期刊
CELL REPORTS
卷 11, 期 10, 页码 1535-1548出版社
CELL PRESS
DOI: 10.1016/j.celrep.2015.05.003
关键词
-
类别
资金
- Science Foundation Ireland [08/IN.1/B2031, 07/SRC/B1144]
- Science Foundation Ireland (SFI) [07/SRC/B1144, 08/IN.1/B2031] Funding Source: Science Foundation Ireland (SFI)
The NLRP3 inflammasome is involved in caspase-1-dependent maturation of IL-1 beta in many contexts. A two-signal model has emerged for IL-1 beta maturation, with LPS providing signal I'' and diverse agents such as ATP, Nigericin, streptolysin O, uric acid crystals, and alum salts capable of acting as signal II.'' In the absence of signal II, pro-IL-1 beta is upregulated but typically fails to be processed or released. What unites signal II stimuli has been debated, with the ability to promote K+ efflux suggested as a common factor, but the mechanism of IL-1 beta release remains unclear. Here, we show that all examined inflammasome signal II agents triggered necrosis, which was highly correlated with their ability to promote IL-1 beta release. IL-1 beta secretion occurred in tandem with the release of many additional proteins and was confined to necrotic cells. Thus, signal II agents initiate inflammation by promoting necrosis-driven IL-1 beta release, suggesting that IL-1 beta represents an inducible danger signal.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据