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Blood, 18 June 2009, Vol. 113, No. 25, pp. 6277-6287. Prepublished online as a Blood First Edition Paper on February 10, 2009; DOI 10.1182/blood-2008-06-161026. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2008-06-161026v1 113/25/6277    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Google Scholar Articles by Swee, L. K. Articles by Rolink, A. PubMed PubMed Citation Articles by Swee, L. K. Articles by Rolink, A. Related Collections Immunobiology Plenary Papers Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  PLENARY PAPER Expansion of peripheral naturally occurring T regulatory cells by Fms-like tyrosine kinase 3 ligand treatment Lee Kim Swee1, Nabil Bosco1, Bernard Malissen2, Rhodri Ceredig1,3, and Antonius Rolink1 1 Departement Biomedizin Basel, Division of Molecular Immunology, University of Basel, Basel, Switzerland; 2 Centre d'Immunologie de Marseille-Luminy, Université de la Méditerrannée, Inserm Unité 631, Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche (UMR) 6102, Marseille, France; and 3 Inserm Unité 645, Université Franche-Comté, Etablissement Français du Sang, Bourgogne Franche-Comté, Institut Fédératif de Recherche 133, Besançon, France Fms-like tyrosine kinase 3 ligand (FLT3L) plays a major role in dendritic cell (DC) biology. Deficiency of FLT3L causes a dramatic decrease in DC numbers, whereas increasing its availability (by repetitive injections for 7-10 days) leads to a 10-fold increase in DC numbers. In this study, we show that FLT3L treatment indirectly leads to an expansion of peripheral naturally occurring T regulatory cells (NTregs). The FLT3L-induced increase in NTregs was still observed in thymectomized mice, ruling out the role of the thymus in this mechanism. Instead, the increased number of NTregs was due to proliferation of preexisting NTregs, most likely due to favored interactions with increased number of DCs. In vitro, we show that DCs induce regulatory T-cell (Treg) proliferation by direct cell contact and in an interleukin-2–dependent, T-cell receptor–independent manner. FLT3L could prevent death induced by acute graft-versus-host disease (GVHD). This study demonstrates unique aspects in the regulation of Treg homeostasis by DCs, which were unappreciated until now. It also reinforces the relevance of FLT3L treatment in GVHD by its ability to increase both the number of tolerizing DCs and NTregs. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Flt3L, DCs, and NTregs: team contra GVHD? Markus G. Manz Blood 2009 113: 6267-6268. [Full Text] [PDF] This article has been cited by other articles: G. Darrasse-Jeze, S. Deroubaix, H. Mouquet, G. D. Victora, T. Eisenreich, K.-h. Yao, R. F. Masilamani, M. L. Dustin, A. Rudensky, K. Liu, et al. Feedback control of regulatory T cell homeostasis by dendritic cells in vivo J. Exp. Med., August 31, 2009; 206(9): 1853 - 1862. [Abstract] [Full Text] [PDF] M. G. Manz Flt3L, DCs, and NTregs: team contra GVHD? Blood, June 18, 2009; 113(25): 6267 - 6268. [Full Text] [PDF]

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