Jan 29, 2002

CD94-NKG2A receptors regulate antiviral CD8(+) T cell responses

Nature Immunology
Janice M MoserAron E Lukacher

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.

Mentioned in this Paper

Tumor Virus Infections
Killer Cell Lectin-Like Receptor Subfamily C, Member 3
Mice, Inbred CBA
T-Lymphocyte
Klrd1 protein, mouse
Leukocyte Differentiation Antigens, Human
Suppressor T-Lymphocytes, CD8-Positive
Neoplasms
CD94 Antigen
KLRD1 wt Allele

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