Inflammasomes are cytosolic multiprotein complexes that sense microbial infections or host cell damage, triggering cytokine production and a proinflammatory form of cell death, called pyroptosis. Whereas pyroptosis and cytokine production may often promote host resistance to infections, uncontrolled inflammasome activation leads to autoinflammatory diseases in humans. Among the multiple inflammasomes described, the neuronal apoptosis inhibitory protein/nucleotide‐binding domain leucine‐rich repeat‐containing protein family caspase activation and recruitment domain‐containing protein 4 (NLRC4) inflammasome emerged as a critical component for the restriction of bacterial infections. Accordingly, our understanding of this inflammasome advanced remarkably over the last 10 yr, expanding our knowledge about ligand‐receptor interaction; cryo‐EM structure; and downstream effectors and substrates, such as gasdermin‐D, caspase‐1, caspase‐8, and caspase‐7. In this review, we discuss recent advances on the biology of the NLRC4 inflammasome, in terms of structure and activation mechanisms, importance in bacterial and nonbacterial diseases, and the identification of NLRC4 gain‐of‐function mutations leading to NLRC4‐associated autoinflammatory diseases in humans.

中文翻译：

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NLRC4在免疫和炎症中的生物学作用。

炎性小体是胞质多蛋白复合物，可感知微生物感染或宿主细胞损伤，从而触发细胞因子的产生和促炎形式的细胞死亡，称为焦磷酸化。发烧和细胞因子的产生通常可以促进宿主对感染的抵抗力，而不受控制的炎症小体激活会导致人类自身炎症性疾病。在所描述的多个炎症小体中，神经元凋亡抑制蛋白/核苷酸结合域富含亮氨酸的重复蛋白家族胱天蛋白酶激活和募集结构域蛋白4（NLRC4）炎症小体成为限制细菌感染的重要组成部分。因此，在过去的10年中，我们对这种炎性体的了解显着发展，扩大了我们对配体-受体相互作用的认识。cryo-EM结构；以及下游效应子和底物，例如gasdermin-D，caspase-1，caspase-8和caspase-7。在这篇综述中，我们讨论了NLRC4炎性小体生物学的最新进展，包括结构和激活机制，在细菌和非细菌性疾病中的重要性以及鉴定导致NLRC4相关的自发炎性疾病的NLRC4功能获得性突变。人类。