Abstract
Cell mediated and humoral immunity to hepatitis B surface antigen (HBsAg) was studied in nine asymptomatic HBsAg carriers, nine patients with natural acquired immunity to HB infection and nine HB-susceptible donors. Peripheral T and B lymphocytes from all asymptomatic HBsAg carriers and all HB-immune donors studied were specifically induced into proliferation and anti-HBs secretion when stimulated with low doses of HBsAg (2-30 ng antigen protein/ml) in vitro. This activation was achieved by mixing purified B and/or T cells with optimal concentrations of autologous monocytic cells. T and B cells from the HB-susceptible donors were non-responsive under identical culture conditions. These data do neither substantiate the existence of a qualitative defect in T cell function, nor the absence of circulatory B cells capable of synthesizing anti-HBs in vitro in asymptomatic HBsAg carriers. Thus, the inability to mount a satisfactory antibody response to HBsAg in vivo might be a consequence of altered immune responsiveness to this antigen, which may be a relevant factor in the pathogenesis of asymptomatic HBsAg carriership.
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