IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v7y2016i1d10.1038_ncomms13696.html
   My bibliography  Save this article

A TNFRSF14-FcɛRI-mast cell pathway contributes to development of multiple features of asthma pathology in mice

Author

Listed:
  • Riccardo Sibilano

    (Stanford University School of Medicine)

  • Nicolas Gaudenzio

    (Stanford University School of Medicine)

  • Marianne K. DeGorter

    (Stanford University School of Medicine
    Stanford University School of Medicine)

  • Laurent L. Reber

    (Stanford University School of Medicine
    Unit of Antibodies in Therapy and Pathology, INSERM U1222, Institut Pasteur)

  • Joseph D. Hernandez

    (Stanford University School of Medicine
    Stanford University School of Medicine)

  • Philipp M. Starkl

    (Stanford University School of Medicine
    Research Laboratory of Infection Biology, Medical University of Vienna)

  • Oliwia W. Zurek

    (Stanford University School of Medicine)

  • Mindy Tsai

    (Stanford University School of Medicine)

  • Sonja Zahner

    (La Jolla Institute for Allergy and Immunology)

  • Stephen B. Montgomery

    (Stanford University School of Medicine
    Stanford University School of Medicine)

  • Axel Roers

    (Institute for Immunology, Technische Universität Dresden)

  • Mitchell Kronenberg

    (La Jolla Institute for Allergy and Immunology)

  • Mang Yu

    (Stanford University School of Medicine)

  • Stephen J. Galli

    (Stanford University School of Medicine
    Stanford University School of Medicine)

Abstract

Asthma has multiple features, including airway hyperreactivity, inflammation and remodelling. The TNF superfamily member TNFSF14 (LIGHT), via interactions with the receptor TNFRSF14 (HVEM), can support TH2 cell generation and longevity and promote airway remodelling in mouse models of asthma, but the mechanisms by which TNFSF14 functions in this setting are incompletely understood. Here we find that mouse and human mast cells (MCs) express TNFRSF14 and that TNFSF14:TNFRSF14 interactions can enhance IgE-mediated MC signalling and mediator production. In mouse models of asthma, TNFRSF14 blockade with a neutralizing antibody administered after antigen sensitization, or genetic deletion of Tnfrsf14, diminishes plasma levels of antigen-specific IgG1 and IgE antibodies, airway hyperreactivity, airway inflammation and airway remodelling. Finally, by analysing two types of genetically MC-deficient mice after engrafting MCs that either do or do not express TNFRSF14, we show that TNFRSF14 expression on MCs significantly contributes to the development of multiple features of asthma pathology.

Suggested Citation

  • Riccardo Sibilano & Nicolas Gaudenzio & Marianne K. DeGorter & Laurent L. Reber & Joseph D. Hernandez & Philipp M. Starkl & Oliwia W. Zurek & Mindy Tsai & Sonja Zahner & Stephen B. Montgomery & Axel R, 2016. "A TNFRSF14-FcɛRI-mast cell pathway contributes to development of multiple features of asthma pathology in mice," Nature Communications, Nature, vol. 7(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms13696
    DOI: 10.1038/ncomms13696
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms13696
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms13696?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_ncomms13696. 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.