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CD26 is essential for normal G-CSF-induced progenitor cell mobilization as determined by CD26-/- mice
Kent W Christopherson1, Scott Cooper, Giao Hangoc
1Department of Microbiology/Immunology and the Walther Oncology Center, Indiana University School of Medicine, and the Walther Cancer Institute, Indianapolis, Ind. 46202-5254, USA.
Objective:
In spite of the wide usage of mobilized peripheral blood hematopoietic stem and progenitor cells (HSC/HPC) for transplantation, the mechanism of granulocyte colony-stimulating factor (G-CSF)-induced HSC/HPC mobilization has yet to be fully determined. Our previous studies suggested that that G-CSF-induced mobilization may involve the extracellular peptidase CD26 (DPPIV/dipeptidylpeptidase IV). We set out to establish whether CD26 was an essential component of normal G-CSF-induced mobilization of HSC/HPC.
Materials And Methods:
Normal wild-type (WT) control C57BL/6 mice and CD26 knockout (CD26(-/-)) mice, also on a C57BL/6 background, were treated with or without G-CSF and peripheral blood cells, bone marrow cells, and spleen cells were assessed for CFU-GM, BFU-E, and CFU-GEMM content.
Results:
No statistical difference in the number of CFU-GM, BFU-E, or CFU-GEMM in the peripheral blood, bone marrow, or spleen of untreated WT vs untreated CD26(-/-) mice was observed. G-CSF treatment of WT mice resulted in the mobilization of HPC into the peripheral blood. The number of HPC detected in G-CSF-treated CD26(-/-) mouse peripheral blood was significantly less than the corresponding number of HPC detected in G-CSF-treated WT mouse peripheral blood after either a 2- or 4-day G-CSF regimen.
Conclusions:
CD26 plays a critical role in G-CSF-induced mobilization of HPC.