Pyroptosis is a programmed and inflammatory cell death initiated by inflammasome. During pyroptosis, cytosolic pattern recognition receptors, apoptosis-associated speck-like protein and pro-Caspase-1 form activated inflammasome together. Caspase-1 activated by inflammasome results in generating an N-terminal cleavage product of gasdermin D (GSDMD), which is a major executor of pyroptosis. As a consequence of pyroptosis, a large number of pro-inflammatory cytokines are released including IL-1β and IL-18. Nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) and absent in melanoma 2 (AIM2)-like receptors (ALRs) belong to cytosolic pattern recognition receptors and assemble inflammasomes by detecting host cell damage signals. Pyroptosis pathways are divided into canonical and non-canonical pathways according to the identification of damage signals by cytoplasmic protein sensors. Pyroptosis not only plays an important role in infection, but also plays a vital role in inflammatory immune diseases. This article reviews the advances research of pyroptosis initiated by inflammasome in inflammatory and immune diseases.

中文翻译：

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炎症小体在炎症和免疫疾病中引发的细胞焦亡进展。

焦亡是由炎症小体引发的程序性炎症性细胞死亡。在细胞焦亡期间，细胞溶质模式识别受体、凋亡相关斑点样蛋白和 pro-Caspase-1 一起形成活化的炎性体。由炎性体激活的 Caspase-1 导致产生 gasdermin D (GSDMD) 的 N 端裂解产物，它是细胞焦亡的主要执行者。由于细胞焦亡，大量促炎细胞因子被释放，包括 IL-1β 和 IL-18。核苷酸结合寡聚化结构域 (NOD) 样受体 (NLR) 和黑色素瘤 2 (AIM2) 样受体 (ALR) 中不存在属于细胞溶质模式识别受体，通过检测宿主细胞损伤信号组装炎性体。根据细胞质蛋白传感器对损伤信号的识别，细胞焦亡途径分为经典途径和非经典途径。焦亡不仅在感染中起重要作用，而且在炎症性免疫疾病中也起着至关重要的作用。本文综述了炎症小体引发的细胞焦亡在炎症和免疫疾病中的研究进展。