Downregulation of the stress-induced ligand ULBP1 following SV40 infection confers viral evasion from NK cell cytotoxicity

被引：18

作者：

Bauman, Yoav ^{[1
]}

Drayman, Nir ^{[2
]}

Ben-Nun-Shaul, Orly ^{[2
]}

Vitenstein, Alon ^{[1
]}

Yamin, Rachel ^{[1
]}

Ophir, Yael ^{[1
]}

Oppenheim, Ariella ^{[2
]}

Mandelboim, Ofer ^{[1
]}

机构：

[1] Hebrew Univ Jerusalem, Hadassah Med Sch, Lautenberg Ctr Gen & Tumor Immunol, BioMed Res Inst Israel Canada,Fac Med IMRIC, IL-91010 Jerusalem, Israel

[2] Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Hematol, IL-91010 Jerusalem, Israel

来源：

ONCOTARGET | 2016年 / 7卷 / 13期

基金：

欧洲研究理事会; 以色列科学基金会;

关键词：

SV40; ULBP1; immune-evasion; NK cells; NKG2D; Immunology and Microbiology Section; Immune response; Immunity; NATURAL-KILLER-CELLS; GENE-EXPRESSION; CAPSID PROTEINS; IMMUNE-RESPONSE; NKG2D LIGANDS; RECOGNITION; VIRUS; SIMIAN-VIRUS-40; RECEPTORS; TUMOR;

D O I：

10.18632/oncotarget.8085

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Polyomaviruses are a diverse family of viruses which are prevalent in the human population. However, the interactions of these viruses with the immune system are not well characterized. We have previously shown that two human polyomaviruses, JC and BK, use an identical microRNA to evade immune attack by Natural Killer (NK) cells. We showed that this viral microRNA suppresses ULBP3 expression, a stress induced ligand for the killer receptor NKG2D. Here we show that Simian Virus 40 (SV40) also evades NK cell attack through the down regulation of another stress-induced ligand of NKG2D, ULBP1. These findings indicate that NK cells play an essential role in fighting polyomavirus infections and further emphasize the importance of various members of the ULBP family in controlling polyomavirus infection.

引用

页码：15369 / 15381

页数：13