Introduction
Food allergy is defined as an adverse reaction to food which is reproducible and arises from a specific immune response.1 Food allergies affect up to 7-8% of the population and have been increasing in prevalence, although the incidence has probably stabilised in Western countries. Prevalence is higher in children compared to adults, with the most common food triggers being peanut, tree nuts and seeds, egg, milk, wheat, soy, fish and shellfish.1-3 The common underlying mechanism is the breakdown of immunological and clinical tolerance to an ingested food, causing either IgE-mediated reactions (including anaphylaxis) or non-IgE-mediated disorders such as eosinophilic eosophagitis (EoE) and food protein induced enterocolitis syndrome (FPIES).4Sensitization to food allergens usually occurs through the skin and/or gastrointestinal tract (and less commonly through the respiratory tract), due to impaired barrier function.5, 6Following sensitization, many – but not all – individuals go on to develop clinical reactivity. The interaction between microbiota, the immune system, epithelial barrier function and genetic factors results in a dysregulated type 2 response to food allergens. Recent studies have demonstrated the possible involvement of a novel cell type, known as innate lymphoid cells (ILCs), in driving food allergy.7 While their role is not currently well-defined, the elevated levels of Interleukin (IL)-25, IL-33 and thymic stromal lymphopoietin (TSLP) observed in allergic patients imply a possible role because these cytokines are strong stimuli of a subset of these cells, the ILC2s.7-9 For instance, recently, it was shown that IL-33 promotes food allergy through the expansion and activation of ILC2s, resulting in the large production of IL-4 that suppresses regulatory T cells function in the skin, lung and small intestine.10 ILC2s have been shown to be potent producers of IL-9, which was highly expressed in a study of children with peanut allergy.11 In addition, the expression of IL-33 was increased in esophageal biopsies of pediatric EoE patients12 and ILC2s density was increased in esophageal biopsies from patients with active EoE.13