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

Psychiatry

Journal of Addiction Research & Therapy

Author(s): Kurebayashi Y, Nagai S, Ikejiri A, Ohtani M, Ichiyama K,

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Abstract The PI3K-Akt-mTORC1 axis contributes to the activation, survival, and proliferation of CD4(+) T cells upon stimulation through TCR and CD28. Here, we demonstrate that the suppression of this axis by deletion of p85α or PI3K/mTORC1 inhibitors as well as T cell-specific deletion of raptor, an essential component of mTORC1, impairs Th17 differentiation in vitro and in vivo in a S6K1/2-dependent fashion. Inhibition of PI3K-Akt-mTORC1-S6K1 axis impairs the downregulation of Gfi1, a negative regulator of Th17 differentiation. Furthermore, we demonstrate that S6K2, a nuclear counterpart of S6K1, is induced by the PI3K-Akt-mTORC1 axis, binds RORγ, and carries RORγ to the nucleus. These results point toward a pivotal role of PI3K-Akt-mTORC1-S6K1/2 axis in Th17 differentiation. Copyright © 2012 The Authors. Published by Elsevier Inc. All rights reserved. This article was published in Cell Rep and referenced in Journal of Addiction Research & Therapy

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