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 Blood, 15 September 2008, Vol. 112, No. 6, pp. 2575-2578.
Prepublished online as a Blood First Edition Paper on July 10, 2008; DOI 10.1182/blood-2008-02-140681.

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TRANSPLANTATION

Brief Report

Role of GM-CSF in tolerance induction by mobilized hematopoietic progenitors

Hassen Kared1,*, Bertrand Leforban1,*, Ruddy Montandon1, Amédée Renand1, Esther Layseca Espinosa1, Lucienne Chatenoud2,3, Yvonne Rosenstein4, Elke Schneider1, Michel Dy1, and Flora Zavala1

1 Université Paris Descartes, Faculté de Médecine, Centre National de la Recherche Scientifique UMR 8147 and 2 Inserm U580, Paris, France; 3 Hôpital Necker-Enfants Malades, Paris, France; and 4 Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Mexico

Mechanisms of protection against autoimmune diseases by transplantation of autologous hematopoietic progenitors remain poorly defined. We recently demonstrated that, unlike medullary hematopoietic stem cells (HSCs), mobilized hematopoietic progenitors (HPCs) stimulate peripheral Foxp3+ regulatory T cell (Treg)–expansion through cell-contact activation of Notch signaling and through as yet undetermined soluble factor(s), distinct from TGF-β1. Herein we identified one such soluble factor as granulocyte macrophage–colony stimulating factor (GM-CSF), which is produced at higher levels by HPCs than HSCs and whose neutralization significantly reduces the growth-promoting effect of HPCs on Treg. Treg express a functional GM-CSF receptor {alpha}-chain CD116 and proliferate in response to this cytokine independently from IL2. GM-CSF–expanded Treg—like HPC-expanded Treg—display enhanced suppressive capacity relative to control Treg. Hence, mobilized progenitors stimulate Treg expansion both by cell-contact dependent mechanisms and by their production of GM-CSF.


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