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Nat Immunol. 2017 Oct;18(10):1084-1093. doi: 10.1038/ni.3821. Epub 2017 Aug 28.

IFN-λ suppresses intestinal inflammation by non-translational regulation of neutrophil function.

Author information

1
Harvard Medical School and Division of Gastroenterology, Boston Children's Hospital, Boston, Massachusetts, USA.
2
Department of Biotechnology and Biosciences, University of Milano-Bicocca, Milan, Italy.

Abstract

Interferon-λ (IFN-λ) is a central regulator of mucosal immunity; however, its signaling specificity relative to that of type I interferons is poorly defined. IFN-λ can induce antiviral interferon-stimulated genes (ISGs) in epithelia, while the effect of IFN-λ in non-epithelial cells remains unclear. Here we report that neutrophils responded to IFN-λ. We found that in addition to inducing ISG transcription, IFN-λ (but not IFN-β) specifically activated a translation-independent signaling pathway that diminished the production of reactive oxygen species and degranulation in neutrophils. In mice, IFN-λ was elicited by enteric viruses and acted on neutrophils to decrease oxidative stress and intestinal damage. Thus, IFN-λ acted as a unique immunomodulatory agent by modifying transcriptional and non-translational neutrophil responses, which might permit a controlled development of the inflammatory process.

PMID:
28846084
PMCID:
PMC5701513
DOI:
10.1038/ni.3821
[Indexed for MEDLINE]
Free PMC Article

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