The Effects of HBcAg and HBeAg on the Expression of Cytokine Genes from Murine Macrophages

• Main Authors: Kung-yen Chang, 章公彥
• Other Authors: Cheng-po Hu
• Format: Others
• Language: en_US
• Published: 1999
• Online Access: http://ndltd.ncl.edu.tw/handle/25243027316972563926

碩士 === 國立陽明大學 === 微生物暨免疫學研究所 === 87 === The hepatitis B virus (HBV) is a noncytopathic, enveloped virus with a circular double-stranded DNA genome that caused acute and chronic necroinflammatory liver disease. Chronically infected patients with active liver disease carry a high risk of developing cirrhosis and hepatocellular carcinoma (HCC). In HBV infection, patients who successfully clear the virus demonstrate strong HLA class I and II-restricted T cell responses to all viral antigens. In contrast, the HBV-specific T cell response of chronic active hepatitis patients are weak or undetectable. Specific defects and interference of immune response leading to a malfunction of the immune system may causes HBV persistence and chronic hepatitis. In this study, the effects of HBV antigens on the expression of cytokine genes from murine macrophages were investigated. HBcAg and HBeAg were able to trigger murine peritoneal exudate cells (PEC) expressing higher levels of mRNA of many mediators, including IL-1, IL-6, IL-10, IL-12p35, IL-12p40, TNF-, TGF-, GM-CSF, iNOS and MIP-2. The production of IL-6 protein was elevated in the supernatants of PEC stimulated with HBeAg. However, such an effect did not occur when PEC were treated with HBsAg. Furthermore, using a binding assay, a specific binding of 125I-HBcAg to RAW264.7 cells was noted. Taken together, our preliminary data in this study suggest that HBV may interfere the host immune response by secreting HBeAg which is able to interact with one of the most important host immune cells, macrophages.