First Author | Klein RS | Year | 2005 |
Journal | J Virol | Volume | 79 |
Issue | 17 | Pages | 11457-66 |
PubMed ID | 16103196 | Mgi Jnum | J:101771 |
Mgi Id | MGI:3605174 | Doi | 10.1128/JVI.79.17.11457-11466.2005 |
Citation | Klein RS, et al. (2005) Neuronal CXCL10 directs CD8+ T-cell recruitment and control of West Nile virus encephalitis. J Virol 79(17):11457-66 |
abstractText | The activation and entry of antigen-specific CD8(+) T cells into the central nervous system is an essential step towards clearance of West Nile virus (WNV) from infected neurons. The molecular signals responsible for the directed migration of virus-specific T cells and their cellular sources are presently unknown. Here we demonstrate that in response to WNV infection, neurons secrete the chemokine CXCL10, which recruits effector T cells via the chemokine receptor CXCR3. Neutralization or a genetic deficiency of CXCL10 leads to a decrease in CXCR3(+) CD8(+) T-cell trafficking, an increase in viral burden in the brain, and enhanced morbidity and mortality. These data support a new paradigm in chemokine neurobiology, as neurons are not generally considered to generate antiviral immune responses, and CXCL10 may represent a novel neuroprotective agent in response to WNV infection in the central nervous system. |