Downregulation of natural killer cell-activating ligand CD155 by human cytomegalovirus UL141

被引:205
作者
Tomasec, P
Wang, ECY
Davison, AJ
Vojtesek, B
Armstrong, M
Griffin, C
McSharry, BP
Morris, RJ
Llewellyn-Lacey, S
Rickards, C
Nomoto, A
Sinzger, C
Wilkinson, GWG
机构
[1] Cardiff Univ, Coll Med, Sect Infect & Immun, Cardiff CF14 4XX, S Glam, Wales
[2] Inst Virol, MRC, Virol Unit, Glasgow G11 5JR, Lanark, Scotland
[3] Masaryk Mem Canc Inst, Brno 65653, Czech Republic
[4] Univ Tokyo, Grad Sch Med, Dept Microbiol, Tokyo, Japan
[5] Univ Tubingen, Tubingen, Germany
基金
英国惠康基金; 英国医学研究理事会;
关键词
D O I
10.1038/ni1156
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Natural killer (NK) cells are crucial in the control of cytomegalovirus infections in mice and humans. Here we show that the viral UL141 gene product has an immunomodulatory function that is associated with low-passage strains of human cytomegalovirus. UL141 mediated efficient protection of cells against killing by a wide range of human NK cell populations, including interferon-alpha- stimulated bulk cultures, polyclonal NK cell lines and most NK cell clones tested. Evasion of NK cell killing was mediated by UL141 blocking surface expression of CD155, which was previously identified as a ligand for NK cell-activating receptors CD226 (DNAM-1) and CD96 (TACTILE). The breadth of the UL141-mediated effect indicates that CD155 has a key role in regulating NK cell function.
引用
收藏
页码:181 / 188
页数:8
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