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Enhanced production of type I IFNs in Axl-\/- dendritic cells (DCs) in vitro have led to speculation that inhibition of AXL would promote antiviral responses. Notwithstanding, type I IFNs also exert potent immunosuppressive functions. Here we demonstrate that ablation of AXL enhances the susceptibility to infection by influenza A virus and West Nile virus. The increased type I IFN response in Axl-\/- mice was associated with diminished DC maturation, reduced production of IL-1\u03b2, and defective antiviral T cell immunity. Blockade of type I IFN receptor or administration of IL-1\u03b2 to Axl-\/- mice restored the antiviral adaptive response and control of infection. Our results demonstrate that AXL is essential for limiting the immunosuppressive effects of type I IFNs and enabling the induction of protective antiviral adaptive immunity.<\/jats:p>","DOI":"10.7554\/elife.12414","type":"journal-article","created":{"date-parts":[[2016,6,28]],"date-time":"2016-06-28T21:40:40Z","timestamp":1467150040000},"source":"Crossref","is-referenced-by-count":78,"title":["AXL receptor tyrosine kinase is required for T cell priming and antiviral immunity"],"prefix":"10.7554","volume":"5","author":[{"given":"Edward T","family":"Schmid","sequence":"first","affiliation":[{"name":"Department of Immunobiology, School of Medicine, Yale University, New Haven, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Iris K","family":"Pang","sequence":"additional","affiliation":[{"name":"Department of Immunobiology, School of Medicine, Yale University, New Haven, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eugenio 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