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Abstract
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.
Highlights
Regulatory T (Treg)5 cells are charged with the important task of maintaining homeostatic T cell reactivity and are thought to prevent autoimmunity by restraining self-reactive T cells that escape thymic deletion [1, 2]
Because -catenin is regulated by glycogen synthase kinase 3 (GSK3)-directed phosphorylation, we focused on GSK-3 and the role it plays in Treg cell function
We focused on the serine/threonine kinase GSK-3, which phosphorylates -catenin, marking it for ubiquitination, resulting in its degradation
Summary
Regulatory T (Treg)5 cells are charged with the important task of maintaining homeostatic T cell reactivity and are thought to prevent autoimmunity by restraining self-reactive T cells that escape thymic deletion [1, 2]. Inhibitor-treated Treg cells exhibited prolonged FoxP3 expression and increased levels of -catenin and of the antiapoptotic protein Bcl-xL.
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