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IFN-λ 'guts' neutrophil-mediated inflammation

Nature Immunology volume 18, pages 1061–1062 (2017)Cite this article

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Interferon-λ (IFN-λ) curbs neutrophil-mediated intestinal inflammation by diminishing the production of reactive oxygen species and subsequent oxidative stress. This regulatory process is unique to IFN-λ and is independent of interferon-induced transcription and translation programs.

A hallmark of inflammation is the infiltration of neutrophils into the site of infection in response to inflammatory cytokines and chemokines released by infected cells. Neutrophil-mediated restriction of pathogens is conferred by phagocytosis, the production of reactive oxygen species (ROS) and the release of cytotoxic antimicrobial molecules1. In this issue of Nature Immunology, Broggi et al. show that the antiviral cytokine IFN-λ (a type III interferon composed of IFN-λ1, IFN-λ2, IFN-λ3 and IFN-λ4) regulates the effector function of neutrophils by diminishing ROS production and degranulation and thereby reducing oxidative stress and tissue damage during intestinal inflammation2. Surprisingly, this regulatory mechanism is unique to IFN-λ, is not mediated by type I interferons (IFN-α and IFN-β) and is independent of canonical interferon-induced antiviral transcription and translation programs.

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Figure 1: IFN-λ produced in response to enteric viruses regulates intestinal inflammation via diminishing neutrophil function.

Kim Caesar/Springer Nature

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Authors and Affiliations

  1. Department of Immunology, University of Washington, Seattle, Washington, USA

    Emily A Hemann, Johannes Schwerk & Ram Savan

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  1. Emily A Hemann
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  2. Johannes Schwerk
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  3. Ram Savan
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Correspondence to Ram Savan.

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Hemann, E., Schwerk, J. & Savan, R. IFN-λ 'guts' neutrophil-mediated inflammation. Nat Immunol 18, 1061–1062 (2017). https://doi.org/10.1038/ni.3834

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