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. Author manuscript; available in PMC: 2015 Jun 1.
Published in final edited form as: Gastroenterol Clin North Am. 2014 Mar 22;43(2):281–296. doi: 10.1016/j.gtc.2014.02.006

Fig 1.

Fig 1

Proposed allergic mechanisms involved in the pathogenesis of Eosinophilic Esophagitis (EoE). TOP: Proposed mechanism of allergic sensitization in EoE. In the presence of epithelial injury, TSLP production is elicited from epithelium. This primes basophils to produce IL-4 which promotes allergic sensitization after antigen presentation to a naïve T-cell which generates antigen-specific Th2 cells. BOTTOM: Proposed mucosal response in EoE. Subsequet antigen challenge leads to recruitment and expansion of Th2 cells which secrete IL-5 and IL-13, both critical in the recruitment of eosinophils and remodeling of the esophagus. Th2 cells locally promote class-switching of B-cells to produce antigen-specific IgE, which binds to the surface of mast cells. Activation of mast cells leads to the releast of pro-inflammatory mediators such as TGF-β, which promotes remodeling and enhances muscle cell contractility.