In contrast to highly specific sensor molecules of the innate immune system, the NLRP 3 receptor detects a broad variety of danger signals including pathogens. Sensing triggers intracellular NLRP 3 inflammasome complex assembly to induce an inflammatory response with the primary aim to eliminate pathogens. However, several of them have developed distinct strategies to hijack NLRP 3‐dependent immunity. In this issue of EMBO Reports , Zhang and colleagues demonstrate that reovirus infection of airway epithelial cells promotes EphA2‐dependent phosphorylation of NLRP 3 that impedes the recruitment of other inflammasome components necessary for its activation [1]. This potentially uncovers a mechanism that may lead to reduced viral clearance in the lung, eventually contributing to life‐threatening respiratory disease.

中文翻译：

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劫持NLRP3炎性体：病毒性呼吸系统疾病的潜在机制？

与先天免疫系统的高度特异性传感器分子相反，NLRP 3受体可检测多种危险信号，包括病原体。传感触发细胞内NLRP 3炎性小体复合物装配，以诱导炎症反应，其主要目的是消除病原体。但是，其中一些已经开发出独特的策略来劫持NLRP 3依赖性免疫。在本期EMBO报告中，Zhang和他的同事证明呼肠孤病毒感染气道上皮细胞会促进EphA2依赖的NLRP 3磷酸化，这阻碍了激活它所需的其他炎性体成分的募集[1]。这潜在地揭示了一种机制，该机制可能导致肺中病毒清除率降低，最终导致威胁生命的呼吸系统疾病。