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Regulation of inflammasome signaling

机译：炎性体信号传导的调节

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Innate immune responses have the ability to both combat infectious microbes and drive pathological inflammation. Inflammasome complexes are a central component of these processes through their regulation of interleukin 1β (IL-1β), IL-18 and pyroptosis. Inflammasomes recognize microbial products or endogenous molecules released from damaged or dying cells both through direct binding of ligands and indirect mechanisms. The potential of the IL-1 family of cytokines to cause tissue damage and chronic inflammation emphasizes the importance of regulating inflammasomes. Many regulatory mechanisms have been identified that act as checkpoints for attenuating inflammasome signaling at multiple steps. Here we discuss the various regulatory mechanisms that have evolved to keep inflammasome signaling in check to maintain immunological balance.
机译：先天性免疫反应具有抵抗传染性微生物和驱动病理性炎症的能力。炎症小体复合物通过调节白介素1β（IL-1β），IL-18和发烧而成为这些过程的重要组成部分。炎症小体通过配体的直接结合和间接机制识别从受损或垂死的细胞释放的微生物产物或内源性分子。 IL-1家族细胞因子引起组织损伤和慢性炎症的潜力强调了调节炎症小体的重要性。已经确定了许多调节机制，这些机制在多个步骤中充当减弱炎症小体信号传导的检查点。在这里，我们讨论了各种调节机制，这些机制已经发展成为可检查炎症小体信号以维持免疫平衡的机制。

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