Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/128420
Citations
Scopus Web of Science® Altmetric
?
?
Type: Journal article
Title: Flt3 ligand expands CD4⁺FoxP3⁺ regulatory T cells in human subjects
Other Titles: Flt3 ligand expands CD4(+)FoxP3(+) regulatory T cells in human subjects
Author: Klein, O.
Ebert, L.
Zanker, D.
Woods, K.
Tan, B.
Fucikova, J.
Behren, A.
Davis, I.
Maraskovsky, E.
Chen, W.
Cebon, J.
Citation: European Journal of Immunology, 2013; 43(2):533-539
Publisher: Wiley
Issue Date: 2013
ISSN: 0014-2980
1521-4141
Statement of
Responsibility: 
Oliver Klein, Lisa M. Ebert, Damien Zanker, Katherine Woods, Bee Shin Tan ... et al.
Abstract: CD4(+) CD25(+) FoxP3(+) naturally occurring regulatory T (Treg) cells play a crucial role in the maintenance of immune tolerance and in preventing autoimmune pathology. Interventions that expand Treg cells are highly desirable, as they may offer novel treatment options in a variety of autoimmune and transplantation settings. Paralleling previous preclinical studies, we demonstrate here that administration of the hematopoietic growth factor Flt3L to human subjects increases the frequency and absolute number of Treg cells, and reduces the ratio of CD8(+) T cells to Treg cells in the peripheral blood. The increase in Treg cells was due to enhanced Treg-cell proliferation rather than release of Treg cells from the thymus. Further studies revealed that Flt3L-induced proliferation of Treg cells was an indirect effect that occurred via the interaction of Treg cells with the Flt3L-expanded pool of CD1c(+) myeloid dendritic cells. On the basis of these findings, Flt3L may represent a promising agent for promoting immune tolerance in a variety of clinical settings.
Keywords: Flt3 ligand; immune tolerance; Regulatory T (Treg) cells
Rights: © 2012 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim
RMID: 1000026722
DOI: 10.1002/eji.201242603
Appears in Collections:Medicine publications

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.