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Published online before print May 29, 2008
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0208109

Received for publication February 14, 2008.
Revised April 16, 2008.
Accepted for publication April 20, 2008.

Article

Conditioning response to granulocyte colony-stimulating factor via the dipeptidyl peptidase IV-adenosine deaminase complex

Daniele Focosi *@, Kast Richard Eric {dagger}, Sara Galimberti *, and Mario Petrini *

*Division of Hematology, Azienda Ospedaliera Santa Chiara, University of Pisa, Pisa, Italy; and {dagger}Department of Psychiatry, University of Vermont, Burlington, Vermont, USA

@ To whom correspondence should be addressed. E-mail: focosi{at}icgeb.org.


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Abstract

G-CSF is routinely used to mobilize hematopoietic stem cells (HSCs) from bone marrow (BM) into peripheral blood before aphaeresis, but HSC harvesting can be suboptimal. On the other hand, transplanted HSCs sometimes fail to engraft a recipient BM microenvironment when G-CSF is used after transplantation, as pushing-CSF will push HSCs away from marrow. So, G-CSF action needs to be potentiated by other drugs. Marrow stromal cells establish a local CXCL12 concentration gradient that is the primary homing signal for HSCs. Pharmacological interventions that modify this gradient, therefore, have potential to help HSC mobilization (by decreasing CXCL12) and engraftment (by increasing CXCL12). CXCL12 inactivation is primarily mediated by dipeptidyl peptidase-IV. We review here the currently available drugs affecting this enzyme that could be used in the clinic to achieve phase-specific help for G-CSF.

Key Words: bone marrow • CXCL12 • DPP-IV • G-CSF • hematopoietic stem cells • gliptins • sitagliptin