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Editorial
. 2016 Nov;138(5):1381-1383.
doi: 10.1016/j.jaci.2016.09.001. Epub 2016 Sep 21.

Linking impaired skin barrier function to esophageal allergic inflammation via IL-33

Affiliations
Editorial

Linking impaired skin barrier function to esophageal allergic inflammation via IL-33

Jared Travers et al. J Allergy Clin Immunol. 2016 Nov.
No abstract available

Keywords: Cytokines; barrier function; basophils; eosinophils; food allergy; innate Immunity.

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Conflict of interest statement

Disclosure of potential conflict of interest: M. E. Rothenberg receives grant support from the National Institutes of Health; consulting fees from Receptos Immune Pharmaceuticals, NKT Therapeutics, and PulmOne Therapeutics; patents with Miraca Life Science; royalties from Teva Pharmaceuticals; and stock options from PulmOne, NKT Therapeutics, and Immune Pharmaceuticals. The rest of the authors declare that they have no relevant conflicts of interest.

Figures

FIG 1
FIG 1
Proposed model for the development of allergic inflammation in patients with EoE. Impaired skin barrier integrity, such as that caused by injury or FLG mutations, allows for increased allergen penetration through the epithelium, causing allergic sensitization and release of IL-33 and TSLP from the epithelium. Secondary to activation by these cytokines, there is increased trafficking of basophils through the bloodstream to the esophagus. Later, direct exposure of allergens to the esophageal epithelium leads to the release of TSLP and IL-33, which induce IL-4 production from basophils and subsequent release of IL-5 and IL-13 from TH2 cells. IL-13 causes esophageal epithelial barrier impairment and increased allergen exposure by decreasing desmoglein 1 (DSG1) and increasing calpain 14 (CAPN14) expression. Additionally, IL-13 induces CCL26 production from the epithelium, which, in combination with IL-5, causes eosinophil infiltration into the esophagus.

Comment on

References

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