期刊
JOURNAL OF IMMUNOLOGY
卷 183, 期 3, 页码 1528-1532出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0901080
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资金
- National Institutes of Health [R2 I A1076835]
Cells undergoing necrosis release endogenous danger signals that possess proinflammatory potential. In this study we show that mature IL-1 beta and IL-18 are released by necrotic cells but not by apoptotic cells. We identify 7-bromoindirubin-3'-oxime, an indirubin oxime derivative that induces necrosis, as a potent inducer of caspase-1 activation and release of mature IL-1 beta and IL-18. Inflammasome activation was triggered by other necrosis-inducing treatments but was not observed in response to apoptosis-inducing stimuli. Necrosis-induced inflammasome activation was mediated by the NLRP3 and ASC molecules. Release of IL-18 and IL-1 beta in response to necrosis-inducing stimuli was observed in THP-I macrophages and the MSTO-211H human mesothelioma cell line independently of LPS priming. Using the in vivo model of naphthalene-induced airway epithelial cell injury, we showed that necrosis activates the ASC inflammasome in vivo. Our study identifies a new mechanism through which necrosis generates proinflammatory molecules that contributes to the sterile inflammatory response. The Journal of Immunology, 2009,183:1528-1532.
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