Article abstract


Nature Medicine 14, 162 - 169 (2008)
Published online: 3 February 2008 | doi:10.1038/nm1707

Beta-catenin stabilization extends regulatory T cell survival and induces anergy in nonregulatory T cells

Yi Ding1,2, Shiqian Shen1, Andreia C Lino1, Maria A Curotto de Lafaille1,3 & Juan J Lafaille1,3


beta-catenin is a central molecule in the Wnt pathway. Expression of a stable form of beta-catenin on CD4+CD25+ regulatory T (Treg) cells resulted in a marked enhancement of survival of these cells in vitro. Furthermore, stable beta-catenin–expressing CD4+CD25+ Treg cells outcompeted control Treg cells in vivo, and the number of Treg cells necessary for protection against inflammatory bowel disease could be substantially reduced when stable beta-catenin–expressing CD4+CD25+ Treg cells were used instead of control Treg 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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  1. Molecular Pathogenesis Program and Skirball Institute for Biomolecular Medicine, New York University School of Medicine, 540 First Avenue, New York, New York 10016, USA.
  2. Sackler Institute of Graduate Biomedical Sciences, New York University School of Medicine, 540 First Avenue, New York, New York 10016, USA.
  3. Department of Pathology, New York University School of Medicine, 540 First Avenue, New York, New York 10016, USA.

Correspondence to: Juan J Lafaille1,3 e-mail: lafaille@saturn.med.nyu.edu



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