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Antiviral immunity

IFNλ offers frontline protection

Nature Reviews Immunology volume 17, pages 404–405 (2017)Cite this article

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In mice infected with IAV, IFNλs were rapidly induced at both low (sublethal) doses and high (lethal) doses, whereas type I IFNs were only induced when the infection dose was high or at later time points when the viral load had increased. Thus, the authors investigated whether initial viral spread after a sublethal infection could be targeted by IFNλs acting alone. Ifnlr1−/− mice (which lack the IFNλ receptor) and Ifnlr1−/−Ifnar1−/− mice (which lack IFNλ and type I IFN receptors) had markedly increased viral loads during the first 5 days of a sublethal IAV infection compared with wild-type and Ifnar1−/− mice. The Ifnlr1−/− mice and Ifnlr1−/−Ifnar1−/− mice also had increased infiltration of the lungs with inflammatory cells, mainly neutrophils, by 5 days after infection, which was associated with increased production of IFNα (presumably owing to increased viral load) and of pro-inflammatory mediators, and increased immunopathology. In contrast to the solo role of IFNλs in inhibiting early viral replication during a sublethal infection, type I IFNs were shown to cooperate with IFNλs during lethal IAV infection. At day 2 after lethal infection, Ifnlr1−/− mice and Ifnlr1−/−Ifnar1−/− mice had higher viral loads, whereas from day 3 onwards, viral loads were higher in Ifnar1−/− mice and Ifnlr1−/−Ifnar1−/− mice.

IFNλs function in an autocrine manner on airway epithelial cells to limit early viral replication

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References

  1. Galani, I. E. et al. Interferon-λ mediates non-redundant front-line antiviral protection against influenza virus infection without compromising host fitness. Immunity http://dx.doi.org/10.1016/j.immuni.2017.04.025 46, 875–890 (2017)

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  1. Kirsty Minton
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Minton, K. IFNλ offers frontline protection. Nat Rev Immunol 17, 404–405 (2017). https://doi.org/10.1038/nri.2017.70

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