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

Essig et al. show that spontaneous activation and aberrant differentiation of Roquin-deficient T cells involves cellintrinsic causes in not only conventional T cells but also impaired Treg cell function. In both cell types, Roquin inhibits the PI3K-mTOR signaling pathway at several levels, thereby controlling protein biosynthesis and limiting differentiation toward Th17 and Tfh cells as well as preventing the conversion and functional specialization of Treg into Tfr cells.

Roquin 抑制 PI3K-mTOR 信号通路抑制 T 辅助细胞分化和 Treg 向 Tfr 细胞转化

Essig Roquin t 细胞的自发活化和异常分化不仅涉及常规T 细胞的 cellintrinsic 原因, 而且也损害 Treg 细胞功能。在这两种细胞类型中, Roquin 抑制 PI3K-mTOR 信号通路的几个层次, 从而控制向 Th17 和Tfh细胞的蛋白质生物合成和限制分化, 并防止Treg向Tfr 细胞的转换和功能专门化。