Compensatory splenic hemopoiesis in beta-thalassemic mice
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Updated: Aug 30, 2026

The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
C van den Bos1, D Kieboom, T P Visser
1Department of Radiobiology, Erasmus University, Rotterdam, The Netherlands.
Abstract:
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.
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