van den Bos C, Kieboom D, Visser T P, Wagemaker G
Department of Radiobiology, Erasmus University, Rotterdam, The Netherlands.
Exp Hematol. 1993 Feb;21(2):350-3.
beta-Thalassemic mice, homozygous for the deletion of the beta major-globin gene, were investigated for compensatory hemopoiesis in bone marrow and spleen. Apart from characteristic severe anemia, these mice have a marked granulocytosis, monocytosis and lymphocytosis. A large compensatory expansion of late (CFU-E) erythroid progenitor cells was demonstrated, predominantly in the spleen. Immature hemopoietic cells (CFU-S) were also expanded, as were early progenitor cells of erythroid (BFU-E), as well as granulocyte/macrophage (GM-CFU) and megakaryocytic (CFU-Meg) lineages. It is concluded that the persistent erythropoietic stress results in a selective expansion of immature hemopoietic cells and inappropriate production of nonerythroid blood cells from excess production of progenitor cells.
对β-珠蛋白生成障碍性贫血小鼠（β-珠蛋白生成障碍性贫血小鼠为β-主要珠蛋白基因缺失的纯合子）的骨髓和脾脏代偿性造血进行了研究。除了典型的严重贫血外，这些小鼠还出现明显的粒细胞增多、单核细胞增多和淋巴细胞增多。结果表明，晚期（CFU-E）红系祖细胞有大量代偿性扩增，主要发生在脾脏。未成熟造血细胞（CFU-S）以及红系早期祖细胞（BFU-E）、粒细胞/巨噬细胞系（GM-CFU）和巨核细胞系（CFU-Meg）也出现了扩增。得出的结论是，持续的红细胞生成应激导致未成熟造血细胞选择性扩增，以及祖细胞过度产生导致非红系血细胞产生不当。
