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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 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.

SUBMITTER: Han H

PROVIDER: S-EPMC5431780 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature

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Intradermal administration of IL-33 induces allergic airway inflammation.

Han Hongwei H Ziegler Steven F SF

Scientific reports 20170510 1

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, deve ...[more]

PMID: 28490737

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Project description: Not available

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