Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4458_Библиотеки_им_академика_М_И_Перельмана

The common mechanism leading to various food allergies is the breakdown of immunologic and clinical tolerance to an ingested food, which results in both IgE and non-IgE-mediated reac­tions. Sensitization to food allergens can occur through the gastrointestinal tract, the skin and, less commonly, the respiratory tract, presumably in conjunction with impaired and/or inamed barrier function. Induction and maintenance of tolerance to food antigens require active genera­tion of food antigen-specic regulatory T (Treg) cells, which are likely inuenced by the resident microbiome. This mucosal barrier might be less efcient or ‘immature’ in infants and young chil­dren. This would explain the increased preva­lence of both gastrointestinal tract infections and food allergy in the rst years of life. The skin is also more recently felt be a route of sensitiza­tion, as exemplied in several mouse models [74] and in epidemiologic studies suggesting that environmental exposure to peanut might promote sensitization and allergy [75, 76]. Thus, the role of the skin barrier has attracted increas­ing attention. Constitutive alterations in the skin, for example, such as a defect in the laggrin gene, might also lead to a great risk of sensitiza­tion [77].

There are extensive data to suggest that food allergies are common (up to 10% affected), [78] have been increasing in prevalence in the last 2–3 decades, appear to disproportionately affect per­sons in industrialized/westernized regions and are more common in children compared with adults and that a shortlist of foods accounts for most of the more serious disease burden, namely, peanut, tree nuts, sh, shellsh, egg, milk, wheat, soy and seeds [79–81].