Downregulation of the stress-induced ligand ULBP1 following SV40 infection confers viral evasion from NK cell cytotoxicity.
Downregulation of the stress-induced ligand ULBP1 following SV40 infection confers viral evasion from NK cell cytotoxicity.
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DOI：
10.18632/oncotarget.8085
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发表时间：
2016-03-29
期刊：
影响因子：
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通讯作者：
Mandelboim O
中科院分区：
文献类型：
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作者：
Bauman Y;Drayman N;Ben-Nun-Shaul O;Vitenstein A;Yamin R;Ophir Y;Oppenheim A;Mandelboim O
多瘤病毒是在人群中流行的病毒的不同家族。然而，这些病毒与免疫系统的相互作用还没有得到很好的表征。我们之前已经证明，两种人类多瘤病毒JC和BK使用相同的microRNA来逃避自然杀伤（NK）细胞的免疫攻击。我们发现这种病毒microRNA抑制ULBP3表达，ULBP3是一种应激诱导的杀伤受体NKG2D配体。在这里，我们表明，猿猴病毒40（SV40）也通过下调另一种应激诱导的NKG2D配体ULBP 1来逃避NK细胞的攻击。这些发现表明NK细胞在对抗多瘤病毒感染中起着至关重要的作用，并进一步强调了ULBP家族的各种成员在控制多瘤病毒感染中的重要性。
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.