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Blood, 22 January 2009, Vol. 113, No. 4, pp. 827-836. Prepublished online as a Blood First Edition Paper on October 21, 2008; DOI 10.1182/blood-2008-04-150524. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2008-04-150524v1 113/4/827    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 Citing Articles via Google Scholar Google Scholar Articles by Kleinewietfeld, M. Articles by Falk, K. Search for Related Content PubMed PubMed Citation Articles by Kleinewietfeld, M. Articles by Falk, K. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY CD49d provides access to "untouched" human Foxp3+ Treg free of contaminating effector cells Markus Kleinewietfeld1, Mireille Starke1, Diletta Di Mitri2, Giovanna Borsellino2, Luca Battistini2, Olaf Rötzschke1,3, and Kirsten Falk1 1 Max-Delbrück-Center for Molecular Medicine, Berlin, Germany; 2 Laboratory of Neuroimmunology, Fondazione Santa Lucia, Rome, Italy; and 3 Singapore Immunology Network, Singapore The adoptive transfer of regulatory Foxp3+ T (Treg) cells has been shown in various animal models to prevent inflammatory immune and autoimmune diseases. Translation into therapeutic applications, however, is hindered by the lack of suitable techniques and markers. CD25, commonly used to isolate Treg cells from mice, has only limited value in humans as it is also present on proinflammatory CD4+ effector cells. Here we show that clean populations of human Foxp3+ Treg cells can be obtained with antibodies directed against CD49d. The marker is present on proinflammatory peripheral blood mononuclear cells but is absent on immune-suppressive Treg cells. Depletion with -CD49d removes contaminating interferon- (IFN-)– and interleukin-17 (IL-17)–secreting cells from Treg preparations of CD4+CD25high cells. More importantly, in combination with -CD127 it allows the isolation of "untouched" Foxp3+ Treg (ie, cells that have not been targeted by an antibody during purification). The removal of CD49d+/CD127+ cells leaves a population of Foxp3+ Treg virtually free of contaminating CD25+ effector cells. The cells can be expanded in vitro and are effective suppressors both in vitro and in vivo. Thus, CD49d provides access to highly pure populations of untouched Foxp3+ Treg cells conferring maximal safety for future clinical applications. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: H. Grindebacke, H. Stenstad, M. Quiding-Jarbrink, J. Waldenstrom, I. Adlerberth, A. E. Wold, and A. Rudin Dynamic Development of Homing Receptor Expression and Memory Cell Differentiation of Infant CD4+CD25high Regulatory T Cells J. Immunol., October 1, 2009; 183(7): 4360 - 4370. [Abstract] [Full Text] [PDF] D. Q. Tran, J. Andersson, D. Hardwick, L. Bebris, G. G. Illei, and E. M. Shevach Selective expression of latency-associated peptide (LAP) and IL-1 receptor type I/II (CD121a/CD121b) on activated human FOXP3+ regulatory T cells allows for their purification from expansion cultures Blood, May 21, 2009; 113(21): 5125 - 5133. [Abstract] [Full Text] [PDF]

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