Editor: Willem van Eden
Role of two distinct γδ T cell subsets during West Nile virus infection
Article first published online: 28 JUN 2008
© 2008 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved
FEMS Immunology & Medical Microbiology
Volume 53, Issue 2, pages 275–283, July 2008
How to Cite
Welte, T., Lamb, J., Anderson, J. F., Born, W. K., O'Brien, R. L. and Wang, T. (2008), Role of two distinct γδ T cell subsets during West Nile virus infection. FEMS Immunology & Medical Microbiology, 53: 275–283. doi: 10.1111/j.1574-695X.2008.00430.x
- Issue published online: 28 JUN 2008
- Article first published online: 28 JUN 2008
- Received 7 March 2008; revised 29 March 2008; accepted 22 April 2008.First published online 30 May 2008.
- West Nile;
- γδ T cell;
γδ T cells respond rapidly following West Nile virus (WNV) infection, limiting viremia and invasion of the central nervous system and thereby protecting the host from lethal encephalitis. Here, we investigated the role of two major subpopulations of peripheral γδ T cells, Vγ1+ and Vγ4+ cells, in host immunity against WNV infection. We found initially that aged mice were more susceptible to WNV infection than young mice. Following WNV challenge, Vγ1+ cells in young mice expanded significantly whereas Vγ4+ cells expanded modestly. In contrast, aged mice exhibited a slower and reduced response of Vγ1+ cells but maintained a higher content of Vγ4+ cells. Vγ1+ cells were the major γδ subset producing IFN-γ during WNV infection. Mice depleted of Vγ1+ cells had an enhanced viremia and higher mortality to WNV encephalitis. Vγ4+ cells had a higher potential for producing tumor necrosis factor-α (TNF-α), a cytokine known to be involved in blood–brain barrier compromise and WNV entry into the brain. Depletion of Vγ4+ cells reduced TNF-α level in the periphery, accompanied by a decreased viral load in the brain and a lower mortality to WN encephalitis. These results suggest that Vγ1+ and Vγ4+ cells play distinct roles in protection and pathogenesis during WNV infection.