Abstract
CD8(+) 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.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Antigens, CD / metabolism*
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CD8-Positive T-Lymphocytes / immunology*
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Cell Transformation, Viral
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Cytotoxicity, Immunologic
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Immunologic Memory
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Immunologic Surveillance
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Lectins, C-Type*
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Membrane Glycoproteins / metabolism*
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Mice
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Mice, Inbred C3H
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Mice, Inbred CBA
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NK Cell Lectin-Like Receptor Subfamily C
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NK Cell Lectin-Like Receptor Subfamily D
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Polyomavirus Infections / immunology*
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Receptors, Immunologic / metabolism*
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Receptors, Natural Killer Cell
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Tumor Virus Infections / immunology*
Substances
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Antigens, CD
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Klrc1 protein, mouse
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Klrd1 protein, mouse
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Lectins, C-Type
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Membrane Glycoproteins
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NK Cell Lectin-Like Receptor Subfamily C
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NK Cell Lectin-Like Receptor Subfamily D
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Receptors, Immunologic
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Receptors, Natural Killer Cell