CD94-NKG2A receptors regulate antiviral CD8+T cell responses

被引：185

作者：

Moser, JM

Gibbs, J

Jensen, PE

Lukacher, AE ^{[1
]}

机构：

[1] Emory Univ, Sch Med, Dept Pathol, Atlanta, GA 30322 USA

[2] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA

来源：

NATURE IMMUNOLOGY | 2002年 / 3卷 / 02期

关键词：

D O I：

10.1038/ni757

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：189 / 195

页数：7

共 51 条

[1] Innate immune response of the human host to exposure with herpes simplex virus type 1: In vitro control of the virus infection by enhanced natural killer activity via interleukin-15 induction [J].