IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v7y2016i1d10.1038_ncomms10888.html
   My bibliography  Save this article

IL-15-dependent balance between Foxp3 and RORγt expression impacts inflammatory bowel disease

Author

Listed:
  • Milena J. Tosiek

    (Unité de Biologie des Populations Lymphocytaires, Institut Pasteur
    CNRS, URA1961)

  • Laurence Fiette

    (Unité d’Histopathologie Humaine et Modèles Animaux, Institut Pasteur
    Université Paris-Descartes, Hôpital Ste Anne)

  • Sary El Daker

    (Unité de Biologie des Populations Lymphocytaires, Institut Pasteur
    CNRS, URA1961)

  • Gérard Eberl

    (CNRS, URA1961
    Unité de Développement des Tissus Lymphoïdes, Institut Pasteur)

  • Antonio A. Freitas

    (Unité de Biologie des Populations Lymphocytaires, Institut Pasteur
    CNRS, URA1961)

Abstract

The ability of CD4+ T cells to change their phenotype and to specialize into different functional subsets may enhance the risk of autoimmune diseases. Here we investigate how a pleiotropic cytokine interleukin (IL)-15 may modify the functional commitment of CD4+ T cells expressing the lineage-associated transcription factors: forkhead box P3 (Foxp3; Treg) and RORγt (Th17) in the context of inflammatory bowel disease (IBD). We demonstrate in mice that impaired delivery of IL-15 to CD4+ T cells in the colon downmodulates Foxp3 expression (diminishing STAT5 phosphorylation) and enhances RORγt expression (by upregulating the expression of Runx1). In consequence, CD4+ T cells deprived of IL-15 rapidly trigger IBD characterized by enhanced production of pro-inflammatory cytokines (interferon-γ, IL-6) and accumulation of Th1/Th17 cells. Overall, our findings indicate a potentially beneficial role of IL-15 in IBD by fine-tuning the balance between Treg and Th17 cells and controlling intestinal inflammation.

Suggested Citation

  • Milena J. Tosiek & Laurence Fiette & Sary El Daker & Gérard Eberl & Antonio A. Freitas, 2016. "IL-15-dependent balance between Foxp3 and RORγt expression impacts inflammatory bowel disease," Nature Communications, Nature, vol. 7(1), pages 1-11, April.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10888
    DOI: 10.1038/ncomms10888
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms10888
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms10888?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10888. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.