A Lack of Burst-Forming Unit (BFU-e) and Lymphocyte-Mediated Suppression of Erythropoiesis in Patients with Aplastic Anemia
The pathogenesis of idiopathic aplastic anemia remains obscure.1 Since all cellular components of the blood are depressed in aplastic anemia, it is reasonable to suggest that the defect resides at the level of the pluripotential hematopoietic stem cells, as a result of a defect in the matrix of the hematopoietic system or of humoral regulation. However, several recent reports2,3 suggest that immune processes may be involved in the pathogenesis of aplastic anemia in some patients. In work reported in this chapter, using a plasma clot assay for the growth of burst-forming unit (BFU-e) including more mature (CFU-e) erythroid precursors in vitro, we examined changes in CFU-e and BFU-e in the marrow and blood of patients with aplastic anemia. Both marrow and circulating CFU-e and BFU-e were found to be markedly reduced in aplastic anemia. In addition, whether or not such a reduction of colony forming capacity in vitro may be related to cell-mediated suppression of erythropoiesis3 was investigated in co-cultures with peripheral blood lymphocytes and normal human bone marrow cells.
KeywordsAgar Heparin Sedimentation Anemia Baran
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