Hepatitis B Virus Down-Regulates Expressions of MHC Class I Molecules on Hepatoplastoma Cell Line

Introduction Hepatitis B virus (HBV) is regarded as one of the most fatal human pathogens. Infection with HBV can cause transient and chronic liver inflammation. Many chronically infected people will gradually acquire severe liver cirrhosis and may eventually progress to hepatocellular carcinoma (1). With an estimated population of 350 million individuals chronically infected and approximately one million deaths annually in the world, it is of great importance to demonstrate the key points…

Hepatitis B Virus Down-Regulates Expressions of MHC Class I Molecules on Hepatoplastoma Cell Line

Chronic HBV infection is associated with a 100-fold high risk of developing hepatocellular carcinoma. Tumor recognition is of the most importance during the immune surveillance process that prevents cancer development in humans. In the present study, the expressions of MHC class I molecules on hepatoplastoma cell line HepG2.2.15 were investigated to indicate the possible effects of HBV on the immune recognition during HBV-associated hepatocellular carcinoma. It was found that the expressions of MHC class I molecules HLA-ABC, HLA-E and MICA were much lower in HepG2.2.15 cells compared with HepG2 cells. The expressing HBV in human hepatoplastoma cell line significantly down-regulated the expressions of MHC class I molecules. Additionally, it was observed that in murine chronic HBsAg carriers the expression of classical MHC-I molecule on hepatocytes was down-regulated. These results demonstrated that HBV might affect the immune recognition during HBV- associated hepatocellular carcinoma such as the recognition of CD8+ T, NK-CTL and NK cells and prevent the immune surveillance against tumors. However, the effects of HBV down-regulation of MHC class I molecules on the target cells in vivo should be further studied