CXCR4 and mobilization of hematopoietic precursors.
作者： Michael P. Rettig , Pablo Ramirez , Bruno Nervi , John F. DiPersio
DOI: 10.1016/S0076-6879(09)05203-3
关键词:
摘要: Abstract The binding of the chemokine [C‐X‐C motif] ligand 12 (CXCL12 or stromal cell–derived factor 1α [SDF‐1α]) constitutively produced by bone marrow cells and osteoblasts, to CXC receptor (CXCR) 4, a transmembrane expressed on hematopoietic stem progenitor (HSPCs), has emerged as key signal for HSPC trafficking from marrow. Disruption CXCL12/CXCR4 signaling causes leukocytosis, with release HSPCs, neutrophils, lymphocytes into peripheral blood. Although mobilized blood become preferred source both autologous allogeneic transplantation, optimum strategy obtaining products donors is subject ongoing study. Granulocyte colony–stimulating (G‐CSF) plerixafor (AMD3100) are two agents used clinically induce mobilization disruption interaction. This chapter describes current procedures phenotypically functionally characterize murine human HSPCs G‐CSF plerixafor.
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