The present knowledge of the inflammatory reaction occurring in situ during hepatitis B favors a T cell-dependent MHC-restricted immune response. However, the reports in the literature are primarily based on the application of monoclonal antibodies directed at different lymphocyte subsets which discern only lymphocytic phenotypes and do not reflect the actual situation adequately. Therefore, we investigated the liver biopsies of patients with hepatitis B (28 patients) and non-A, non-B (21 patients) by immunoelectron microscopy with monoclonal antibodies directed at lymphocyte subtypes (pan-B, pan-T, T8, T4 and NKH1) and at activation epitopes (IL-2 receptor, TA1 and T11/3) as well, in order to determine the phenotype in association with the activation status of the lymphocytes that are in close contact with hepatocytes; thus, establishing an effector-target cell relationship on the ultrastructural level.
We were able to confirm the central role of T8 lymphocytes being the predominant type of lymphocytes in close contact with liver cells in the space of Disse. A certain percentage of these cells expressed “activation” markers as IL-2 receptor, TA1 and T11/3. In acute hepatitis, the NK lymphocytes made up a fifth of all lymphocytes, whereas their number dropped below 10% in the chronic stage. There was a vague correlation between the inflammatory activity of the disease and the expression of HLA antigens (both classes I and II) on inflammatory cells and also on hepatocytes. The results did not show significant differences between hepatitis B and non-A, non-B.
Our findings underline the significance of a T lymphocyte-dependent, MHC-restricted immune response in chronic hepatitis B and non-A, non-B as the decisive mechanism which seems to be flanked by NK cell activity in the acute phase. The expression of the T11/3 antigen on many lymphocytes indicates that a certain proportion of the T lymphocytes may be activated by an antigen-independent alternative pathway.
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