Down-regulation of the NKG2D ligand MICA by the human cytomegalovirus glycoprotein UL142

被引：144

作者：

Chalupny, NJ ^{[1
]}

Rein-Weston, A ^{[1
]}

Dosch, S ^{[1
]}

Cosman, D ^{[1
]}

机构：

[1] Amgen Inc, Seattle, WA 98119 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2006年 / 346卷 / 01期

关键词：

NK cell; cytotoxicity; HCMV; MICA; UL142;

D O I：

10.1016/j.bbrc.2006.05.092

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Human cytomegalovirus (HCMV) employs a variety of strategies to modify or evade the host immune response, and natural killer (NK) cells play a crucial role in controlling cytomegalovirus infections in mice and humans. Activation of NK cells through the receptor NKG2D/DAP10 leads to killing of NKG2D ligand-expressing cells. We have previously shown that HCMV is able to down-regulate the surface expression of some NKG2D ligands, ULBP1, ULBP2, and MICB via the viral glycoprotein UL16. Here, we show that the viral gene product UL142 is able to down-regulate another NKG2D ligand, MICA, leading to protection from NK cytotoxicity. UL142 is not able to affect surface expression of all MICA alleles, however, which may reflect selective pressure on the host to thwart viral immune evasion, further supporting an important role for the MICA-NKG2D interaction in immune surveillance. (c) 2006 Elsevier Inc. All rights reserved.

引用

页码：175 / 181

页数：7

共 44 条

[1] Lentivirus vectors encoding both central polypurine tract and posttranscriptional regulatory element provide enhanced transduction and transgene expression [J].