Ontology type: schema:ScholarlyArticle Open Access: True
2011-09
AUTHORSMarc Beyer, Yasser Thabet, Roman-Ulrich Müller, Timothy Sadlon, Sabine Classen, Katharina Lahl, Samik Basu, Xuyu Zhou, Samantha L Bailey-Bucktrout, Wolfgang Krebs, Eva A Schönfeld, Jan Böttcher, Tatiana Golovina, Christian T Mayer, Andrea Hofmann, Daniel Sommer, Svenja Debey-Pascher, Elmar Endl, Andreas Limmer, Keli L Hippen, Bruce R Blazar, Robert Balderas, Thomas Quast, Andreas Waha, Günter Mayer, Michael Famulok, Percy A Knolle, Claudia Wickenhauser, Waldemar Kolanus, Bernhard Schermer, Jeffrey A Bluestone, Simon C Barry, Tim Sparwasser, James L Riley, Joachim L Schultze
ABSTRACTRegulatory T cells (T(reg) cells) are essential for self-tolerance and immune homeostasis. Lack of effector T cell (T(eff) cell) function and gain of suppressive activity by T(reg) cells are dependent on the transcriptional program induced by Foxp3. Here we report that repression of SATB1, a genome organizer that regulates chromatin structure and gene expression, was crucial for the phenotype and function of T(reg) cells. Foxp3, acting as a transcriptional repressor, directly suppressed the SATB1 locus and indirectly suppressed it through the induction of microRNAs that bound the SATB1 3' untranslated region. Release of SATB1 from the control of Foxp3 in T(reg) cells caused loss of suppressive function, establishment of transcriptional T(eff) cell programs and induction of T(eff) cell cytokines. Our data support the proposal that inhibition of SATB1-mediated modulation of global chromatin remodeling is pivotal for maintaining T(reg) cell functionality. More... »
PAGES898
http://scigraph.springernature.com/pub.10.1038/ni.2084
DOIhttp://dx.doi.org/10.1038/ni.2084
DIMENSIONShttps://app.dimensions.ai/details/publication/pub.1002295466
PUBMEDhttps://www.ncbi.nlm.nih.gov/pubmed/21841785
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