fig1

Figure 1. Pathophysiology of eosinophilic esophagitis. Barrier integrity is essential in the gastrointestinal tract to protect against inappropriate inflammation. Impaired barrier defenses and allergic sensitization to food and aeroallergens can then initiate inflammation in the esophageal epithelium. Tissue resident antigen-presenting cells are thought to process and present allergenic peptides to CD4+ T lymphocytes, activating and skewing T cell differentiation towards T helper type 2 (Th2) lymphocyte development. When activated by antigen, Th2 cells produce pathogenic and inflammatory cytokines, IL-13, IL-5, and IL-4. IL-13 induces non-traditional immune cells, like the epithelium, to produce chemoattractant cytokines. One chemokine, CCL26 (also called Eotaxin-3) attracts and recruits eosinophils to the esophageal tissue. IL-5 promotes eosinophil maturation, differentiation, and activation, leading to the release of allergic mediators. IL-4 activates B cells to differentiate into plasma cells, undergo class switching, and produce antigen-specific IgE. IgE can then bind to Fc receptors on mast cells, triggering degranulation and release of histamine and proteases. Activated mast cells also produce TGF-β, a key cytokine implicated in fibrotic processes that lead to stenotic disease and esophageal narrowing