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前沿:NKG2C(高表达)CD57+NK 细胞特异性地对巨细胞病毒的急性感染产生应答,而不是对 EBV 产生应答。

Cutting edge: NKG2C(hi)CD57+ NK cells respond specifically to acute infection with cytomegalovirus and not Epstein-Barr virus.

机构信息

Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143;

出版信息

J Immunol. 2014 May 15;192(10):4492-6. doi: 10.4049/jimmunol.1303211. Epub 2014 Apr 16.

DOI:10.4049/jimmunol.1303211
PMID:24740502
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4013527/
Abstract

CMV induces the expansion of a unique subset of human NK cells expressing high levels of the activating CD94-NKG2C receptor that persist after control of the infection. We investigated whether this subset is CMV specific or is also responsive to acute infection with EBV. We describe a longitudinal study of CMV(-) and CMV(+) students who were acutely infected with EBV. The NKG2C(hi) NK subset was not expanded by EBV infection. However, EBV infection caused a decrease in the absolute number of immature CD56(bright)CD16(-) NK cells in the blood and, in CMV(+) individuals, induced an increased frequency of mature CD56(dim)NKG2A(+)CD57(+) NK cells in the blood that persisted into latency. These results provide further evidence that NKG2C(+) NK cells are CMV specific and suggest that EBV infection alters the repertoire of NK cells in the blood.

摘要

巨细胞病毒(CMV)诱导表达高水平激活型 CD94-NKG2C 受体的独特人类 NK 细胞亚群扩增,这种扩增在感染得到控制后仍然存在。我们研究了这个亚群是否是 CMV 特异性的,还是也对 EBV 的急性感染有反应。我们描述了一项对 CMV(-)和 CMV(+)学生的纵向研究,他们急性感染 EBV。EBV 感染并没有使 NKG2C(hi)NK 亚群扩增。然而,EBV 感染导致血液中不成熟 CD56(bright)CD16(-)NK 细胞的绝对数量减少,并且在 CMV(+)个体中,诱导血液中成熟 CD56(dim)NKG2A(+)CD57(+)NK 细胞的频率增加,这种增加持续到潜伏阶段。这些结果进一步证明了 NKG2C(+)NK 细胞是 CMV 特异性的,并表明 EBV 感染改变了血液中 NK 细胞的 repertoire。

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