The preferential expression of CD7 and CD34 in myeloid blast crisis in chronic myeloid leukemia.

karyocyte colony formation. These data indicate that the IgG autoantibodies can specifically neutralize the in vitro biologic activity of TPO. The effectiveness of cyA in improving thrombocytopenia strongly suggests an immune-mediated pathogenetic mechanism in the patient. Although it is unclear that anti-TPO autoantibody is the sole cause of the thrombocytopenia, the recovery of serum TPO levels and peripheral platelet counts appeared to be closely related to the decrease in the antibody levels. Low levels of measurable TPO before cyA therapy could be due to the antibody-mediated increased clearance of TPO or the interference by the antibody in the detection of serum TPO. In either case, the autoantibodies might result in a decrease in the effective TPO concentrations for stimulating megakaryocytopoiesis, leading to thrombocytopenia. In recent clinical trials of pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF), a very small proportion of healthy volunteers who had received repeated subcutaneous injections of PEG-rHuMGDF-developed antibodies against endogenous TPO and eventually became thrombocytopenic (unpublished data). The present results, together with these observations, suggest that an autoantibody against TPO should be included in the pathogenetic mechanisms underlying AMTP.