Immunoregulation oftheinvitro anti-HBs antibody synthesis inchronic HBsAgcarriers andinrecently boosted anti-hepatitis Bvaccine recipients

SUMMARY Wereport astudy onimmunoregulation ofinvitro antibody tohepatitis Bsurface antigen (anti-HBs) synthesis induced bypokeweed mitogen (PWM)fromperipheral blood mononuclear cells (PBMC)inchronic hepatitis Bsurface antigen (HBsAg) carriers andin 'high responders' (anti-HBs RIAratio >20inserum), recently boosted withanti-hepatitis Bvaccine. Anti-HBs wasdetected in11days PBMCsupernatants (SN)from24outof36 'high responders', butinnonefrom31chronic HBsAgcarriers, despite detectable amounts ofpolyclonal IgGandantibody tohepatitis Bcoreantigen (anti-HBc) were produced. Thelack ofanti-HBs production bychronic HBsAgcarriers didnotseemtobe determined bysuppressor influences because Tlymphocytes fromthemajority ofchronic HBsAgcarriers, co-cultured with'high responders' PBMC didnotsuppress anti-HBs production. Co-cultures between HBsAgcarriers T4positive (helper/inducer) cells and allogenic 'high responder' non-Tcells produced anti-HBs antibody, indicating that HBsAgcarrier T cells arenotdeficient inthis allogenic helper function underPWM stimulation. Allogenic cocultures between HBsAgcarrier non-Tcells and'high responder' T4positive cells failed inanti-HBs production: aspecific Blymphocyte defect might be involved inthelacking anti-HBs synthesis inchronic HBV patients. Antigen-induced specific anti-HBs synthesis experiments indicate that Bcells themselves seemtobethe target forHBsAg-induced suppression ofanti-HBs antibody response.