A TNFRSF14-FcɛRI-mast cell pathway contributes to development of multiple features of asthma pathology in mice
| العنوان: | A TNFRSF14-FcɛRI-mast cell pathway contributes to development of multiple features of asthma pathology in mice |
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| المؤلفون: | Mindy Tsai, Joseph D. Hernandez, Mang Yu, Sonja Zahner, Stephen B. Montgomery, Axel Roers, Oliwia W Zurek, Nicolas Gaudenzio, Philipp Starkl, Stephen J. Galli, Mitchell Kronenberg, Laurent L. Reber, Marianne K. DeGorter, Riccardo Sibilano |
| المساهمون: | Department of Pathology [Stanford], Stanford Medicine, Stanford University-Stanford University, Department of Genetics [Stanford], Anticorps en thérapie et pathologie - Antibodies in Therapy and Pathology, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Pediatrics [Stanford], Research Center for Molecular Medicine of the Austrian Academy of Sciences [Vienna, Austria] (CeMM ), Austrian Academy of Sciences (OeAW), La Jolla Institute for Immunology [La Jolla, CA, États-Unis], Technische Universität Dresden = Dresden University of Technology (TU Dresden), Sean N. Parker Center for Allergy and Asthma Research [Stanford], This work was supported by US National Institutes of Health (NIH) grants to S.J.G. (U19AI104209 and R01AR067145), M.K. (R01AI61516) and L.L.R. (K99AI110645), fellowships from the Lucile Packard Foundation for Children’s Health to R.S. (UL1 RR025744) and J.D.H. (UL1 TR001085), the Fondation pour la Recherche Medicale (FRM) SPE20130326582 and Philippe foundation to N.G., a Schroedinger Fellowship of the Austrian Science Fund (FWF) J3399-B21 to P.M.S., an NIH postdoctoral fellowship (2T32AI007290-31) to O.W.Z., the Department of Pathology and the Sean N. Parker Center for Allergy and Asthma Research, Stanford University., Pistre, Karine |
| المصدر: | Nature Communications Nature Communications, 2016, 7, pp.13696. ⟨10.1038/ncomms13696⟩ Nature Communications, Vol 7, Iss 1, Pp 1-15 (2016) |
| بيانات النشر: | HAL CCSD, 2016. |
| سنة النشر: | 2016 |
| مصطلحات موضوعية: | 0301 basic medicine, Pathology, General Physics and Astronomy, Immunoglobulin E, MESH: Mice, Knockout, MESH: Ovalbumin / immunology, Immunoglobulin G, MESH: Receptors, IgE / metabolism, MESH: Genotype, MESH: Ovalbumin / toxicity, Mice, 0302 clinical medicine, Antigen Sensitization, MESH: Asthma / pathology, MESH: Animals, MESH: Mast Cells / physiology, Mast Cells, Mice, Knockout, MESH: Immunoglobulin G, Multidisciplinary, biology, MESH: Gene Expression Regulation / drug effects, MESH: Bronchoalveolar Lavage Fluid / cytology, MESH: Immunoglobulin E, Chronic inflammation, Mast cell, MESH: Antigens, Dermatophagoides / toxicity, 3. Good health, medicine.anatomical_structure, MESH: Receptors, IgE / genetics, Airway Remodeling, Mucosal immunology, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, Tumor necrosis factor alpha, Antibody, medicine.symptom, [SDV.IMM.IMM] Life Sciences [q-bio]/Immunology/Immunotherapy, Bronchoalveolar Lavage Fluid, Receptors, Tumor Necrosis Factor, Member 14, MESH: Antigens, Dermatophagoides / immunology, medicine.medical_specialty, Genotype, [SDV.IMM] Life Sciences [q-bio]/Immunology, Ovalbumin, Science, MESH: Asthma / metabolism, Inflammation, Article, Antibodies, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, Mediator, medicine, Animals, Antigens, Dermatophagoides, MESH: Mice, Receptors, IgE, business.industry, MESH: Asthma / chemically induced, MESH: Antibodies, General Chemistry, [SDV.IMM.IMM]Life Sciences [q-bio]/Immunology/Immunotherapy, MESH: Receptors, Tumor Necrosis Factor, Member 14 / genetics, Asthma, respiratory tract diseases, MESH: Airway Remodeling, 030104 developmental biology, Gene Expression Regulation, Immunology, biology.protein, MESH: Receptors, Tumor Necrosis Factor, Member 14 / metabolism, business, MESH: Female, 030215 immunology |
| الوصف: | 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. TNFSF14 (LIGHT) contributes to airway inflammation and remodelling. Here the authors show that TNFSF14 acting on its receptor TNFRSF14 on mast cells enhances their IgE-dependent activation and that interference with this pathway attenuates features of asthma pathology in mice. |
| وصف الملف: | application/pdf |
| اللغة: | English |
| تدمد: | 2041-1723 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::975c634ea018b0399cc2423e074d9a7fTest https://ut3-toulouseinp.hal.science/hal-03521499/file/2016_Sibliano.pdfTest |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....975c634ea018b0399cc2423e074d9a7f |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 20411723 |
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