The C-type lectin member 5A (CLEC5A) is a pattern recognition receptor for members of the Flavivirus family and has critical functions in response to dengue virus and Japanese encephalitis virus. Here we show that CLEC5A is involved in neutrophil extracellular trap formation and the production of reactive oxygen species and proinflammatory cytokines in response to Listeria monocytogenes. Inoculation of Clec5a ^-/- mice with L. monocytogenes causes rapid bacterial spreading, increased bacterial loads in the blood and liver, and severe liver necrosis. In these mice, IL-1β, IL-17A, and TNF expression is inhibited, CCL2 is induced, and large numbers of CD11b⁺Ly6C^hiCCR2^hiCX3CR1^low inflammatory monocytes infiltrate the liver. By day 5 of infection, these mice also have fewer IL-17A⁺ γδ T cells, severe liver necrosis and a higher chance of fatality. Thus, CLEC5A has a pivotal function in the activation of multiple aspects of innate immunity against bacterial invasion.The lectin receptor CLEC5A is a pattern recognition receptor that has been shown to detect dengue and Japanese encephalitis virus. Here the authors show that CLEC5A is needed for optimal ROS production, NET formation and other immune responses to Listeria monocytogenes in mice.

中文翻译：

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CLEC5A是天然抗李斯特菌感染的关键受体。

C型凝集素成员5A（CLEC5A）是黄病毒家族成员的模式识别受体，对登革热病毒和日本脑炎病毒具有关键作用。在这里，我们显示CLEC5A参与嗜中性粒细胞胞外陷阱的形成以及响应单核细胞增生性李斯特菌的活性氧和促炎细胞因子的产生。用单核细胞增生李斯特氏菌接种Clec5a ^-/-小鼠会导致细菌迅速扩散，血液和肝脏中细菌含量增加以及严重的肝坏死。在这些小鼠中，IL-1β，IL-17A和TNF表达被抑制，CCL2被诱导，大量CD11b ⁺ Ly6C ^hi CCR2 ^hi CX3CR1^低炎性单核细胞浸润肝。到感染的第5天，这些小鼠还具有较少的IL-17A ⁺ γδT细胞，严重的肝坏死和更高的致死率。因此，CLEC5A在激活针对细菌入侵的先天免疫的多个方面具有关键作用。凝集素受体CLEC5A是一种模式识别受体，已被证明可以检测登革热和日本脑炎病毒。在这里，作者表明CLEC5A是小鼠中最佳ROS产生，NET形成和其他针对单核细胞增生李斯特菌的免疫反应所必需的。