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The Journal of Immunology, 2003, 171: 2524-2531.
Copyright © 2003 by The American Association of Immunologists

IFN-{gamma}-Producing {gamma}{delta} T Cells Help Control Murine West Nile Virus Infection 1

Tian Wang*, Eileen Scully*,{ddagger}, Zhinan Yin*, Jung H. Kim{dagger}, Sha Wang{dagger}, Jun Yan*, Mark Mamula*, John F. Anderson§, Joe Craft*,{ddagger} and Erol Fikrig*,2

* Department of Internal Medicine, Section of Rheumatology and {dagger} Department of Pathology, Yale University School of Medicine, New Haven, CT 06520; {ddagger} Section of Immunobiology, Yale University, New Haven, CT 06520; and § Department of Entomology, Connecticut Agricultural Experiment Station, New Haven, CT 06504

West Nile (WN) virus causes fatal meningoencephalitis in laboratory mice, thereby partially mimicking human disease. Using this model, we have demonstrated that mice deficient in {gamma}{delta} T cells are more susceptible to WN virus infection. TCR{delta}-/- mice have elevated viral loads and greater dissemination of the pathogen to the CNS. In wild-type mice, {gamma}{delta} T cells expanded significantly during WN virus infection, produced IFN-{gamma} in ex vivo assays, and enhanced perforin expression by splenic T cells. Adoptive transfer of {gamma}{delta} T cells to TCR{delta}-/- mice reduced the susceptibility of these mice to WN virus, and this effect was primarily due to IFN-{gamma}-producing {gamma}{delta} T cells. These data demonstrate a distinct role for {gamma}{delta} T cells in the control of and prevention of mortality from murine WN virus infection.


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