ULBP1 is induced by hepatitis C virus infection and is the target of the NK cell-mediated innate immune response in human hepatocytes

被引：9

作者：

Dansako, Hiromichi ^{[1
]}

Imai, Hirotaka ^{[1
]}

Ueda, Youki ^{[1
]}

Satoh, Shinya ^{[1
]}

Wakita, Takaji ^{[2
]}

Kato, Nobuyuki ^{[1
]}

机构：

[1] Okayama Univ, Dept Tumor Virol, Grad Sch Med Dent & Pharmaceut Sci, Okayama, Japan

[2] Natl Inst Infect Dis, Dept Virol 2, Tokyo, Japan

来源：

FEBS OPEN BIO | 2018年 / 8卷 / 03期

关键词：

HCV RNA replication; hepatitis C virus; innate immune response; NK cell; ULBP1; NATURAL-KILLER-CELLS; NKG2D RECEPTOR; HEPATOCELLULAR-CARCINOMA; SIGNALING PATHWAY; INTERFERON-BETA; CORE PROTEIN; DNA-DAMAGE; LIGANDS; CYTOTOXICITY; SUPPRESSION;

D O I：

10.1002/2211-5463.12373

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Natural killer (NK) cells through their NK group 2 member D (NKG2D) receptors recognize NKG2D ligands such as UL16-binding proteins (ULBPs) on virus-infected cells and subsequently trigger the host innate immune response. In the present study, we demonstrated that hepatitis C virus (HCV) induced the cell surface expression of ULBP1 in human immortalized hepatocyte PH5CH8 cells and human hepatoma HuH-7 cell-derived RSc cells. Interestingly, NK cell line NK-92 induced cytotoxicity and interferon- mRNA expression and subsequently reduced the levels of HCV RNA replication during co-culture with HCV-infected RSccells. From these results, we conclude that ULBP1 is a target of the NK cell-mediated innate immune response in HCV-infected human hepatocytes.

引用

收藏

页码：361 / 371

页数：11

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