NLRP3炎性小体激活的机制与调控
Mechanism and Regulation of NLRP3 Inflammasome Activation.
作者信息
He Yuan, Hara Hideki, Núñez Gabriel
机构信息
Department of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Department of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
出版信息
Trends Biochem Sci. 2016 Dec;41(12):1012-1021. doi: 10.1016/j.tibs.2016.09.002. Epub 2016 Sep 23.
Members of the nucleotide-binding domain and leucine-rich repeat (LRR)-containing (NLR) family and the pyrin and HIN domain (PYHIN) family can form multiprotein complexes termed 'inflammasomes'. The biochemical function of inflammasomes is to activate caspase-1, which leads to the maturation of interleukin 1 beta (IL-1β) and IL-18 and the induction of pyroptosis, a form of cell death. Unlike other inflammasomes, the NLRP3 inflammasome can be activated by diverse stimuli. The importance of the NLRP3 inflammasome in immunity and human diseases has been well documented, but the mechanism and regulation of its activation remain unclear. In this review we summarize current understanding of the mechanism and regulation of NLRP3 inflammasome activation as well as recent advances in the noncanonical and alternative inflammasome pathways.
核苷酸结合结构域和富含亮氨酸重复序列（LRR）的（NLR）家族以及含pyrin和HIN结构域（PYHIN）家族的成员可形成称为“炎性小体”的多蛋白复合物。炎性小体的生化功能是激活半胱天冬酶-1，这会导致白细胞介素1β（IL-1β）和IL-18成熟，并诱导细胞焦亡，这是一种细胞死亡形式。与其他炎性小体不同，NLRP3炎性小体可被多种刺激激活。NLRP3炎性小体在免疫和人类疾病中的重要性已有充分记载，但其激活机制和调节仍不清楚。在这篇综述中，我们总结了目前对NLRP3炎性小体激活机制和调节的理解，以及非经典和替代炎性小体途径的最新进展。
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