IgE-Mediated Food Allergy

Abstract

Food allergies are defined as adverse immune responses to food proteins that result in typical clinical symptoms involving the dermatologic, respiratory, gastrointestinal, cardiovascular, and/or neurologic systems. IgE-mediated food-allergic disease differs from non-IgE-mediated disease because the pathophysiology results from activation of the immune system, causing a T helper 2 response which results in IgE binding to F c ε receptors on effector cells like mast cells and basophils. The activation of these cells causes release of histamine and other preformed mediators, and rapid symptom onset, in contrast with non-IgE-mediated food allergy which is more delayed in onset. The diagnosis of IgE-mediated food allergy requires a history of classic clinical symptoms and evidence of food-specific IgE by either skin-prick or serum-specific IgE testing. Symptoms of IgE-mediated food allergies range from mild to severe. The severity of symptoms is not predicted by the level of specific IgE or skin test wheal size, but the likelihood of symptom onset is directly related. Diagnosis is excluded when a patient can ingest the suspected food without clinical symptoms and may require an in-office oral food challenge if testing for food-specific IgE by serum or skin testing is negative or low. Anaphylaxis is the most severe form of the clinical manifestation of IgE-mediated food allergy, and injectable epinephrine is the first-line treatment. Management of food allergies requires strict avoidance measures, counseling of the family about constant vigilance, and prompt treatment of allergic reactions with emergency medications. Guidelines have changed recently to include early introduction of peanuts at 4-6 months of life. Early introduction is recommended to prevent the development of peanut allergy. Future treatments for IgE-mediated food allergy evaluated in clinical trials include epicutaneous, sublingual, and oral immunotherapy.

IgE reactivity to components of fish allergens in Pacific cod (Gadus macrocephalus) in atopic dogs

“…Moreover, we showed that the rate of IgE reactivity to crude cod allergens among dogs with cod allergy was 44% (12/27) (Fig. 1), which was comparable to that reported in humans [26,27]. Atopic dermatitis with food allergy can be a manifestation of an IgE-or a non-IgE-mediated reaction to food [28,29].…”

Protective Effect of Glycomacropeptide on Food Allergy with Gastrointestinal Manifestations in a Rat Model through Down-Regulation of Type 2 Immune Response

“…In IgE-mediated FA, the immune response to food proteins that pass through the disrupted epithelial barrier is developed within a tissue environment governed by inflammatory cytokines that activates dendritic cells to in turn activate T-cells into a T helper 2 (Th2) phenotype, which then prime the production of allergen specific IgE by B lymphocytes. Afterwards, IgE is bound to the high affinity receptor FcεRI on mast cells and the individual becomes allergen-sensitized [ 10 ]. The subsequent intake of the food allergen triggers the activation of mast cells, inducing the release of preformed and de novo produced vasoactive and inflammatory mediators, that causes the immediate manifestations of the allergic response [ 4 , 11 ].…”

Mechanisms of allergen-specific immunotherapy for allergic rhinitis and food allergies

“…FA is defined as an adverse immunological reaction to food [8,15], which may be IgE-mediated, non-IgE mediated (cell-mediated) or mixed (IgE and cell-mediated). IgE-mediated food reactions usually occur within minutes to 2 hours after exposure to allergen [16,17] while non-IgE-mediated food reactions are typically delayed from hours to weeks after intake of the allergen [18]. FA are diagnosed based on detailed clinical history and physical examination together with skin-prick test or serum-specific IgE testing, elimination diet for diagnostic purposes and oral food challenge [19].…”