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Roquin Suppresses the PI3K-mTOR Signaling Pathway to Inhibit T Helper Cell Differentiation and Conversion of Treg to Tfr Cells.

Immunity | Dec 19, 2017

Roquin proteins preclude spontaneous T cell activation and aberrant differentiation of T follicular helper (Tfh) or T helper 17 (Th17) cells. Here we showed that deletion of Roquin-encoding alleles specifically in regulatory T (Treg) cells also caused the activation of conventional T cells. Roquin-deficient Treg cells downregulated CD25, acquired a follicular Treg (Tfr) cell phenotype, and suppressed germinal center reactions but could not protect from colitis. Roquin inhibited the PI3K-mTOR signaling pathway by upregulation of Pten through interfering with miR-17∼92 binding to an overlapping cis-element in the Pten 3' UTR, and downregulated the Foxo1-specific E3 ubiquitin ligase Itch. Loss of Roquin enhanced Akt-mTOR signaling and protein synthesis, whereas inhibition of PI3K or mTOR in Roquin-deficient T cells corrected enhanced Tfh and Th17 or reduced iTreg cell differentiation. Thereby, Roquin-mediated control of PI3K-mTOR signaling prevents autoimmunity by restraining activation and differentiation of conventional T cells and specialization of Treg cells.

Pubmed ID: 29246441 RIS Download

Mesh terms: Animals | B-Lymphocytes | Cell Differentiation | Colitis | Disease Models, Animal | Female | Forkhead Box Protein O1 | Gene Expression Regulation | Germinal Center | Interleukin-2 Receptor alpha Subunit | Lymphocyte Activation | Mice | Mice, Inbred C57BL | Mice, Transgenic | MicroRNAs | PTEN Phosphohydrolase | Phosphatidylinositol 3-Kinases | Primary Cell Culture | Repressor Proteins | Signal Transduction | Spleen | T-Lymphocytes, Regulatory | TOR Serine-Threonine Kinases | Th17 Cells | Ubiquitin-Protein Ligases

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