PI3K-Akt-mTORC1-S6K1/2 axis controls Th17 differentiation by regulating Gfi1 expression and nuclear translocation of RORγ

Abstract

(Cell Reports 1, 360–373; April 19, 2012) In the originally published version of this article, we reported that a dose of 100 nanogram/kg body weight rapamycin was administered to EAE model mice and a CD4+ T cell transfer model of colitis. The actual dose was 100 microgram/kg body weight. This error does not affect the interpretation of the experiment. The authors regret this error. PI3K-Akt-mTORC1-S6K1/2 Axis Controls Th17 Differentiation by Regulating Gfi1 Expression and Nuclear Translocation of RORγKurebayashi et al.Cell ReportsMarch 29, 2012In BriefThe PI3K-Akt-mTORC1 axis contributes to the activation, survival, and proliferation of CD4+ T cells upon stimulation through TCR and CD28. Koyasu and colleagues demonstrate that this axis positively regulates Th17 differentiation in a fashion dependent upon the ribosomal protein S6 kinase (S6K1/2). Inhibition of the PI3K-Akt-mTORC1-S6K1 axis impairs downregulation of Gfi-1, a negative regulator of Th17 differentiation. Furthermore, the authors show that S6K2, a nuclear counterpart of S6K1, is induced by the PI3K-Akt-mTORC1 axis, binds RORγ, and carries RORγ into the nucleus. Full-Text PDF Open Access