Inflammasomes are multi-component signaling complexes critical to the initiation of pyroptotic cell death in response to invading pathogens and cellular damage. A number of innate immune receptors have been reported to serve as inflammasome sensors. Activation of these sensors leads to the proteolytic activation of caspase-1, a proinflammatory caspase responsible for the cleavage of proinflammatory cytokines interleukin-1β and interleukin-18 and the effector of pyroptotic cell death, gasdermin D. Though crucial to the innate immune response to infection, dysregulation of inflammasome activation can lead to the development of inflammatory diseases, neurodegeneration, and cancer. Therefore, clinical interest in the modulation of inflammasome activation is swiftly growing. As such, it is imperative to develop a mechanistic understanding of the regulation of these complexes. In this review, we divide the regulation of inflammasome activation into three parts. We discuss the transcriptional regulation of inflammasome components and related proteins, the post-translational mechanisms of inflammasome activation, and advances in the understanding of the structural basis of inflammasome activation.

炎症小体是多组分信号复合物，对于响应入侵病原体和细胞损伤而启动焦亡细胞死亡至关重要。据报道，许多先天免疫受体可充当炎症小体传感器。这些传感器的激活导致 caspase-1 的蛋白水解激活，caspase-1 是一种促炎性 caspase，负责裂解促炎性细胞因子 IL-1β 和 IL-18，以及焦亡细胞死亡的效应子 Gasdermin D。感染、炎症小体激活失调可导致炎症性疾病、神经退行性变和癌症的发生。因此，临床对调节炎症小体激活的兴趣正在迅速增长。因此，必须对这些复合物的调节产生机械性的理解。在这篇综述中，我们将炎症小体激活的调节分为三个部分。我们讨论了炎症小体成分和相关蛋白的转录调控、炎症小体激活的翻译后机制，以及对炎症小体激活结构基础的理解进展。