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• W2980765413 abstract "Abstract The functions of the IL-36 cytokines remain poorly understood. We report a previously unrecognized mechanism whereby IL-36 promotes innate antiviral immunity in mouse and human models of herpes simplex virus-1 (HSV-1) infections. HSV-1 actively suppresses production of type I interferon (IFN); our data reveal that IL-36 overcomes this immune evasion strategy by increasing cellular sensitivity to IFN. IL-36β deficient mice display impaired IFN responses and poorly restrict viral replication in skin keratinocytes. In mouse and human keratinocytes IL-36 elicits an antiviral state driven by STAT1 and STAT2 via enhanced expression of IFNAR1 and IFNAR2 subunits of the type I IFN receptor. The degree of IFN regulatory factor 1 (IRF1) involvement is species dependent, with IRF1 playing a more prominent role in human cells. Similar mechanisms are activated by IL-1. Overall, IL-36 acts as an antiviral cytokine by potentiating type I IFN signaling and thereby upholds immune responses to viruses that limit the production of IFNs." @default.
• W2980765413 created "2019-10-25" @default.
• W2980765413 creator A5014073749 @default.
• W2980765413 creator A5044581763 @default.
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• W2980765413 date "2019-10-16" @default.
• W2980765413 modified "2023-10-02" @default.
• W2980765413 title "IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners" @default.
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• W2980765413 doi "https://doi.org/10.1038/s41467-019-12318-y" @default.
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• W2980765413 hasPublicationYear "2019" @default.
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