IgA bound in vivo was shown by immunofluorescence on the plasma membrane of isolated hepatocytes from subjects with normal liver and patients with liver cirrhosis, chronic active hepatitis or fatty liver. IgA in sera with elevated IgA concentrations, especially from cases with alcoholic cirrhosis, was bound in vitro to isolated hepatocytes from rabbit and mouse. This was not due to the high IgA concentration per se. Moreover, polyclonal polymeric serum-type and secretory IgA, and three of ten polymeric monoclonal IgA preparations, showed similar binding properties. Conversely, purified polyclonal and monoclonal monemeric IgA did not show affinity for the hepatocytes. The binding of polymeric IgA did not seem to depend on the proportion of dimers and larger polymers, kappa- or lambda-type light chains, heavy-chain subclasses, content of J chain or affinity for secetory component. The in vivo binding of IgA by hepatocytes is probably a physiological phenomenon which in part may explain the normal clearance of polymeric IgA from serum.
During a period of 3 years we observed 5 patients with chronic active hepatitis B and 2 with hepatitis B virus-induced liver cirrhosis who cleared HBsAg from their sera after 2–14 years of HBsAg carriership. 4 of them developed anti-HBs. After HBsAg clearance there was no evidence of persisting inflammatory activity within their livers. 5 of the 7 patients had been treated for 1–39 months with prednisolone, sometimes in combination with azathioprine. This therapy, however, had been stopped more than 3 years before these patients terminated their HBsAg carriership. Our observations indicate that even after long-standing chronic active hepatitis B or hepatitis B virus-induced liver cirrhosis HBsAg may be eliminated in a considerable number of patients.
The effect of alpha-interferon treatment on serum levels of hepatitis B virus-encoded proteins was analyzed in eight patients with chronic type B hepatitis who participated in a pilot study of interferon therapy. Three individuals became HBsAg-negative, 4 lost HBeAg but remained HBsAg-positive and 1 remained positive for both HBsAg and HBeAg. Initiation of interferon treatment was rapidly followed by reduction or loss of hepatitis B virus DNA in the serum but by little immediate change in hepatitis B virus antigen levels. Changes in hepatitis B virus antigens were usually delayed. Loss of HBsAg from the serum was preceded by the sequential disappearance of pre-S-encoded proteins (pre-S1 and polymerized human serum albumin) and HBeAg. In patients who lost HBeAg but remained HBsAg-positive, serum levels of pre-S1 and polymerized human serum albumin usually, but did not always, decrease. The individual who remained HBsAg- and HBeAg-positive had unchanged serum levels of pre-S1, polymerized human serum albumin and HBsAg. These results suggest that alpha-interferon inhibits hepatitis B virus DNA replication but has little direct effect on synthesis of hepatitis B virus gene products.
spontaneous (SCMC) and antibody-dependent (ADCC) cellular cytotoxicity was studied in patients with aucte viral hepatitis B and chronic active hepatitis (CAH) B and non-A, non-B. Chang cells displaying the liver-specific protein LSP on the plasma membrane were used as target cells. SCMC and ADCC in acute hepatitis B were not different from normal controls. SCMC and ADCC in chronic active hepatitis B as well as in non-A, non-B were significantly elevated in comparison to normal controls. In additional experiments, the influence of patients sera on SCMC and ADCC was studied. Autologous serum from CAH patients significantly reduced cytotoxicity in SCMC and ADCC assays. This inhibitory capacity of patients sera was attributable to immune complexes, as ultracentrifugation studies and determination of immune complexes of fractionated sera demonstrated.
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