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IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners
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IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners
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Journal Article
IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners
2019
Overview
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.
Herpes simplex virus-1 (HSV-1) suppresses the induction of interferon to evade antiviral immunity. Here, Wang et al. show that during HSV-1 infection, IL-36 increases cellular sensitivity to interferon through induction of IRF1 and the interferon receptor.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/106
/ 13/21
/ 13/51
/ 13/95
/ 38/1
/ 38/77
/ 64/60
/ 82/1
/ 82/29
/ 82/80
/ 96/106
/ 96/95
/ Animals
/ Humanities and Social Sciences
/ Humans
/ Immunity
/ Interferon regulatory factor 1
/ Interferon Regulatory Factor-1 - immunology
/ Interferon Type I - immunology
/ Mice
/ Receptor, Interferon alpha-beta - genetics
/ Receptor, Interferon alpha-beta - metabolism
/ Science
/ STAT1 Transcription Factor - immunology
/ STAT2 Transcription Factor - immunology
/ Viruses
