期刊
SCIENCE
卷 352, 期 6284, 页码 463-466出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aaf3926
关键词
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资金
- NIH [AI081884, AI062428, AI064705, HHSN272201100019C, K24 AG02489, T32 AI007019-36, T32 AI007019-38, T32 AI055403, 5T32HL066987-13, F31 AG039163, R01HL102101, R01HL125501, K24 AG042489, P30 AG21342]
- Deutsche Forschungsgemeinschaft (DFG) [SFB1160/P13]
Influenza A virus (IAV) causes up to half a million deaths worldwide annually, 90% of which occur in older adults. We show that IAV-infected monocytes from older humans have impaired antiviral interferon production but retain intact inflammasome responses. To understand the in vivo consequence, we used mice expressing a functional Mx gene encoding a major interferon-induced effector against IAV in humans. In Mx1-intact mice with weakened resistance due to deficiencies in Mavs and Tlr7, we found an elevated respiratory bacterial burden. Notably, mortality in the absence of Mavs and Tlr7 was independent of viral load or MyD88-dependent signaling but dependent on bacterial burden, caspase-1/11, and neutrophil-dependent tissue damage. Therefore, in the context of weakened antiviral resistance, vulnerability to IAV disease is a function of caspase-dependent pathology.
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