Eosinophilic esophagitis (EoE) is a chronic, food-mediated Type-2 (T2) inflammatory disease of the esophagus [1,2]. The disease was initially described in the early 1990s by Stephen Attwood and Alex Straumann [3,4], who independently documented the clinical presentation of a handful of patients with esophageal eosinophilia. However, it was not until a decade later that the first publication exploring its potential Th2 cytokine-driven pathophysiology was released [2]. Initially being considered a rare disease, EoE has emerged as an important clinical entity with increasing prevalence and incidence over the last 30 years [5,6]. Currently, it is estimated that 1 out of 700 suffers from EoE, and it represents the most common cause of solid food dysphagia in the Western hemisphere [7]. Dysphagia, mainly for solids, is the leading symptom in most patients, but a non-specific presentation including burning sensation within the esophagus, chest pain and reflux is not infrequent, particularly in children and adolescents [8]. The natural history of EoE has been well documented with most patients progressing from an inflammatory phenotype towards an inflammatory-fibrotic phenotype [9]. In fact, after 10 years of undiagnosed EoE 70 % of patients present with an esophageal stricture [10].

Treatment strategies consist of the 3D's: drugs, diet, and dilation [11]. However, endoscopic dilation should not be used as a standalone therapy, but rather as an add-on for managing severe fibrosis or strictures [11]. Both drug therapy and dietary modification are valid first-line treatment strategies. In general, these approaches are used separately, as combining them has not shown any additional benefit. Drugs include proton-pump inhibitors, topical steroids and the anti IL-4/IL-13 antibody dupilumab. All medications have proven to be efficacious in inducing and maintaining clinical, endoscopic and histological remission, although the strongest evidence supports the use of topical steroids and dupilumab. Diets are also highly effective. Since EoE is triggered by certain foods, eliminating these triggers can successfully induce and maintain remission. The classical food categories are: milk, wheat/gluten, eggs, soy, nuts and fish/seafood [12]. While EoE is a benign disease without evidence for progression towards cancer, it can significantly affect quality of life, particularly in patients with severe disease [13]. Nonetheless, it is important to also consider patients with milder forms of the disease, as many of them may not experience relevant dysphagia due to adjustments in their eating habits. These modifications can nicely be summarized by the mnemonic IMPACT: Imbibe fluid with meals; Modify food (cut, puree); Prolong mealtime; Avoid hard texture foods; Chew excessively; Turn away tables/pills [14]. Therefore, during patient consultations, it is of utmost importance to inquire about these strategies in order to unmask underlying dysphagia. In the following review, we will summarize current knowledge about the role and impact of different food antigens in EoE pathophysiology with a particular focus on therapeutic implications.