Accuri C6 Flow Cytometer System
Originally published online as doi:10.1189/jlb.0208109 on May 29, 2008

Published online before print May 29, 2008
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
jlb.0208109v1
84/2/331    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Focosi, D.
Right arrow Articles by Petrini, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Focosi, D.
Right arrow Articles by Petrini, M.
(Journal of Leukocyte Biology. 2008;84:331-337.)
© 2008 by Society for Leukocyte Biology

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

Daniele Focosi*,1,2, Richard Eric Kast{dagger},1, 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

2 Correspondence: Division of Hematology, Azienda Ospedaliera Santa Chiara, University of Pisa, via Roma 56, 56100 Pisa, Italy. E-mail: dfocosi{at}fin.org

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