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