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J Biol Chem. 2010 Oct 22;285(43):32852-9. doi: 10.1074/jbc.M110.150904. Epub 2010 Aug 20.

Suppressive regulatory T cell activity is potentiated by glycogen synthase kinase 3{beta} inhibition.

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Transplantation Unit, Massachusetts General Hospital, Department of Surgery, Harvard Medical School, Boston, Massachusetts 02114, USA.


The mechanism by which regulatory T (Treg) cells suppress the immune response is not well defined. A recent study has shown that β-catenin prolongs Treg cell survival. Because β-catenin is regulated by glycogen synthase kinase 3β (GSK-3β)-directed phosphorylation, we focused on GSK-3β and the role it plays in Treg cell function. Inhibition of GSK-3β led to increased suppression activity by Treg cells. Inhibitor-treated Treg cells exhibited prolonged FoxP3 expression and increased levels of β-catenin and of the antiapoptotic protein Bcl-xL. Systemic administration of GSK-3β inhibitor resulted in prolonged islet survival in an allotransplant mouse model. Our data suggest that GSK-3β could be a useful target in developing strategies designed to increase the stability and function of Treg cells for inducing allotransplant tolerance or treating autoimmune conditions.

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