Nature Immunology
3, 189 - 195 (2002)
Published online: 22 January 2002; | doi:10.1038/ni757
CD94-NKG2A receptors regulate antiviral CD8+ T cell responsesJanice M. Moser1, James Gibbs2, Peter E. Jensen1
& Aron E. Lukacher11
Department of Pathology, Emory University School of Medicine, Atlanta, GA 30322, USA. 2
Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Correspondence should be addressed to Aron E. Lukacher alukach@emory.eduCD8+ T lymphocytes mediate immunosurveillance against persistent virus infections and virus-induced neoplasia. Polyoma virus, a highly oncogenic natural mouse DNA virus, establishes persistent infection, but only a few mice are highly susceptible to tumors induced by the virus. Mature antiviral CD8+ T cells expand in tumor-susceptible mice, but their cytotoxic effector activity is nonfunctional in vivo. Here we show that the natural killer cell inhibitory receptor, CD94-NKG2A, is up-regulated by antiviral CD8+ T cells during acute polyoma infection and is responsible for down-regulating their antigen-specific cytotoxicity during both viral clearance and virus-induced oncogenesis.
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