炎症小体信号的调控。
Regulation of inflammasome signaling.
机构信息
Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
出版信息
Nat Immunol. 2012 Mar 19;13(4):333-42. doi: 10.1038/ni.2237.
Abstract
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.
摘要
先天免疫反应既有抵抗感染微生物的能力，也能引发病理性炎症。炎性体复合物是这些过程的一个核心组成部分，通过调节白细胞介素 1β（IL-1β）、IL-18 和细胞焦亡来发挥作用。炎性体通过直接结合配体和间接机制识别微生物产物或受损或死亡细胞释放的内源性分子。细胞因子白细胞介素 1 家族有引起组织损伤和慢性炎症的潜力，这强调了调节炎性体的重要性。已经确定了许多调节机制，它们作为在多个步骤减弱炎性体信号的检查点。在这里，我们讨论了为了保持免疫平衡而进化出来的各种调节机制，以控制炎性体信号。
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