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Immune Network ; : 126-134, 2010.
Article in English | WPRIM | ID: wpr-96923

ABSTRACT

BACKGROUND: CD8+ T cells contribute to the clearance of Hepatitis B virus (HBV) infection and an insufficient CD8+ T cell response may be one of the major factors leading to chronic HBV infection. Since the HBx antigen of HBV can up-regulate cellular expression of several immunomodulatory molecules, we hypothesized that HBx expression in hepatocytes might affect CD8+ T cell activity. METHODS: We analyzed the activation and apoptosis of CD8+ T cells co-cultured with primary hepatocytes rendered capable of expressing HBx by recombinant baculovirus infection. RESULTS: Expression of HBx in hepatocytes induced low production of interferon-gamma and apoptosis of CD8+ T cells, with no effect on CD8 T cell proliferation. However, transcriptional levels of H-2K, ICAM-1 and PD-1 ligand did not correlate with HBx expression in hepatocytes. CONCLUSION: Our results suggest that HBx may inhibit CD8+ T cell response by regulation of interferon-gamma production and apoptosis.


Subject(s)
Apoptosis , Baculoviridae , Cell Proliferation , Hepadnaviridae , Hepatitis , Hepatitis B , Hepatitis B virus , Hepatocytes , Intercellular Adhesion Molecule-1 , Interferon-gamma , T-Lymphocytes , Trans-Activators , Viral Proteins
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