- Author:
Mi Jin LEE
1
;
Young hee JIN
;
Kyongmin KIM
;
Yangkyu CHOI
;
Hyoung Chin KIM
;
Sun PARK
Author Information
- Publication Type:Original Article
- Keywords: Hepadnaviridae; T-lymphocytes; Cytotoxic; Viral proteins; Apoptosis; Interferon-gamma
- MeSH: Apoptosis; Baculoviridae; Cell Proliferation; Hepadnaviridae; Hepatitis; Hepatitis B; Hepatitis B virus; Hepatocytes; Intercellular Adhesion Molecule-1; Interferon-gamma; T-Lymphocytes; Trans-Activators; Viral Proteins
- From:Immune Network 2010;10(4):126-134
- CountryRepublic of Korea
- Language:English
- 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.