Approximately 5% of young children and 3-4% of adults exhibit adverse immune responses to foods in westernized countries, with a tendency to increase. The pathophysiology of
food allergy (FA) relies on immune reactions triggered by
epitopes, i.e. small amino-acid sequences able to bind to
antibodies or cells. Some food
allergens share specific physicochemical characteristics that allow them to resist digestion, thus enhancing allergenicity. These
allergens encounter specialized dendritic cell populations in the gut, which leads to T-cell priming. In case of
IgE-mediated
allergy, this process triggers the production of
allergen-specific
IgE by B cells. Tissue-resident reactive cells, including mast cells, then bind
IgE, and
allergic reactions are elicited when these cells, with adjacent
IgE molecules bound to their surface, are re-exposed to
allergen.
Allergic reactions occurring in the absence of detectable
IgE are labeled non-
IgE mediated. The abrogation of oral tolerance which leads to FA is likely favored by genetic disposition and environmental factors (e.g. increased hygiene or enhanced allergenicity of some foods). For an accurate diagnosis, complete medical history, laboratory tests and, in most cases, an oral food challenge are needed. Noticeably, the detection of food-specific
IgE (sensitization) does not necessarily indicate clinical
allergy. Novel diagnostic methods currently under study focus on the immune responses to specific food
proteins or
epitopes of specific
proteins. Food-induced
allergic reactions represent a large array of symptoms involving the skin and gastrointestinal and respiratory systems. They can be attributed to
IgE-mediated and non-
IgE-mediated (cellular) mechanisms and thus differ in their nature, severity and outcome. Outcome also differs according to
allergens.