Intradermal administration of IL-33 induces allergic airway inflammation

Abstract Approximately half of all atopic dermatitis (AD) patients subsequently develop asthma, particularly those with severe AD. This association, suggesting a role for AD as an entry point for subsequent allergic disease, is a phenomenon known as the “atopic march”. While the underlying cause of...

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Autores principales:	Hongwei Han, Steven F. Ziegler
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/ab8cca8a85174759966757d08a42ecb6
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spelling	oai:doaj.org-article:ab8cca8a85174759966757d08a42ecb62021-12-02T12:32:42ZIntradermal administration of IL-33 induces allergic airway inflammation10.1038/s41598-017-01863-52045-2322https://doaj.org/article/ab8cca8a85174759966757d08a42ecb62017-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-01863-5https://doaj.org/toc/2045-2322Abstract Approximately half of all atopic dermatitis (AD) patients subsequently develop asthma, particularly those with severe AD. This association, suggesting a role for AD as an entry point for subsequent allergic disease, is a phenomenon known as the “atopic march”. While the underlying cause of the atopic march remains unknown, recent evidence suggests that epithelial cell (EC)-derived cytokines play a major role. We showed that mice exposed to antigen through the skin, in the presence of IL-33, developed antigen-specific airway inflammation when later challenged in the lung. IL-33 signaling was dispensable during effector/challenge phase. These data reveal critical roles for IL-33 in the “atopic march” and will offer a new therapeutic target in the treatment and prevention of allergic asthma.Hongwei HanSteven F. ZieglerNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-8 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Hongwei Han Steven F. Ziegler Intradermal administration of IL-33 induces allergic airway inflammation
description	Abstract Approximately half of all atopic dermatitis (AD) patients subsequently develop asthma, particularly those with severe AD. This association, suggesting a role for AD as an entry point for subsequent allergic disease, is a phenomenon known as the “atopic march”. While the underlying cause of the atopic march remains unknown, recent evidence suggests that epithelial cell (EC)-derived cytokines play a major role. We showed that mice exposed to antigen through the skin, in the presence of IL-33, developed antigen-specific airway inflammation when later challenged in the lung. IL-33 signaling was dispensable during effector/challenge phase. These data reveal critical roles for IL-33 in the “atopic march” and will offer a new therapeutic target in the treatment and prevention of allergic asthma.
format	article
author	Hongwei Han Steven F. Ziegler
author_facet	Hongwei Han Steven F. Ziegler
author_sort	Hongwei Han
title	Intradermal administration of IL-33 induces allergic airway inflammation
title_short	Intradermal administration of IL-33 induces allergic airway inflammation
title_full	Intradermal administration of IL-33 induces allergic airway inflammation
title_fullStr	Intradermal administration of IL-33 induces allergic airway inflammation
title_full_unstemmed	Intradermal administration of IL-33 induces allergic airway inflammation
title_sort	intradermal administration of il-33 induces allergic airway inflammation
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/ab8cca8a85174759966757d08a42ecb6
work_keys_str_mv	AT hongweihan intradermaladministrationofil33inducesallergicairwayinflammation AT stevenfziegler intradermaladministrationofil33inducesallergicairwayinflammation
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Intradermal administration of IL-33 induces allergic airway inflammation

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