Vanaja Sivapriya K, Rathinam Vijay A K, Fitzgerald Katherine A
Department of Immunology, University of Connecticut Health Center, Farmington, CT, USA.
Program in Innate Immunity, Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA; Centre of Molecular Inflammation Research, Department of Cancer Research and Molecular Medicine, NTNU, 7491 Trondheim, Norway.
Trends Cell Biol. 2015 May;25(5):308-15. doi: 10.1016/j.tcb.2014.12.009. Epub 2015 Jan 29.
Inflammasomes are cytosolic multiprotein platforms assembled in response to invading pathogens and other danger signals. Typically inflammasome complexes contain a sensor protein, an adaptor protein, and a zymogen - procaspase-1. Formation of inflammasome assembly results in processing of inactive procaspase-1 into an active cysteine-protease enzyme, caspase-1, which subsequently activates the proinflammatory cytokines, interleukins IL-1β and IL-18, and induces pyroptosis, a highly-pyrogenic inflammatory form of cell death. Studies over the past year have unveiled exciting new players and regulatory pathways that are involved in traditional inflammasome signaling, some of them even challenging the existing dogma. This review outlines these new insights in inflammasome research and discusses areas that warrant further exploration.
炎性小体是一种胞质多蛋白平台,可响应入侵病原体和其他危险信号而组装。典型的炎性小体复合物包含一种传感器蛋白、一种衔接蛋白和一种酶原——前半胱天冬酶-1。炎性小体组装的形成会导致无活性的前半胱天冬酶-1加工成活性半胱氨酸蛋白酶——半胱天冬酶-1,后者随后激活促炎细胞因子白细胞介素IL-1β和IL-18,并诱导细胞焦亡,这是一种高度致热的炎症性细胞死亡形式。过去一年的研究揭示了参与传统炎性小体信号传导的令人兴奋的新参与者和调节途径,其中一些甚至挑战了现有的教条。这篇综述概述了炎性小体研究中的这些新见解,并讨论了值得进一步探索的领域。