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Article
Nature Immunology  4, 1177 - 1182 (2003)
Published online: 9 November 2003; | doi:10.1038/ni1008

Deletion of bold beta-catenin impairs T cell development

Youyuan Xu1, 5, Daliya Banerjee2, 5, Joerg Huelsken3, Walter Birchmeier3 & Jyoti Misra Sen1, 4

1  Dana Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA.

2  Rosensteil Center for Biomedical Research, Brandeis University, Waltham, Massachusetts 02540, USA.

3  Max-Delbrueck-Centrum for Molecular Medicine, Robert-Roessle-Strasse 10, D-13092 Berlin, Germany.

4  Harvard Medical School, 44 Binney Street, Boston, Massachusetts 02115, USA.

5  These authors contributed equally to this work.

Correspondence should be addressed to Jyoti Misra Sen jyoti_sen@dfci.harvard.edu
T cells encounter two main checkpoints during development in the thymus. These checkpoints are critically dependent on signals derived from the thymic microenvironment as well as from the pre-T cell receptor (pre-TCR) and the alphabeta TCR. Here we show that T cell−specific deletion of beta-catenin impaired T cell development at the beta-selection checkpoint, leading to a substantial decrease in splenic T cells. In addition, beta-catenin also seemed to be a target of TCR-CD3 signals in thymocytes and mature T cells. These data indicate that beta-catenin-mediated signals are required for normal T cell development.

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Nature Immunology
ISSN: 1529-2908
EISSN: 1529-2916
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