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

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 Roers, Mitchell Kronenberg, Mang Yu () and Stephen J. Galli ()
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Riccardo Sibilano: Stanford University School of Medicine
Nicolas Gaudenzio: Stanford University School of Medicine
Marianne K. DeGorter: Stanford University School of Medicine
Laurent L. Reber: Stanford University School of Medicine
Joseph D. Hernandez: Stanford University School of Medicine
Philipp M. Starkl: Stanford University School of Medicine
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
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

Nature Communications, 2016, vol. 7, issue 1, 1-15

Abstract: 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.

Date: 2016
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DOI: 10.1038/ncomms13696

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