期刊
NATURE IMMUNOLOGY
卷 18, 期 10, 页码 1084-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3821
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资金
- US National Institutes of Health [1R01DK115217, 1R01AI121066-01A1]
- Harvard Digestive Diseases Center [P30 DK034854]
- Harvard Medical School
- Crohn's and Colitis Foundation of America
- Cariplo Foundation
- Associazione Italiana per la Ricerca sul Cancro
- Fondazione Italiana di Ricerca per la SLA-Sclerosi Laterale Amiotrofica (ARISLA)
- Fondazione Regionale per la Ricerca Biomedica
- Jane Coffin Child's Memorial Fund for Medical Research
Interferon-lambda (IFN-lambda) is a central regulator of mucosal immunity; however, its signaling specificity relative to that of type I interferons is poorly defined. IFN-lambda can induce antiviral interferon-stimulated genes (ISGs) in epithelia, while the effect of IFN-lambda in non-epithelial cells remains unclear. Here we report that neutrophils responded to IFN-lambda. We found that in addition to inducing ISG transcription, IFN-lambda (but not IFN-beta) specifically activated a translation-independent signaling pathway that diminished the production of reactive oxygen species and degranulation in neutrophils. In mice, IFN-lambda was elicited by enteric viruses and acted on neutrophils to decrease oxidative stress and intestinal damage. Thus, IFN-lambda acted as a unique immunomodulatory agent by modifying transcriptional and non-translational neutrophil responses, which might permit a controlled development of the inflammatory process.
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