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  • Allinne, JeanneRegeneron Pharmaceuticals, Inc. (author)

IL-33 blockade affects mediators of persistence and exacerbation in a model of chronic airway inflammation

  • Article/chapterEnglish2019

Publisher, publication year, extent ...

  • Elsevier BV,2019
  • 24 s.

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  • LIBRIS-ID:oai:lup.lub.lu.se:34a61787-87be-4c81-8742-e546b4df2559
  • https://lup.lub.lu.se/record/34a61787-87be-4c81-8742-e546b4df2559URI
  • https://doi.org/10.1016/j.jaci.2019.08.039DOI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:art swepub-publicationtype
  • Subject category:ref swepub-contenttype

Notes

  • Background: Severe inflammatory airway diseases are associated with inflammation that does not resolve, leading to structural changes and an overall environment primed for exacerbations. Objective: We sought to identify and inhibit pathways that perpetuate this heightened inflammatory state because this could lead to therapies that allow for a more quiescent lung that is less predisposed to symptoms and exacerbations. Methods: Using prolonged exposure to house dust mite in mice, we developed a mouse model of persistent and exacerbating airway disease characterized by a mixed inflammatory phenotype. Results: We show that lung IL-33 drives inflammation and remodeling beyond the type 2 response classically associated with IL-33 signaling. IL-33 blockade with an IL-33 neutralizing antibody normalized established inflammation and improved remodeling of both the lung epithelium and lung parenchyma. Specifically, IL-33 blockade normalized persisting and exacerbating inflammatory end points, including eosinophilic, neutrophilic, and ST2+CD4+ T-cell infiltration. Importantly, we identified a key role for IL-33 in driving lung remodeling because anti–IL-33 also re-established the presence of ciliated cells over mucus-producing cells and decreased myofibroblast numbers, even in the context of continuous allergen exposure, resulting in improved lung function. Conclusion: Overall, this study shows that increased IL-33 levels drive a self-perpetuating amplification loop that maintains the lung in a state of lasting inflammation and remodeled tissue primed for exacerbations. Thus IL-33 blockade might ameliorate symptoms and prevent exacerbations by quelling persistent inflammation and airway remodeling.

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Added entries (persons, corporate bodies, meetings, titles ...)

  • Scott, GeorgeRegeneron Pharmaceuticals, Inc. (author)
  • Lim, Wei KeatRegeneron Pharmaceuticals, Inc. (author)
  • Birchard, DylanRegeneron Pharmaceuticals, Inc. (author)
  • Erjefält, Jonas S.Lund University,Lunds universitet,Luftvägsinflammation,Forskargrupper vid Lunds universitet,Airway Inflammation and Immunology,Lund University Research Groups,Medetect AB(Swepub:lu)mphy-jer (author)
  • Sandén, CarolineMedetect AB(Swepub:lu)mphy-cgu (author)
  • Ben, Li HongRegeneron Pharmaceuticals, Inc. (author)
  • Agrawal, AmitRegeneron Pharmaceuticals, Inc. (author)
  • Kaur, NavneetRegeneron Pharmaceuticals, Inc. (author)
  • Kim, Jee HaeRegeneron Pharmaceuticals, Inc. (author)
  • Kamat, VishalRegeneron Pharmaceuticals, Inc. (author)
  • Fury, WenRegeneron Pharmaceuticals, Inc. (author)
  • Huang, TammyRegeneron Pharmaceuticals, Inc. (author)
  • Stahl, NeilRegeneron Pharmaceuticals, Inc. (author)
  • Yancopoulos, George D.Regeneron Pharmaceuticals, Inc. (author)
  • Murphy, Andrew J.Regeneron Pharmaceuticals, Inc. (author)
  • Sleeman, Matthew A.Regeneron Pharmaceuticals, Inc. (author)
  • Orengo, Jamie M.Regeneron Pharmaceuticals, Inc. (author)
  • Regeneron Pharmaceuticals, Inc.Luftvägsinflammation (creator_code:org_t)

Related titles

  • In:Journal of Allergy and Clinical Immunology: Elsevier BV144:6, s. 1624-16370091-6749

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