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Jeffrey M Wilson, Rung-chi Li, Emily C McGowan Division of Allergy and Immunology, University of Virginia, Charlottesville, VA, USACorrespondence: Jeffrey M WilsonDivision of Allergy & Clinical Immunology, University of Virginia, Charlottesville, VA 22908-1355, USATel +1 (434) 924-5917Fax +1 (434) 924-5779Email jmw2gc@virginia.eduAbstract: Food allergy is often understood as an IgE-mediated hypersensitivity, characterized by allergic symptoms which occur “immediately” after the ingestion of a relevant food allergen. Increasingly, however, other food-related immune-mediated disorders are recognized in which symptoms can have a delayed onset and IgE does not play a central role. One of the described examples of the latter is eosinophilic esophagitis (EoE) – a disease defined pathologically by local eosinophilic inflammation in the esophagus in the setting of symptoms of esophageal dysfunction. The evidence that EoE is a food-mediated allergic disease includes i) almost all patients respond to an elemental diet and many respond to a diet in which dairy, wheat, eggs and/or soy are eliminated, ii) the presence of food-specific IgE and Th2 cells are consistent with a loss of tolerance to trigger foods and iii) many EoE patients have concomitant IgE-mediated food allergy and other allergic co-morbidities. This narrative review focuses on the hypothesis that EoE is a form of chronic food allergy. The goal is to describe similarities and differences in EoE and IgE-mediated food allergy, and to consider ways that these two increasingly common forms of food allergy are related to each other.Keywords: food allergy, eosinophilic esophagitis, IgE, IgG4, Th2, Treg, barrier hypothesis |
