PI3 kinase signalling blocks Foxp3 expression by sequestering Foxo factors

M Merkenschlager, H von Boehmer - Journal of Experimental Medicine, 2010 - rupress.org
M Merkenschlager, H von Boehmer
Journal of Experimental Medicine, 2010rupress.org
Expression of the regulatory T (T reg) cell–associated transcription factor Foxp3 can be
induced by signals from the T cell receptor (TCR), interleukin-2 (IL-2), and transforming
growth factor (TGF)-β. These signals are integrated by a network involving
phosphatidylinositol 3 kinase (PI3K), protein kinase B (PKB; here referred to as Akt), and the
mammalian target of rapamycin (mTOR). New studies show that the Foxo proteins Foxo1
and Foxo3a, which are inactivated by Akt, drive Foxp3 expression. These studies therefore …
Expression of the regulatory T (T reg) cell–associated transcription factor Foxp3 can be induced by signals from the T cell receptor (TCR), interleukin-2 (IL-2), and transforming growth factor (TGF)-β. These signals are integrated by a network involving phosphatidylinositol 3 kinase (PI3K), protein kinase B (PKB; here referred to as Akt), and the mammalian target of rapamycin (mTOR). New studies show that the Foxo proteins Foxo1 and Foxo3a, which are inactivated by Akt, drive Foxp3 expression. These studies therefore explain the negative regulation of Foxp3 by PI3K signaling, and add Foxo proteins to the growing list of nuclear factors capable of modulating Foxp3 expression.
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