Human Factors and Behavioral Neurobiology
CD8 T cells are crucial components of immunity and play a vital role in recovery from West Nile virus (WNV) infection. Here, we identify a previously unrecognized function of interleukin-17A (IL-17A) in inducing cytotoxic-mediator gene expression and promoting CD8 T cell cytotoxicity against WNV infection in mice. We find that IL-17A-deficient (Il17a/) mice are more susceptible to WNV infection and develop a higher viral burden than wild-type (WT) mice. Interestingly, the CD8 T cells isolated from Il17a/ mice are less cytotoxic and express lower levels of cytotoxic-mediator genes, which can be restored by supplying recombinant IL-17A in vitro and in vivo. Importantly, treatment of WNV-infected mice with recombinant IL17A, as late as day 6 post infection, significantly reduces the viral burden and increases survival, suggesting a therapeutic potential for IL-17A. In conclusion, we report a novel function of IL-17A in promoting CD8 T cell cytotoxicity, which may have broad implications in other microbial infections and cancers.
Journal of Virology
American Society for Microbiology
Grant or Award Name
National Institutes of Health grants AI099625 and AI103807
Scholarly Commons Citation
Acharya D, Wang P, Paul AM, Dai J, Gate D ,Lowery JE,Stokic DS, Leis AA, Flave llRA, TownT,FikrigE,BaiF.2017.Interleukin-17A promotesCD8+Tcellcytotoxicitytofacilitate WestNilevirusclearance.JVirol91:e01529-16. https://doi.org/10.1128/JVI.01529-16.