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Biomedical subjects

U Hopf

Publications and source records attributed to U Hopf.

At least 163 records · Page 9Linked to original sources
PubMed1976

Demonstration of binding sites for IgG Fc and the third complement component (C3) on isolated hepatocytes.

Isolated hepatocytes from rabbits with experimental acute serum sickness showed immune complexes bound to the hepatocellular membrane with a coarse granular fluorescent pattern. Also in vitro preformed immune complexes (BSA-anti-BSA) or aggregated gamma-globulin from human and rabbit could be bound to the surface of isolated hepatocytes. In contrast, immune complexes with F(ab')2 anti-BSA were not fixed on the membranes. Hepatocytes incubated in fresh serum showed membrane-fixed C3 in a coarse granular pattern. This deposition could be abolished by heating (56 degrees C, 30 min) the serum or by adding EDTA (0.02 M). Also, purified human or guinea pig C3 could be bound to the hepatocellular membrane but in a linear fluorescent pattern. Thus, fixation of immune complexes on hepatocytes appears to operate through binding sites for IgG Fc and, possibly, also through binding sites for C3. It is suggested that these hepatocellular-binding sites may have a physiologic clearance function. In vivo fixed IgA could be detected on the membranes of isolated hepatocytes from healthy persons. It is assumed that the membrane-fixed IgA has a carrier function for antigens from the gut.

Animals↗
PubMed1975

[Investigations concerning the fixation of hepatitis B-antigen (HBAg) on peripheral lymphocytes and isolated hepatocytes in patients with inflammatory liver diseases. (author's transl)].

The fixation of HBAg on lymphocytes was investigated in 127 patients with various inflammatory liver diseases. The fixation of HBAg on lymphocytes and isolated hepatocytes as well as the fixation of IgG on isolated hepatocytes were studied in 60 cases. Membrane-fixed HBAg could in no case be demonstrated on isolated hepatocytes whether these cells were derived from patients with or without HBAg in the serum. HBAg on hymphocytes was detectable in most cases of acute hepatitis during the phase when HBAg disappeared from the serum. HBAg on lymphocytes was detectable in most cases of acute hepatitis during the phase when HBAg disappeared from the serum (time of immunoelimination). Membrane-fixed IgG could be mainly demonstrated in HBAg positive acute hepatitis with a protracted course or in HBAg-positive active chronic hepatitis and signs of inflammatory activity. The results obtained for HBAg-carriers indicate (a) an immunological tolerance against HBAg, (b) a persistance of the virus infection in liver cells, and (c) an antibody-mediated cyto- and histotoxicity as a pathogenetic principle for the course of certain chronic liver diseases. The antigenic determinant of the membrane-fixed antibody is not known until now.

Binding Sites, Antibody↗
PubMed1975

Studies on the pathogenesis of chronic inflammatory liver diseases. I. Membrane-fixed IgG on isolated hepatocytes from patients.

Membrane-fixed IgG on isolated hepatocytes from biopsy material could be demonstrated by direct immunofluorescence in nine of thirty-four patients with acute virus-B hepatitis and in seventeen of forty-nine cases with chronic active hepatitis (CAH). Patients with acute virus-A hepatitis, chronic persistent hepatitis (CPH) or metabolic liver diseases did not show this phenomenon. Cases with CAH and IgG on the hepatocytes-HBsAg-positive as well as HBsAg-negative-had high inflammatory activity. Antibodies against HBsAg were not present in any serum. Autoimmune phenomena (antibodies against smooth muscle, mitochondria and nuclei) were only rarely demonstrable. The findings suggest that an antibody- or immune complex-mediated lymphocyte cytotoxicity may be involved in the pathogenesis of chronic liver diseases.

Antibodies↗