Abstract

EoE is an increasingly common inflammatory condition of the esophagus, however, the underlying immunologic mechanisms remain poorly understood. The epithelium-derived cytokine IL-33 is associated with type 2 responses and is elevated in esophageal biopsies from EoE subjects. We hypothesized that overexpression of secreted and active IL-33 by the esophageal epithelium would result in innate and adaptive immune responses associated with type 2 inflammation representative of human disease.

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