Defective monocyte-to-macrophage maturation in patients with aplastic anemia.

摘要: Macrophages (MAC) are important effector cells of the immune system but also play an essential role as regulatory in hematopoiesis. They originate from circulating monocytes (MO) immature precursor that undergo terminal differentiation upon migration capillary bed into various tissues. In presence serum, MAC maturation blood MO is observed vitro and can be followed by expression maturation-associated antigens (MAX.1, .3, .11, .26; transferrin receptor, 13C2, CD16). We have tested 22 patients with aplastic anemia (AA) for their capacity to vitro. After isolation, six expressed CD14 molecules at low density when compared normals. On culture 7 days, 15 abnormalities could shown phenotype analysis using cell-enzyme-linked immunosorbent assay (ELISA) immunoperoxidase staining technique single cells. Abnormalities ranged distinctive failure mature express surface (eg, gp64-MAX.1) complete inhibition development a phenotype. three maturational defect was found persist remission after successful therapy antileukocyte globulin (ALG). Neither other immunosuppressed or multiple-transfused nor those bone marrow hypoplasia secondary cancer chemotherapy during hematologic reconstitution following autologous transplantation (BMT), defective seen. Our data provide evidence existence serious disorders within MO-MAC lineage AA. This observation may either reflect stem-cell indicate involvement pathogenesis disease.