期刊
MOLECULAR CELL
卷 74, 期 4, 页码 801-+出版社
CELL PRESS
DOI: 10.1016/j.molcel.2019.02.038
关键词
-
资金
- NIH [AI27463, AI118916, AI100625, AI104002, AI083019]
- [T32AI106677-03]
Interleukin-1 beta (IL-1 beta) is a pleiotropic mediator of inflammation and is produced in response to a wide range of stimuli. During infection, IL-1 beta production occurs in parallel with the onset of innate antimicrobial defenses, but the contribution of IL-1 beta signaling to cell-intrinsic immunity is not defined. Here, we report that exogenous IL-1 beta induces interferon regulatory factor 3 (IRF3) activation in human myeloid, fibroblast, and epithelial cells. IRF3 activation by IL-1 beta is dependent upon the DNA-sensing pathway adaptor, stimulator of interferon genes (STING), through the recognition of cytosolic mtDNA by cyclic guanosine monophosphate (GMP)-AMP synthase (cGAS). IL-1 beta treatment results in interferon (IFN) production and activation of IFN signaling to direct a potent innate immune response that restricts dengue virus infection. This study identifies a new function for IL-1 beta in the onset or enhancement of cell-intrinsic immunity, with important implications for cGAS-STING in integrating inflammatory and microbial cues for host defense.
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