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

Hiromichi Dansako; Hirotaka Imai; Youki Ueda; Shinya Satoh; Takaji Wakita; Nobuyuki Kato

doi:10.1002/2211-5463.12373

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

Hiromichi Dansako, Hirotaka Imai, Youki Ueda, Shinya Satoh, Takaji Wakita, Nobuyuki Kato

Research output: Contribution to journal › Article › peer-review

7 Citations (Scopus)

Abstract

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-γ mRNA expression and subsequently reduced the levels of HCV RNA replication during co-culture with HCV-infected RSc cells. From these results, we conclude that ULBP1 is a target of the NK cell-mediated innate immune response in HCV-infected human hepatocytes.

Original language	English
Pages (from-to)	361-371
Number of pages	11
Journal	FEBS Open Bio
Volume	8
Issue number	3
DOIs	https://doi.org/10.1002/2211-5463.12373
Publication status	Published - Mar 2018

Keywords

HCV RNA replication
NK cell
ULBP1
hepatitis C virus
innate immune response

ASJC Scopus subject areas

Biochemistry, Genetics and Molecular Biology(all)

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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

abstract = "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-γ mRNA expression and subsequently reduced the levels of HCV RNA replication during co-culture with HCV-infected RSc cells. From these results, we conclude that ULBP1 is a target of the NK cell-mediated innate immune response in HCV-infected human hepatocytes.",

keywords = "HCV RNA replication, NK cell, ULBP1, hepatitis C virus, innate immune response",

author = "Hiromichi Dansako and Hirotaka Imai and Youki Ueda and Shinya Satoh and Takaji Wakita and Nobuyuki Kato",

note = "Funding Information: We thank Marie Iwado, Masayo Takemoto, Hiroki Hiramoto and Takashi Nakamura for their technical assistance. We also thank Dr Tsuyoshi Akagi for pCX4bsr, pCX4pur and pCX4bleo retroviral vectors. This work was supported by the Practical Research on Hepatitis from Japan Agency for Medical Research and Development (AMED), and by JSPS KAKENHI Grant Number 15K08498. Publisher Copyright: {\textcopyright} 2018 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.",

year = "2018",

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doi = "10.1002/2211-5463.12373",

language = "English",

volume = "8",

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T1 - ULBP1 is induced by hepatitis C virus infection and is the target of the NK cell-mediated innate immune response in human hepatocytes

AU - Dansako, Hiromichi

AU - Imai, Hirotaka

AU - Ueda, Youki

AU - Satoh, Shinya

AU - Wakita, Takaji

AU - Kato, Nobuyuki

N1 - Funding Information: We thank Marie Iwado, Masayo Takemoto, Hiroki Hiramoto and Takashi Nakamura for their technical assistance. We also thank Dr Tsuyoshi Akagi for pCX4bsr, pCX4pur and pCX4bleo retroviral vectors. This work was supported by the Practical Research on Hepatitis from Japan Agency for Medical Research and Development (AMED), and by JSPS KAKENHI Grant Number 15K08498. Publisher Copyright: © 2018 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.

PY - 2018/3

Y1 - 2018/3

N2 - 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-γ mRNA expression and subsequently reduced the levels of HCV RNA replication during co-culture with HCV-infected RSc cells. From these results, we conclude that ULBP1 is a target of the NK cell-mediated innate immune response in HCV-infected human hepatocytes.

AB - 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-γ mRNA expression and subsequently reduced the levels of HCV RNA replication during co-culture with HCV-infected RSc cells. From these results, we conclude that ULBP1 is a target of the NK cell-mediated innate immune response in HCV-infected human hepatocytes.

KW - HCV RNA replication

KW - NK cell

KW - ULBP1

KW - hepatitis C virus

KW - innate immune response

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

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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