“…EoE is induced by food or aeroallergen exposure, characterized by intraepithelial eosinophil accumulation, eosinophil granule deposition in the extracellular tissue, and epithelial cell hyperplasia and is resistant to acid suppression therapy (10,11,14,20,27,31). Eosinophils and mast cells are increased in the esophageal mucosa of experimental and human EoE (2,9,17,19,25,30), but their role in disease pathogenesis is unclear. Mast cells express the high-affinity receptor for IgE on their surface (3,4,15,16) that initiates a complex process of signal transduction that releases proinflammatory mediators, cytokines, and chemokines (3,4,12,16).…”