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首页> 外文期刊>Nature immunology >Systemic activation of dendritic cells by Toll-like receptor ligands or malaria infection impairs cross-presentation and antiviral immunity
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Systemic activation of dendritic cells by Toll-like receptor ligands or malaria infection impairs cross-presentation and antiviral immunity

机译：Toll样受体配体对树突状细胞的全身激活或疟疾感染削弱了交叉呈递和抗病毒免疫

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The mechanisms responsible for the immunosuppression associated with sepsis or some chronic blood infections remain poorly understood. Here we show that infection with a malaria parasite (Plasmodium berghei) or simple systemic exposure to bacterial or viral Toll-like receptor ligands inhibited cross-priming. Reduced cross-priming was a consequence of downregulation of cross-presentation by activated dendritic cells due to systemic activation that did not otherwise globally inhibit T cell proliferation. Although activated dendritic cells retained their capacity to present viral antigens via the endogenous major histocompatibility complex class I processing pathway, antiviral responses were greatly impaired in mice exposed to Toll-like receptor ligands. This is consistent with a key function for cross-presentation in antiviral immunity and helps explain the immunosuppressive effects of systemic infection. Moreover, inhibition of cross-presentation was overcome by injection of dendritic cells bearing antigen, which provides a new strategy for generating immunity during immunosuppressive blood infections.
机译：与败血症或某些慢性血液感染相关的免疫抑制的机制仍知之甚少。在这里，我们显示感染疟疾寄生虫（伯氏疟原虫）或简单地全身性暴露于细菌或病毒Toll样受体配体会抑制交叉启动。交叉引发的减少是由于系统性激活而被激活的树突状细胞的交叉呈递下调的结果，而全身性激活原本不会全面抑制T细胞增殖。尽管活化的树突状细胞保留了通过内源性主要组织相容性复合体I类加工途径呈递病毒抗原的能力，但在暴露于Toll样受体配体的小鼠中，抗病毒反应受到了极大损害。这与抗病毒免疫中交叉呈递的关键功能是一致的，并有助于解释全身感染的免疫抑制作用。此外，交叉呈递的抑制作用通过注射带有抗原的树突状细胞得以克服，这为在免疫抑制性血液感染过程中产生免疫力提供了新的策略。

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