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Increased susceptibility to liver injury in hepatitis B virus transgenic mice involves NKG2D-ligand interaction and natural killer cells

The innate immunopathogenesis responsible for the susceptibility to hepatocyte injury in chronic hepatitis B surface antigen carriers is not well defined. In this study, hepatitis B virus (HBV) transgenic mice (named HBs-Tg) were oversensitive to liver injury after immunologic [polyinosinic:polycyti... Full description

Journal Title: Hepatology (Baltimore Md.), September 2007, Vol.46(3), pp.706-15
Main Author: Chen, Yongyan
Other Authors: Wei, Haiming , Sun, Rui , Dong, Zhongjun , Zhang, Jian , Tian, Zhigang
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0270-9139 ; PMID: 17626270 Version:1
Link: http://pubmed.gov/17626270
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recordid: medline17626270
title: Increased susceptibility to liver injury in hepatitis B virus transgenic mice involves NKG2D-ligand interaction and natural killer cells
format: Article
creator:
  • Chen, Yongyan
  • Wei, Haiming
  • Sun, Rui
  • Dong, Zhongjun
  • Zhang, Jian
  • Tian, Zhigang
subjects:
  • Carrier State -- Immunology
  • Chemical and Drug Induced Liver Injury -- Immunology
  • Hepatitis B Surface Antigens -- Immunology
  • Hepatitis B Virus -- Immunology
  • Killer Cells, Natural -- Immunology
  • Receptors, Immunologic -- Metabolism
ispartof: Hepatology (Baltimore, Md.), September 2007, Vol.46(3), pp.706-15
description: The innate immunopathogenesis responsible for the susceptibility to hepatocyte injury in chronic hepatitis B surface antigen carriers is not well defined. In this study, hepatitis B virus (HBV) transgenic mice (named HBs-Tg) were oversensitive to liver injury after immunologic [polyinosinic:polycytidylic acid or concanavalin A (ConA)] or chemical (CCl4) triggering. It was then found that the nonhepatotoxic low dose of ConA for wild-type mice induced severe liver injury in HBs-Tg mice, which was dependent on the accumulated intraheptic natural killer (NK) cells. Expressions of NKG2D ligands (Rae-1 and Mult-1) in hepatocytes were markedly enhanced upon ConA stimulation in HBs-Tg mice, which greatly activated hepatic NK cells via NKG2D/Rae-1 or Mult-1 recognition. Interestingly, the presence of NK T cells was necessary for NK cell activation and worked as positive helper cell possibly by producing interferon-gamma and interleukin-4 in this process. Our findings for the first time suggested the critical role of NKG2D recognition of hepatocytes by NK cells in oversensitive liver injury during chronic HBV infection.
language: eng
source:
identifier: ISSN: 0270-9139 ; PMID: 17626270 Version:1
fulltext: fulltext
issn:
  • 02709139
  • 0270-9139
url: Link


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titleIncreased susceptibility to liver injury in hepatitis B virus transgenic mice involves NKG2D-ligand interaction and natural killer cells
creatorChen, Yongyan ; Wei, Haiming ; Sun, Rui ; Dong, Zhongjun ; Zhang, Jian ; Tian, Zhigang
ispartofHepatology (Baltimore, Md.), September 2007, Vol.46(3), pp.706-15
identifierISSN: 0270-9139 ; PMID: 17626270 Version:1
subjectCarrier State -- Immunology ; Chemical and Drug Induced Liver Injury -- Immunology ; Hepatitis B Surface Antigens -- Immunology ; Hepatitis B Virus -- Immunology ; Killer Cells, Natural -- Immunology ; Receptors, Immunologic -- Metabolism
descriptionThe innate immunopathogenesis responsible for the susceptibility to hepatocyte injury in chronic hepatitis B surface antigen carriers is not well defined. In this study, hepatitis B virus (HBV) transgenic mice (named HBs-Tg) were oversensitive to liver injury after immunologic [polyinosinic:polycytidylic acid or concanavalin A (ConA)] or chemical (CCl4) triggering. It was then found that the nonhepatotoxic low dose of ConA for wild-type mice induced severe liver injury in HBs-Tg mice, which was dependent on the accumulated intraheptic natural killer (NK) cells. Expressions of NKG2D ligands (Rae-1 and Mult-1) in hepatocytes were markedly enhanced upon ConA stimulation in HBs-Tg mice, which greatly activated hepatic NK cells via NKG2D/Rae-1 or Mult-1 recognition. Interestingly, the presence of NK T cells was necessary for NK cell activation and worked as positive helper cell possibly by producing interferon-gamma and interleukin-4 in this process. Our findings for the first time suggested the critical role of NKG2D recognition of hepatocytes by NK cells in oversensitive liver injury during chronic HBV infection.
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abstractThe innate immunopathogenesis responsible for the susceptibility to hepatocyte injury in chronic hepatitis B surface antigen carriers is not well defined. In this study, hepatitis B virus (HBV) transgenic mice (named HBs-Tg) were oversensitive to liver injury after immunologic [polyinosinic:polycytidylic acid or concanavalin A (ConA)] or chemical (CCl4) triggering. It was then found that the nonhepatotoxic low dose of ConA for wild-type mice induced severe liver injury in HBs-Tg mice, which was dependent on the accumulated intraheptic natural killer (NK) cells. Expressions of NKG2D ligands (Rae-1 and Mult-1) in hepatocytes were markedly enhanced upon ConA stimulation in HBs-Tg mice, which greatly activated hepatic NK cells via NKG2D/Rae-1 or Mult-1 recognition. Interestingly, the presence of NK T cells was necessary for NK cell activation and worked as positive helper cell possibly by producing interferon-gamma and interleukin-4 in this process.
pmid17626270
doi10.1002/hep.21872
eissn15273350
date2007-09