生物学杂志

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NLRP3炎症小体负调控研究进展

  

  1. 厦门医学院 病原生物与免疫学教研室, 厦门 361023
  • 出版日期:2018-08-18 发布日期:2018-08-18
  • 作者简介:陈淑珍,讲师,博士,主要从事病原生物与免疫学教学及研究,E-mail:cszlotus@126.com
  • 基金资助:
    福建省高校青年自然基金重点项目(JZ160496);福建省中青年教师教育科研项目(JA15816);厦门医学院博士科研项目(Z2014-04)

Research advances in negative regulation of NLRP3 inflammasome

  1. Department of Pathogenic Biology and Immunology, Xiamen Medical College, Xiamen 361023, China
  • Online:2018-08-18 Published:2018-08-18

摘要: 炎症小体是细胞内的一类多蛋白复合物,激活后释放IL-1β和IL-18等促炎细胞因子,诱导细胞焦亡,促进炎症反应。在目前已研究报道的多种炎症小体中,NLRP3炎症小体可被多种病原体和危险信号活化,并参与多种疾病的发生发展,其激活机制及功能研究得最为深入。NLRP3炎症小体激活需要精确调控,适度激活有利于清除病原体或有害物质;而持续过度激活可导致慢性炎症等疾病。目前诸多研究表明,机体可通过多种分子机制对活化的NLRP3炎症小体进行负调控以维持炎症反应平衡。

关键词: NLRP3炎症小体, 负调控, 分子机制

Abstract: Inflammasomes are muti-protein complexes that promote the maturation and secretion of pro-inflammatory cytokines, including interleukin-1β (IL-1β)and IL-18, leading to pyroptosis and inflammation. Among the known inflammasomes, the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3)-dependent inflammasome has been the most extensively studied, which responds to numerous pathogens and damage-associated signals, and is involved in a series of diseases. Precise regulation is required for activation of NLRP3 inflammasome. The moderate activation of NLRP3 inflammasome contributes to eliminate pathogens or hazardous substances, while excessive activation may lead to chronic inflammation. Many molecular mechanisms have been identified to attenuate NLRP3 inflammasome signaling to maintain the homeostasis of inflammatory response.

Key words: NLRP3 inflammasome, negative regulation, molecular mechanism