Journal
JOURNAL OF VIROLOGY
Volume 79, Issue 17, Pages 11457-11466Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.79.17.11457-11466.2005
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Funding
- NCI NIH HHS [R01 CA069212, R01CA069212] Funding Source: Medline
- NINDS NIH HHS [R01 NS052632, K02NS045607, R01NS052632-01, K02 NS045607] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA069212] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [K02NS045607, R01NS052632] Funding Source: NIH RePORTER
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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.
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