Inflammasomes assemble in the cytosol of myeloid and epithelial cells on sensing of cellular stress and pathogen-associated molecular patterns and serve as scaffolds for recruitment and activation of inflammatory caspases. Inflammasomes play beneficial roles in host and immune responses against diverse pathogens but may also promote inflammatory tissue damage if uncontrolled. Gasdermin D (GSDMD) is a recently identified substrate of murine caspase-1 and caspase-11, and human caspases-1, -4, and -5 that mediates a regulated lytic cell death mode termed pyroptosis. Recent studies have identified pyroptosis as a critical inflammasome effector mechanism that controls inflammasome-dependent cytokine secretion and contributes to antimicrobial defense and inflammasome-mediated autoinflammatory diseases. Here, we review recent developments on inflammasome-associated effector functions with an emphasis on the emerging roles of gasdermin pores and pyroptosis.

中文翻译：

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最近对炎症小体、Gasdermin 毛孔和细胞焦亡的见解。

炎症小体在感知细胞应激和病原体相关分子模式时聚集在骨髓和上皮细胞的胞质溶胶中，并用作募集和激活炎症半胱天冬酶的支架。炎症小体在宿主和针对多种病原体的免疫反应中发挥有益作用，但如果不受控制，也可能促进炎症组织损伤。Gasdermin D (GSDMD) 是最近发现的鼠 caspase-1 和 caspase-11 以及人类 caspase-1、-4 和 -5 的底物，可介导一种称为细胞焦亡的受调节的裂解细胞死亡模式。最近的研究已将细胞焦亡确定为一种关键的炎症小体效应机制，可控制炎症小体依赖性细胞因子的分泌，并有助于抗菌素防御和炎症小体介导的自身炎症性疾病。这里，