Increasing complexity of NLRP3 inflammasome regulation,Journal of Leukocyte Biology

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Increasing complexity of NLRP3 inflammasome regulation
Journal of Leukocyte Biology ( IF 3.6 ) Pub Date : 2020-06-12 , DOI: 10.1002/jlb.3mr0520-104rr
Julien Moretti _{1,

2} , J Magarian Blander _{1,

2,

3,

4,

5}

Affiliation

Inflammasomes are multiprotein complexes that assemble upon detection of danger signals to activate the inflammatory enzyme caspase‐1, trigger secretion of the highly proinflammatory cytokine IL‐1β, and induce an inflammatory cell death called pyroptosis. Distinctiveness of the nucleotide‐binding oligomerization (NOD), Leucine‐rich repeat (LRR)‐containing protein (NLRP3) inflammasome resides in the diversity of molecules that induce its activation, indicating a certain intricacy. Furthermore, besides the canonical activation of NLRP3 in response to various stimuli, caspase‐11‐dependent detection of intracellular LPS activates NLRP3 through a noncanonical pathway. Several aspects of the NLRP3 inflammasome are not characterized or remain unclear. In this review, we summarize the different modes of NLRP3 activation. We describe recent insights into post‐translational and cellular regulation that confer further complexity to NLRP3 inflammasomes.

中文翻译：

NLRP3炎症小体调控的复杂性增加

炎症小体是多蛋白复合物，它们在检测到危险信号后组装以激活炎症酶 caspase-1，触发高度促炎细胞因子 IL-1β 的分泌，并诱导称为细胞焦亡的炎症细胞死亡。核苷酸结合寡聚化 (NOD)、富含亮氨酸重复 (LRR) 蛋白 (NLRP3) 炎性体的独特性在于诱导其激活的分子的多样性，这表明了一定的复杂性。此外，除了响应各种刺激的 NLRP3 的典型激活外，细胞内 LPS 的 caspase-11 依赖性检测通过非典型途径激活 NLRP3。NLRP3 炎性体的几个方面没有表征或仍不清楚。在这篇综述中，我们总结了 NLRP3 激活的不同模式。

更新日期：2020-06-12

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