Novel Foxo1-dependent transcriptional programs control Treg cell function View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2012-11-07

AUTHORS

Weiming Ouyang, Will Liao, Chong T. Luo, Na Yin, Morgan Huse, Myoungjoo V. Kim, Min Peng, Pamela Chan, Qian Ma, Yifan Mo, Dies Meijer, Keji Zhao, Alexander Y. Rudensky, Gurinder Atwal, Michael Q. Zhang, Ming O. Li

ABSTRACT

Regulatory T (Treg) cells, characterized by expression of the transcription factor forkhead box P3 (Foxp3), maintain immune homeostasis by suppressing self-destructive immune responses1,2,3,4. Foxp3 operates as a late-acting differentiation factor controlling Treg cell homeostasis and function5, whereas the early Treg-cell-lineage commitment is regulated by the Akt kinase and the forkhead box O (Foxo) family of transcription factors6,7,8,9,10. However, whether Foxo proteins act beyond the Treg-cell-commitment stage to control Treg cell homeostasis and function remains largely unexplored. Here we show that Foxo1 is a pivotal regulator of Tregcell function. Treg cells express high amounts of Foxo1 and display reduced T-cell-receptor-induced Akt activation, Foxo1 phosphorylation and Foxo1 nuclear exclusion. Mice with Treg-cell-specific deletion of Foxo1 develop a fatal inflammatory disorder similar in severity to that seen in Foxp3-deficient mice, but without the loss of Treg cells. Genome-wide analysis of Foxo1 binding sites reveals ∼300 Foxo1-bound target genes, including the pro-inflammatory cytokine Ifng, that do not seem to be directly regulated by Foxp3. These findings show that the evolutionarily ancient Akt–Foxo1 signalling module controls a novel genetic program indispensable for Treg cell function. More... »

PAGES

554-559

References to SciGraph publications

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  • Journal

    TITLE

    Nature

    ISSUE

    7425

    VOLUME

    491

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nature11581

    DOI

    http://dx.doi.org/10.1038/nature11581

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1002551801

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/23135404


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