TGF-β is a key profibrotic factor, but targeting TGF-β to prevent fibrosis also abolishes its
protective anti-inflammatory effects. Here, we investigated the hypothesis that we can
redirect TGF-β signaling by preventing downstream profibrotic interaction of β-catenin with T
cell factor (TCF), thereby enhancing the interaction of β-catenin with Foxo, a transcription
factor that controls differentiation of TGF-β induced regulatory T cells (iTregs), and thus,
enhance anti-inflammatory effects of TGF-β. In iTregs derived from EL4 T cells treated with …