| First Author | Schmid ET | Year | 2016 |
| Journal | Elife | Volume | 5 |
| PubMed ID | 27350258 | Mgi Jnum | J:234329 |
| Mgi Id | MGI:5789810 | Doi | 10.7554/eLife.12414 |
| Citation | Schmid ET, et al. (2016) AXL receptor tyrosine kinase is required for T cell priming and antiviral immunity. Elife 5:e12414 |
| abstractText | The receptor tyrosine kinase (RTK) AXL is induced in response to type I interferons (IFNs) and limits their production through a negative feedback loop. 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-1beta, and defective antiviral T cell immunity. Blockade of type I IFN receptor or administration of IL-1beta 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. |
