炎症体
NALP3
白细胞介素18
半胱氨酸蛋白酶1
目标2
促炎细胞因子
细胞内
化学
上睑下垂
细胞生物学
生物
微生物学
受体
生物化学
炎症
免疫学
细胞因子
作者
Virgine Pétrilli,Stéphanie Papin,Catherine Dostert,Annick Mayor,Fabio Martinon,Jürg Tschopp
标识
DOI:10.1038/sj.cdd.4402195
摘要
Inflammasomes are Nod-like receptor(NLR)- and caspase-1-containing cytoplasmic multiprotein complexes, which upon their assembly, process and activate the proinflammatory cytokines interleukin (IL)-1beta and IL-18. The inflammasomes harboring the NLR members NALP1, NALP3 and IPAF have been best characterized. While the IPAF inflammasome is activated by bacterial flagellin, activation of the NALP3 inflammasome is triggered not only by several microbial components, but also by a plethora of danger-associated host molecules such as uric acid. How NALP3 senses these chemically unrelated activators is not known. Here, we provide evidence that activation of NALP3, but not of the IPAF inflammasome, is blocked by inhibiting K(+) efflux from cells. Low intracellular K(+) is also a requirement for NALP1 inflammasome activation by lethal toxin of Bacillus anthracis. In vitro, NALP inflammasome assembly and caspase-1 recruitment occurs spontaneously at K(+) concentrations below 90 mM, but is prevented at higher concentrations. Thus, low intracellular K(+) may be the least common trigger of NALP-inflammasome activation.
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