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《Science，6月11日，Type I and III interferons disrupt lung epithelial repair during recovery from viral infection》

  • 来源专题：COVID-19科研动态监测
  • 编译者： xuwenwhlib
  • 发布时间：2020-06-14

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    Type I and III interferons disrupt lung epithelial repair during recovery from viral infection

    View ORCID ProfileJack Major1, View ORCID ProfileStefania Crotta1, Miriam Llorian2, View ORCID ProfileTeresa M. McCabe1,*, View ORCID ProfileHans Henrik Gad3, Simon L. Priestnall4,5, View ORCID ProfileRune Hartmann3, View ORCID ProfileAndreas Wack1,†

    See all authors and affiliations

    Science 11 Jun 2020:

    eabc2061

    DOI: 10.1126/science.abc2061

    Abstract

    Excessive cytokine signaling frequently exacerbates lung tissue damage during respiratory viral infection. Type I (IFN-α/β) and III (IFN-λ) interferons are host-produced antiviral cytokines. Prolonged IFN-α/β responses can lead to harmful proinflammatory effects, whereas IFN-λ mainly signals in epithelia, inducing localized antiviral immunity. Here we show that IFN signaling interferes with lung repair during influenza recovery, with IFN-λ driving these effects most potently. IFN-induced p53 directly reduces epithelial proliferation and differentiation, increasing disease severity, and susceptibility to bacterial superinfections. Thus, excessive or prolonged IFN-production aggravates viral infection by impairing lung epithelial regeneration. Therefore, timing and duration are critical parameters of endogenous IFN action and should be considered carefully for IFN therapeutic strategies against viral infections like influenza and coronavirus disease 2019 (COVID-19).

  • 原文来源：https://science.sciencemag.org/content/early/2020/06/10/science.abc2061
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