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CD49d provides access to 'untouched' human Foxp3+ Treg free of contaminating effector cells

Official URL:https://doi.org/10.1182/blood-2008-04-150524
PubMed:View item in PubMed
Creators Name:Kleinewietfeld, M. and Starke, M. and Mitri, D.D. and Borsellino, G. and Battistini, L. and Roetzschke, O. and Falk, K.
Journal Title:Blood
Journal Abbreviation:Blood
Volume:113
Number:4
Page Range:827-836
Date:22 January 2009
Keywords:Cell Separation, Cultured Cells, Forkhead Transcription Factors, Integrin alpha1, Interleukin-2 Receptor alpha Subunit, Interleukin-7 Receptor alpha Subunit, Helper-Inducer T-Lymphocytes, Regulatory T-Lymphocytes, Time Factors, Animals, Mice
Abstract:The adoptive transfer of regulatory Foxp3+ T cells (Treg) has been shown in various animal models to prevent inflammatory (auto-) immune 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 present also on pro-inflammatory 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 pro-inflammatory PBMC but is absent on immune-suppressive Treg cells. Depletion with alpha-CD49d removes contaminating IFN-gamma- and IL-17-secreting cells from Treg preparations of CD4+CD25(high) cells. More importantly, in combination with alpha-CD127 it allows the isolation of 'untouched' Foxp3+ Treg, i.e. 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.
ISSN:0006-4971
Publisher:American Society of Hematology (U.S.A.)
Item Type:Article

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