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IL-33 blockade affe...
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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
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LIBRIS-ID:oai:lup.lub.lu.se:34a61787-87be-4c81-8742-e546b4df2559
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https://lup.lub.lu.se/record/34a61787-87be-4c81-8742-e546b4df2559URI
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https://doi.org/10.1016/j.jaci.2019.08.039DOI
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Language:English
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Summary in:English
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Subject category:art swepub-publicationtype
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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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Scott, GeorgeRegeneron Pharmaceuticals, Inc.
(author)
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Lim, Wei KeatRegeneron Pharmaceuticals, Inc.
(author)
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Birchard, DylanRegeneron Pharmaceuticals, Inc.
(author)
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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)
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Sandén, CarolineMedetect AB(Swepub:lu)mphy-cgu
(author)
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Ben, Li HongRegeneron Pharmaceuticals, Inc.
(author)
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Agrawal, AmitRegeneron Pharmaceuticals, Inc.
(author)
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Kaur, NavneetRegeneron Pharmaceuticals, Inc.
(author)
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Kim, Jee HaeRegeneron Pharmaceuticals, Inc.
(author)
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Kamat, VishalRegeneron Pharmaceuticals, Inc.
(author)
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Fury, WenRegeneron Pharmaceuticals, Inc.
(author)
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Huang, TammyRegeneron Pharmaceuticals, Inc.
(author)
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Stahl, NeilRegeneron Pharmaceuticals, Inc.
(author)
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Yancopoulos, George D.Regeneron Pharmaceuticals, Inc.
(author)
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Murphy, Andrew J.Regeneron Pharmaceuticals, Inc.
(author)
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Sleeman, Matthew A.Regeneron Pharmaceuticals, Inc.
(author)
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Orengo, Jamie M.Regeneron Pharmaceuticals, Inc.
(author)
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Regeneron Pharmaceuticals, Inc.Luftvägsinflammation
(creator_code:org_t)
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In:Journal of Allergy and Clinical Immunology: Elsevier BV144:6, s. 1624-16370091-6749
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Allinne, Jeanne
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Scott, George
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Lim, Wei Keat
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Birchard, Dylan
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Erjefält, Jonas ...
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Sandén, Caroline
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Ben, Li Hong
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Agrawal, Amit
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Kaur, Navneet
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Kim, Jee Hae
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Kamat, Vishal
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Fury, Wen
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Huang, Tammy
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Stahl, Neil
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Yancopoulos, Geo ...
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Murphy, Andrew J ...
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Sleeman, Matthew ...
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Orengo, Jamie M.
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Lund University