[Immunopathological mechanisms responsible for hepatic lesions caused by B virus]

Clinical and experimental observations suggested that liver lesions related to Hepatitis B Virus infection were the result of an immunological process similar to that observed in graft rejection. Virus-antigens (Ag) and particularly, HBsAg expressed on the hepatocyte-membrane are the best candidates as target-Ag. Constituents of the hepatocyte membrane itself and particularly Liver Specific Protein (LSP) are also susceptible to represent targets for an auto-immune attack. Humoral immunity does not seem to be involved in the pathogenesis of the liver lesions; specific antibodies have a protective more than an aggressive role in hepatitis, and immune-complexes are responsible for extra-hepatic lesions. In vitro studies of lymphocytotoxicity against autologous liver cells or rabbit hepatocytes have demonstrated the predominant role of T-lymphocytes in acute hepatitis and that of K lymphocytes in HBsAg positive chronic active hepatitis. The role of Natural Killer cells has not been clearly precised up to now. Analysis of the experimental data has to be cautious because of the diversity of in vitro models and difficulty in interpretation of the results. A better understanding of the immune mechanisms involved in the progression of the disease to chronicity, cirrhosis and hepatocellular carcinoma could allow more suitable treatments according to immunological status of the patients and virus-markers in the serum and the liver.