RAPID COMMUNICATION The Granulocyte Colony-Stimulating Factor Receptor Is Required for the Mobilization of Murine Hematopoietic Progenitors Into Peripheral Blood by Cyclophosphamide or Interleukin-8 But Not Flt-3 Ligand

Hematopoietic progenitor cells (HPC) can be mobilized from CSFR–deficient mice after cyclophosphamide administration. This defect was not due to a failure to regenerate HPC the bone marrow into the peripheral circulation in response to a number of stimuli including hematopoietic growth facfollowing cyclophosphamide administration as the number of CFU-C in the bone marrow of G-CSFR–deficient mice was tors, cytotoxic agents, and certain chemokines. Despite significant differences in their biological activities, these stimuli increased relative to wild-type mice. Likewise, no increase in circulating CFU-C was detected in G-CSFR–deficient mice result in the mobilization of HPC with a similar phenotype, suggesting that a common mechanism for mobilization may following interleukin-8 (IL-8) administration. In contrast, mobilization of HPC in response to flt-3 ligand was nearly norexist. In this study, the role of granulocyte colony-stimulating factor (G-CSF) in progenitor mobilization was examined mal. These results show that the G-CSFR is required for mobilization in response to cyclophosphamide or IL-8 but using G-CSF receptor (G-CSFR)–deficient mice. In contrast to wild-type mice, no increase in circulating colony-forming not flt-3 ligand and suggest that the G-CSFR may play an important and previously unexpected role in HPC migration. cells (CFU-C), CD34 lineage progenitors, or day 12 colonyforming unit-spleen progenitors (CFU-S) was detected in Gq 1997 by The American Society of Hematology.