期刊
IMMUNITY
卷 46, 期 5, 页码 875-+出版社
CELL PRESS
DOI: 10.1016/j.immuni.2017.04.025
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资金
- Hellenic Ministry of Education (MIDAS, RESOLVE-ASTHMA)
- European Commission
Lambda interferons (IFN lambda s) or type III IFNs share homology, expression patterns, signaling cascades, and antiviral functions with type I IFNs. This has complicated the unwinding of their unique non-redundant roles. Through the systematic study of influenza virus infection in mice, we herein show that IFN lambda s are the first IFNs produced that act at the epithelial barrier to suppress initial viral spread without activating inflammation. If infection progresses, type I IFNs come into play to enhance viral resistance and induce pro-inflammatory responses essential for confronting infection but causing immunopathology. Central to this are neutrophils which respond to both cytokines to upregulate antimicrobial functions but exhibit pro-inflammatory activation only to type I IFNs. Accordingly, Ifnlr1(-/-) mice display enhanced type I IFN production, neutrophilia, lung injury, and lethality, while therapeutic administration of PEG-IFN lambda potently suppresses these effects. IFN lambda s therefore constitute the front line of antiviral defense in the lung without compromising host fitness.
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