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1: Nat Med. 2008 Feb;14(2):162-9. Epub 2008 Feb 3.
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Comment in:
Beta-catenin stabilization extends regulatory T cell survival and induces anergy in nonregulatory T cells.

Ding Y, Shen S, Lino AC, Curotto de Lafaille MA, Lafaille JJ.

Molecular Pathogenesis Program and Skirball Institute for Biomolecular Medicine, New York University School of Medicine, 540 First Avenue, New York, New York 10016, USA.

Beta-catenin is a central molecule in the Wnt pathway. Expression of a stable form of beta-catenin on CD4+CD25+ regulatory T (T(reg)) cells resulted in a marked enhancement of survival of these cells in vitro. Furthermore, stable beta-catenin-expressing CD4+CD25+ T(reg) cells outcompeted control T(reg) cells in vivo, and the number of T(reg) cells necessary for protection against inflammatory bowel disease could be substantially reduced when stable beta-catenin-expressing CD4+CD25+ T(reg) cells were used instead of control T(reg) cells. Expression of stable beta-catenin on potentially pathogenic CD4+CD25- T cells rendered these cells anergic, and the beta-catenin-mediated induction of anergy occurred even in Foxp3-deficient T cells. Thus, through enhanced survival of existing regulatory T cells, and through induction of unresponsiveness in precursors of T effector cells, beta-catenin stabilization has a powerful effect on the prevention of inflammatory disease.

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PMID: 18246080 [PubMed - indexed for MEDLINE]