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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 (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 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 Citing Articles via Google Scholar Google Scholar Articles by Swee, L. K. Articles by Rolink, A. Search for Related Content PubMed PubMed Citation Articles by Swee, L. K. Articles by Rolink, A. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted June 2, 2008 Accepted February 7, 2009 Expansion of peripheral NTreg by FLT3L treatment Lee Kim Swee, Nabil Bosco, Bernard Malissen, Rhodri Ceredig, and Antonius Rolink* Departement Biomedizin Basel, Division of Molecular Immunology, University of Basel, Basel, Switzerland Centre d'immunologie de Marseille-Luminy, Universite de la Mediterrannee, INSERM U631, CNRS UMR6102, Marseille, France Regenerative Medicine Institute, National Centre for Biomedical Engineering Science, Department of Physiology, National University of Ireland Galway, Galway, Ireland, Eire * Corresponding author; email: antonius.rolink{at}unibas.ch. 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. Here, we show that FLT3L treatment indirectly leads to an expansion of peripheral naturally occurring T regulatory (NTreg) cells. The FLT3L-induced increase in NTreg was still observed in thymectomized mice, ruling out the role of the thymus in this mechanism. Instead, the increased number of NTreg was due to proliferation of pre-existing NTreg, likely due to favoured interactions with increased number of DC. In vitro, we show that DC induce Treg proliferation by direct cell contact and in an IL-2 dependent, TCR independent manner. FLT3L could prevent death induced by acute Graft vs Host Disease (GvHD). This study demonstrates unique aspects in the regulation of Treg homeostasis by DC, which were unappreciated until now. It also re-enforces the relevance of FLT3L treatment in GvHD by its ability to increase both the number of tolerizing DC and NTreg. 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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