1990 Fiscal Year Final Research Report Summary
Molecular Biological Study on the Mechanism of Hepatocellular Injury of type B Hepatitis
| Project/Area Number |
01570390
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Osaka University |
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Principal Investigator |
FUSAMOTO Hideyuki Osaka University Medical School Lecturer, 医学部, 講師 (90124776)
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| Co-Investigator(Kenkyū-buntansha) |
SASAKI Yutaka Osaka University Medical School Assistant, 医学部, 助手
KASAHARA Akinori Osaka University Medical School Assistant, 医学部, 助手 (70214286)
HAYASHI Norio Osaka University Medical School Lecturer, 医学部, 講師 (00144478)
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| Project Period (FY) |
1989 – 1990
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| Keywords | Type B Hepatitis / HBV / Molecular Biology |
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| Research Abstract |
In order to clarify the mechanism of hepatocellular injury in patients with type B hepatitis, we examined gamma-interferon production of peripheral blood mononuclear cells (PBMCs) from patients with type B hepatitis. Gamma-interferon production of PBMCs from patients with active liver injury were enhanced by HBcAg but not HBsAg, whereas those with inactive liver injury were not affected by HBcAg nor HBsAg. Further, These responsiveness of PBMCs to HBcAg closely correlated to serum levels of aminotransferase during their clinical course, but those to HBsAg did not at all. These results indicated that cellular immune response to HBcAg was responsible for hepatocellular injury in patients with type B hepatitis. Moreover, activated T cells in the liver had significantly increased compared with those in peripheral blood, and there were significantly more activated T cells in the livers of the patients with active liver disease than in those with inactive liver injury. HLA class I Ag was also expressed on the membrane of hapatocyte of patients with active liver injury. In contrast, we also showed that, in HBV-DNA integrated hepatoblastoma cell line, HBV replication suppressed the expression of HLA class I Ag on the membrane induced by gamma-interferon, and that pre-incubation of PBMCs with HBcAg/HBeAg suppressed gamma-interferon production of PHA-stimulated PBMCs. Our conclusion reached is that cellular immune response to HBcAg may cause liver injury and the poor responsiveness in patients with type B hepatitis can be responsible for establishment of chronicity of HBV infection.
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