virus, signaling through the interleukin 1 receptor (IL-1R) was required for productive priming of CD8 + T cells, but signaling through the PRRs TLR7 and RIG-I was not. DCs activated by IL-1 in trans were both required and sufficient for the generation of virus-specific CD8 + T cell immunity. Our data demonstrate a critical role for a bystander cytokine in the priming of CD8 + T cells during infection with a live virus.
机译:对疫苗的免疫反应需要通过树突状细胞(DC)上的模式识别受体(PRR)直接识别病原体相关分子模式(PAMP)。与疫苗接种不同,活病原体的感染通常会损害DC功能,并对宿主造成额外的损害。在这里,我们发现感染活甲型流感病毒后,通过白介素1受体(IL-1R)进行信号传导对于CD8 + T细胞的生产性启动是必需的,而通过PRR TLR7和RIG-I则不需要。由IL-1反式激活的DC既需要又足以产生病毒特异性CD8 + T细胞免疫力。我们的数据表明,在活病毒感染期间,旁观者细胞因子在引发CD8 + T细胞方面起着关键作用。

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