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Published on: February 28, 2019
Functional implications of hepatitis B surface antigen (HBsAg) in the T cells of chronic HBV carriers
1Department of Immunology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India.
This study was undertaken to investigate the role of T-lymphocyte-derived soluble factors in the maintenance of the hepatitis B virus (HBV) chronic carrier state. Cell-free supernatants from the peripheral blood T lymphocytes of chronic HBV carriers were produced by incubating them for 48 h in tissue culture medium. These supernatants were added to in vitro hepatitis B s antibody (HBsAb)-producing cultures of peripheral blood mononuclear cells from hepatitis B surface antigen (HBsAg) vaccinees stimulated with HBsAg or pokeweed mitogen. T-cell supernatants from chronic carriers suppressed in vitro HBsAb antibody synthesis, whereas those from control subjects did not. This suppression was antigen specific as the supernatants did not suppress synthesis of total IgG or IgM. HBV viral sequences were demonstrable, by Southern and dot-blot hybridization, in the T cells secreting this factor. We also demonstrated the presence of HBsAg in T-cell supernatants derived from these cells. These results show that HBsAg of T-cell origin may have a role in suppressing HBsAb production. Our observations point to the role of HBsAg-specific cellular and humoral responses in favouring persistence of the chronic HBV carrier state.
This study was undertaken to investigate the role of T-lymphocyte-derived soluble factors in the maintenance of the hepatitis B virus (HBV) chronic carrier state. Cell-free supernatants from the peripheral blood T lymphocytes of chronic HBV carriers were produced by incubating them for 48 h in tissue culture medium. These supernatants were added to in vitro hepatitis B s antibody (HBsAb)-producing cultures of peripheral blood mononuclear cells from hepatitis B surface antigen (HBsAg) vaccinees stimulated with HBsAg or pokeweed mitogen. T-cell supernatants from chronic carriers suppressed in vitro HBsAb antibody synthesis, whereas those from control subjects did not. This suppression was antigen specific as the supernatants did not suppress synthesis of total IgG or IgM. HBV viral sequences were demonstrable, by Southern and dot-blot hybridization, in the T cells secreting this factor. We also demonstrated the presence of HBsAg in T-cell supernatants derived from these cells. These results show that HBsAg of T-cell origin may have a role in suppressing HBsAb production. Our observations point to the role of HBsAg-specific cellular and humoral responses in favouring persistence of the chronic HBV carrier state.
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