title: Platelets promote liver immunopathology contributing to hepatitis B virus-mediated hepatocarcinogenesis.
abstract: Chronic hepatitis B virus (HBV) infection is a major risk factor for the development of hepatocellular carcinoma (HCC). Among the pathogenetic factors triggered by HBV, virus-specific CD8(+) T cells play and important role in disease pathogenesis by promoting necroinflammatory liver damage. Accordingly, amelioration of immune-mediated chronic liver injury may prevent HCC. Platelets facilitate this process by sustaining the hepatic accumulation of virus-specific CD8(+) T cells and subsequently other virus nonspecific inflammatory cells that contribute to liver disease. Importantly, a recent study shows that the long-term use of clinically relevant doses of the anti-platelet drugs aspirin and clopidogrel, administered after the onset of liver disease, in an HBV transgenic mouse model of immune-mediated chronic hepatitis and HCC, can prevent hepatocarcinogenesis improving overall survival. Platelets therefore, act as key players in the pathogenesis of HBV-associated liver cancer supporting the notion that immune-mediated necroinflammatory liver disease is sufficient to trigger HCC and that interference with platelet activation may have clinical implications for HCC prevention.
authors.affiliation: Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milan, Italy. Electronic address: sitia.giovanni@hsr.it.
authors.forename: Giovanni
authors.initials: G
authors.lastname: Sitia
mesh_terms: D000818:Animals; D001792:Blood Platelets / Q000276:immunology* / Q000473:pathology; D006509:Hepatitis B / Q000150:complications*; D006515:Hepatitis B virus / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology*; D008113:Liver Neoplasms / Q000097:blood / Q000209:etiology* / Q000473:pathology*; D051379:Mice