Work

PI3 kinase signalling blocks Foxp3 expression by sequestering Foxo factors

Year: 2010

Type: article

Abstract: 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.

Source: The Journal of Experimental Medicine

DOI: 10.1084/jem.20101156

Authors: Matthias Merkenschlager, Harald von Boehmer

Institutions: Imperial College London, Medical Research Council, Dana-Farber Cancer Institute, Dana-Farber/Harvard Cancer Center

Language: English

Topic: T-cell and B-cell Immunology

Subfield: Immunology

Field: Immunology and Microbiology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: hybrid

Funder: National Institute of Allergy and Infectious Diseases