Please use this identifier to cite or link to this item:
Title: Epigenetic modification of the human CCR6 gene is associated with stable CCR6 expression in T cells
Authors: Steinfelder, S.
Floess, S.
Engelbert, D.
Haeringer, B.
Baron, U.
Rivino, L. 
Steckel, B.
Gruetzkau, A.
Olek, S.
Geginat, J.
Huehn, J.
Hamann, A.
Issue Date: 10-Mar-2011
Citation: Steinfelder, S., Floess, S., Engelbert, D., Haeringer, B., Baron, U., Rivino, L., Steckel, B., Gruetzkau, A., Olek, S., Geginat, J., Huehn, J., Hamann, A. (2011-03-10). Epigenetic modification of the human CCR6 gene is associated with stable CCR6 expression in T cells. Blood 117 (10) : 2839-2846. ScholarBank@NUS Repository.
Abstract: CCR6 is a chemokine receptor expressed on Th17 cells and regulatory T cells that is induced by T-cell priming with certain cytokines, but how its expression and stability are regulated at the molecular level is largely unknown. Here, we identified and characterized a noncoding region of the human CCR6 locus that displayed unmethylated CpG motifs (differentially methylated region [DMR]) selectively in CCR6+ lymphocytes. CCR6 expression on circulating CD4+ T cells was stable on cytokine-induced proliferation but partially down-regulated on T-cell receptor stimulation. However, CCR6 down-regulation was mostly transient, and the DMR within the CCR6 locus remained demethylated. Notably, in vitro induction of CCR6 expression with cytokines in T-cell receptor-activated naive CD4+ T cells was not associated with a demethylated DMR and resulted in unstable CCR6 expression. Conversely, treatment with the DNA methylation inhibitor 5′-azacytidine induced demethylation of the DMR and led to increased and stable CCR6 expression. Finally, when cloned into a reporter gene plasmid, the DMR displayed transcriptional activity in memory T cells that was suppressed by DNA methylation. In summary, we have identified a noncoding region of the human CCR6 gene with methylation-sensitive transcriptional activity in CCR6+ T cells that controls stable CCR6 expression via epigenetic mechanisms. © 2011 by The American Society of Hematology.
Source Title: Blood
ISSN: 00064971
DOI: 10.1182/blood-2010-06-293027
Appears in Collections:Staff Publications

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


checked on Nov 25, 2022


checked on Nov 25, 2022

Page view(s)

checked on Nov 24, 2022

Google ScholarTM



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