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Title 

Hepatitis B virus X protein induced expression of interleukin 18 (IL-18) : a potential mechanism for liver injury caused by hepatitis B virus (HBV) infection

Authors 

M O LeeY H ChoiE C ShinH J KangY M KimS Y JeongJ K SeongDae Yeul YuH S ChoJ H ParkS J Kim

Publisher 

Elsevier

Issue Date 

2002

Citation 

Journal of Hepatology, vol. 37, no. 3, pp. 380-386

Keywords 

fas ligandhepatitis B virus X proteininterleukin 18liver injurydoxycyclineFAS ligandneutralizing antibodyunclassified drugvirus proteinFasl protein, mouse

Abstract 

Background/Aims: The hepatitis B virus X protein (HBx), a major viral transactivator, is implicated in hepatic inflammation, since it induces many pro-inflammatory cytokines at transcriptional level. The aim of this study was to investigate role of HBx in expression of interleukin 18 (IL-18), a newly identified cytokine that up-regulates Fas ligand (FasL) expression. Methods: Chang X-34 that expressing HBx under the control of a doxycycline-inducible promoter, and hepatitis B virus (HBV)-integrated hepatoma cell lines were examined for IL-18 expression by Northern and Western blotting analysis. To test the role of IL-18 produced by hepatoma cells, FasL expression was examined by flow cytometry after treatment with neutralizing anti-IL-18 antibodies. Further, IL-18 expression was examined in the liver tissues of HBx-transgenic mice. Results: Induction of IL-18 following HBx expression in Chang X-34 and the pattern of IL-18 expression in HBV-integrated cell lines, implicated that HBx transcriptionally induces IL-18 expression. Neutralizing anti-IL-18 antibodies blocked the expression of FasL, suggesting that IL-18 plays a critical role in FasL expression. Further, IL-18 expression in the HBx-transgenic liver, was correlated with the degree of hepatitis. Conclusions: Our results demonstrated that HBx induces IL-18 expression in liver, which may be associated with hepatic injury by amplifying FasL expression during HBV infection.

ISSN 

0168-8278

Link 

http://dx.doi.org/10.1016/S0168-8278(02)00181-2

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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