Summary:on normal hemopoietic stem cells. [1][2][3] The treatment of bone marrow (BM) and mobilized peripheral blood stem cell (PBSC) with Campath-1, has proved to be an effective Campath-1G is a CD52 (rat IgG2b) moAb used in bone marrow transplantation (BMT) to prevent graft-versusmethod for preventing graft-versus-host disease (GVHD). [4][5][6][7] Exposing BM or PBSC cells to Campath-1G host disease (GVHD) by the elimination of T cells via antibody-dependent cell cytotoxicity (ADCC) in vivo.prior to transplantation results in efficient removal of T cells bound to the moAb most probably by the recipient Fc We have previously reported that Campath-1G induces T cell proliferation, activation, and production of cytoreceptor-positive reticuloendothelial cell system. [7][8][9] In addition, Campath-1 is sometimes given to patients as part kines which in turn causes an enhancement of megakaryocytopoiesis in vitro. In view of the fact that recent of the pre-BMT conditioning in order to increase immunosuppression of the host by effective depletion of residual studies have indicated that natural killer (NK) cells may also be involved in the regulation of megakaryocytopoimmunocompetent lymphocytes in an attempt to prevent graft rejection. 8,9 iesis, we undertook the study of the in vitro effect of Campath-1G-treated NK cells on the regulation ofDelayed platelet engraftment is a serious complication in patients undergoing bone marrow transplantation (BMT) or megakaryocytopoiesis. Early burst-forming BFU-MK and late colony-forming CFU-MK were grown from aggressive chemotherapy for cancer treatment resulting in an unpredictable period of protracted thrombocytopenia and 2 × 10 5 peripheral blood non-adherent mononuclear cells (NAMC) in plasma clots in the presence of aplastic bleeding episodes. The production of platelets is thought to be regulated by multi-lineage and lineage-specific (ie canine plasma (PICS-J) which was used as megakaryocyte colony-stimulating factor (MK-CSF). The first step thrombopoietin) growth factors which stimulate megakaryocyte (MK) proliferation and maturation. 10-13 It has been in elucidating this series of events was to investigate the direct influence of NK cells on megakaryocytopoiesis.previously demonstrated that the regulation of MK development within the BM is multi-factorial and involves the Co-culturing NK cells (Ͼ85% CD16 + ) with autologous NAMC at a ratio of 1:1 resulted in a significant increase interaction of both stroma and immune effector cells. 14-18 T cells and soluble T cell factors stimulate megakaryocytic in the proliferation of CFU-MK and BFU-MK over NAMC cultured alone. This effect was further enhanced development. 14-24 Activated lymphocytes produce cytokines that suppport megakaryocyte proliferation and matuupon exposure of NK to Campath-1G (0.1-3 g/ml). To investigate the possible influence of soluble factors ration. [19][20][21][22][23][24] Conditioned medium (CM) from spleen cells or blood lymphocytes stimulated with lectins and PHAreleased from NK cells treated with Camp...

Auj~zky' ~ fueaAe, IgG, blood ~~wn, 60Wc.ulaJL 6lu.id, ova, enzyme-immunoaA~ay.