Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 207, Issue 7, Pages 1347-1350Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20101156
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Funding
- Medical Research Council, UK
- National Institutes of Health [R37 AI 53102]
- MRC [MC_U120027516] Funding Source: UKRI
- Medical Research Council [MC_U120027516] Funding Source: researchfish
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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)-beta. 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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