Cellular and molecular immunological mechanisms in eosinophilic esophagitis: an updated overview of their clinical implications

Eosinophilic esophagitis (EoE) is a pathophysiologically complex disorder driven by distinct, multiple mechanisms involving a large number of cells, molecules, and genes. Associated with food allergy from its initial descriptions, a key role for the Th2-type cytokines IL-5 and IL-13 in recruiting and activating eosinophils has been described. Epithelial cells have been recognized as major effectors in initiating EoE, both through their recruitment of iNKT cells towards the esophageal epithelium, which constitutes a major cytokine source, and through the release of eotaxin-3 and other chemoattractants. Epithelial and mesenchymal-released TSLP is a key regulator for which a connecting role between the adaptive and innate mucosal-associated immune response has been suggested. Finally, activated eosinophil-and mast cell-derived TGF beta 1 secretion is crucial in EoE-associated tissue remodeling.