CD94-NKG2A receptors regulate antiviral CD8+T cell responses
CD94-NKG2A receptors regulate antiviral CD8+T cell responses
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DOI：
10.1038/ni757
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发表时间：
2002-02-01
影响因子：
30.5
通讯作者：
Lukacher, AE
中科院分区：
文献类型：
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作者：
Moser, JM;Gibbs, J;Lukacher, AE
CD8(+) T淋巴细胞介导对持续病毒感染和病毒诱导的肿瘤的免疫监视。多瘤病毒是一种高致癌性的天然小鼠DNA病毒，可建立持续感染，但只有少数小鼠对该病毒诱导的肿瘤高度敏感。成熟的抗病毒CD8(+) T细胞在肿瘤易感小鼠体内扩增，但其细胞毒效应活性在体内无功能。在这里，我们发现自然杀伤细胞抑制受体CD94-NKG2A在急性多瘤感染期间被抗病毒CD8(+) T细胞上调，并在病毒清除和病毒诱导的肿瘤发生期间负责下调其抗原特异性细胞毒性。
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.