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- W4313381710 abstract "Abstract Foxp3-deficient regulatory T (Treg) cells lack suppressor function and manifest a T effector (Teff) cell-like phenotype. We demonstrate that Foxp3 deficiency dysregulates mTORC2 signaling and gives rise to augmented aerobic glycolysis and oxidative phosphorylation. Mutant Treg cell-specific deletion of the mTORC2 adaptor gene Rictor or expression of a Foxo1 transgene improved regulatory function and ameliorated disease. Rictor deficiency reestablished a subset of Treg cell genetic circuits and suppressed the Teff cell-like metabolic program. Treatment of mutant Treg cells of patients with FOXP3 deficiency with mTOR inhibitors similarly antagonized their Teff cell-like program and restored suppressive function. Thus, regulatory function can be reestablished in Foxp3-deficient Treg cells by targeting their metabolic pathways, providing opportunities to restore tolerance in Treg cell disorders." @default.
- W4313381710 created "2023-01-06" @default.
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- W4313381710 date "2018-05-01" @default.
- W4313381710 modified "2023-09-27" @default.
- W4313381710 title "Functional reprogramming of regulatory T cells in the absence of Foxp3" @default.
- W4313381710 doi "https://doi.org/10.4049/jimmunol.200.supp.176.2" @default.
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