Journal
SCIENCE ADVANCES
Volume 6, Issue 14, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciadv.aay3245
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Categories
Funding
- NIH [R01 AI139207, R21AI139207, R21NS100545, R21AI129851, T32-CA009111, NIAMS P30-AR075043]
- Dermatology Foundation Award
- Duke PhysicianScientist Strong Start Award
- Silab company partnership grant
- NIH, National Institute of Allergy and Infectious Diseases [UC6-AI058607]
- Eugene A. Stead Student Research Fellowship
- Poindexter Fellowship
- Burroughs Wellcome Fund [1016810]
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In the skin, antiviral proteins and other immune molecules serve as the first line of innate antiviral defense. Here, we identify and characterize the induction of cutaneous innate antiviral proteins in response to IL-27 and its functional role during cutaneous defense against Zika virus infection. Transcriptional and phenotypic profiling of epidermal keratinocytes treated with IL-27 demonstrated activation of antiviral proteins OAS1, OAS2, OASL, and MX1 in the skin of both mice and humans. IL-27-mediated antiviral protein induction was found to occur in a STAT1- and IRF3-dependent but STAT2-independent manner. Moreover, using IL27ra mice, we demonstrate a significant role for IL-27 in inhibiting Zika virus morbidity and mortality following cutaneous, but not intravenous, inoculation. Together, our results demonstrate a critical and previously unrecognized role for IL-27 in cutaneous innate antiviral immunity against Zika virus.
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