Spontane (SCMC) und antikörperabhängige (ADCC) zelluläre Zytotoxizität bei Patienten mit akuter Hepatitis und chronisch aktiver Hepatitis

Hütteroth, T. H.; Poralla, T.; Büschenfelde, K H Meyer zum

doi:10.1007/bf02593863

Cited by 16 publications

(5 citation statements)

References 26 publications

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“…The deposits of immunoglobulins, especially of IgG type seems to indicate that a ADCC may at least represent one of the immune mechanisms by which the organism tries to eliminate viruses or HBV-infected cells (15,16).…”

Section: Discussionmentioning

confidence: 99%

Immunoelectron microscopic observations on the inflammatory infiltrates and HLA antigens in hepatitis B and non-A, Non-B

et al. 1987

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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.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 99%

Immunoelectron microscopic observations on the inflammatory infiltrates and HLA antigens in hepatitis B and non-A, Non-B

et al. 1987

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“…However, the alterations observed in immune cellular reactions, particularly NK function, are contradictory. For example, NK activity was augmented (14,15) (17). Furthermore, Colucci et al (18) failed to demonstrate non-T lymphocytes in the mononuclear cells liver infiltrate of patients CAH suggesting either poor sensitivity of the staining method used for NK cells detection or lack of non-T cytotoxic activity in situ.…”

Section: Discussionmentioning

confidence: 99%

Lack ofin vivo activation of the interferon system in HBsAg-positive chronic active hepatitis

Poitrine

Chousterman

et al. 1985

Hepatology

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The in vivo activation state of the interferon system was biochemically evaluated in patients with HBsAg-positive liver disease by assaying the interferon-induced enzyme, 2'5'-oligoadenylate synthetase, in peripheral blood mononuclear cells. All patients with chronic active hepatitis had normal levels of enzyme activity. Increased values were found in 77% of patients with acute hepatitis, 50% of those with chronic persistent hepatitis and 54% chronic healthy carriers. These results provide evidence for lack of activation of the interferon system in HBsAg-positive chronic active hepatitis and support the hypothesis that an in vivo defective interferon response may aid in development of chronic active hepatitis.

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“…(26,27). This redistribution may be responsible for the increased hepatocellular injury due to antibody-dependent, cell-mediated cytotoxicity or T-cell mediated cytotoxicity (28,29). Presence of anti-HBc IgM superimposed on already existing anti-HBc IgG may reflect activity of B-cells exposed for the first time to HBcAg released from hepatocytes.…”

Section: )mentioning

confidence: 99%

Detection of Anti-HBc IgM Following Prednisone Treatment in Patients with Chronic Active Hepatitis B Virus Infection

et al. 1984

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The effect of a short course of prednisone therapy on serum IgM type antibody to the hepatitis B core antigen (anti-HBc IgM) was studied in 14 male patients with chronic active type B hepatitis. Eleven patients (78.5%) became positive for serum anti-HBc IgM either during or shortly after prednisone withdrawal. Detection of anti-HBc IgM correlated with an increase in hepatitis B virus specific DNA-polymerase activity and was followed by a rise in serum transaminase levels. Six patients with histologic evidence of cirrhosis developed anti-HBc IgM which lasted six or more months after prednisone therapy and had a rapid onset of hepatic decompensation manifested by encephalopathy with ascites and/or variceal bleeding. In 17 untreated chronic active type B hepatitis patients who served as controls, anti-HBc IgM was detected at low levels in only a single serum sample from each of two patients during the same observation period.

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Spontane (SCMC) und antikörperabhängige (ADCC) zelluläre Zytotoxizität bei Patienten mit akuter Hepatitis und chronisch aktiver Hepatitis

Cited by 16 publications

References 26 publications

Immunoelectron microscopic observations on the inflammatory infiltrates and HLA antigens in hepatitis B and non-A, Non-B

Immunoelectron microscopic observations on the inflammatory infiltrates and HLA antigens in hepatitis B and non-A, Non-B

Lack ofin vivo activation of the interferon system in HBsAg-positive chronic active hepatitis

Detection of Anti-HBc IgM Following Prednisone Treatment in Patients with Chronic Active Hepatitis B Virus Infection

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