Introduction B cell activating factor, a member of tumor necrosis factor family, isa crucial homeostatic cytokine for B cells. It has been shown to enhance theexpression of CD19+ cells and mediate the maturation of autoreactive B cells.BAFF is elevated in several autoimmune diseases including immunethrombocytopenic purpura (ITP). Increased survival of CD8+ T cells also maypromote the apoptosis of platelets through cytotoxic T lymphocyte-mediatedplatelet lysis. Blockade of BAFF receptor has demonstrated a clinical benefit inimmunologic diseases.Methods PBMCs and platelets from 15 acute ITP patients and 15 healthycontrols were analyzed by flow cytometry for apoptosis after culture with rhBAFFor a combination of rhBAFF and BR3-Fc.Results Blockade of BAFF receptor by BR3-Fc significantly increased theapoptosis of CD19+ cells in patients only and decreased the apoptosis of plateletsin both patients and controls. Apoptotic CD8+ cells were significantly increased inpatients only, following the addition of BR3-Fc.Conclusion These findings suggest that blockade of BAFF receptor (BR3-FC)could successfully correct the effects of BAFF by promoting the apoptosis ofCD19+ and CD8+ cells and decreasing the apoptosis of platelets. Furtherresearch will indicate whether blocking BAFF-BR3 will have a therapeuticapplicability in the management of ITP or not.