Immune reactions elicited via IgE antibodies are well characterised and have a close temporal relationship to the responsible allergen. They are dependent on an initial sensitising event where there is exposure to the allergen in the absence of any overt clinical reactivity. This sensitising event can occur as a result of oral, epicutaneous, inhalational, subcutaneous, intradermal, intramuscular or intravenous exposure. The route and dose of allergen, the immune status of the individual, their genetic predisposition, gender and lifestyle are all likely to be influencing factors. Once allergen-specific IgE antibodies are produced by B cells, they bind to high affinity IgE receptors on tissue-resident mast cells and circulating basophils. Subsequent allergen exposure cross-links these allergen-specific IgE antibodies and causes degranulation of these cells with the release of histamine and other inflammatory mediators such as leukotrienes. Mast cell activation also results in the de novo production of various cytokines and chemokines resulting in the activation and tissue infiltration of various other inflammatory cells such as eosinophils and basophils. These are generally associated with the delayed manifestations secondary to allergen exposure including tissue oedema and hyperresponsiveness.
The mechanisms underlying non-IgE mediated food allergies are less well characterised and possibly involve a variety of mechanisms depending on the dose of allergen, the route of exposure and the tissue involved. The best described allergen-associated non-IgE mediated reaction is the infiltration of lymphocytes and eosinophils which occurs in eczema and eosinophilic oesophagitis. Other inflammatory cells have been implicated in various delayed food allergies such as neutrophils in FPIES
IgE mediated food allergic symptoms often occur soon after ingesting the trigger food, typically within 30 minutes of eating. Early symptoms might include mild oropharyngeal symptoms such as tingling or itching, which might progress onto oedema (swelling), and could be followed by other more systemic signs or symptoms such as flushing, urticaria (hives), nausea, vomiting, abdominal pain and diarrhoea; rhino-conjunctivitis and asthma. Anaphylaxis is a rapid, progressive multi-system reaction which is likely when there is acute onset of symptoms (e.g. urticaria, swelling, gastro-intestinal) and either airway compromise or hypotension. The amount of allergen which provokes a reaction cannot predict the severity of the reaction or the likelihood of anaphylaxis. However, co-factors such as exercise or fatigue are known to lower the threshold for an allergic reaction. Some foods, such as peanut, tree nuts, milk and seafood, are more likely to provoke anaphylaxis, although the type of foods involved may vary with age, geography, and dietary norms.
Food allergy is more prevalent in children, with milk, egg, wheat and soy allergies usually developing very early on in life and most often resolving in childhood or adolescence. Fish allergy often occurs on first exposure, and although thought to always be lifelong, there is some evidence that it might resolve in some children. Peanut and tree nut allergies are also most likely to develop in childhood, and although they are often life-long allergies for the majority, resolution can occur. Adult-onset triggers include shellfish, fruits and vegetables. New-onset symptoms to seeds such as sesame, can manifest at any age. People who have a food allergy are more likely to have an allergic co-morbidity such as eczema in children and allergic rhinitis in adults. Those with food allergy and concomitant asthma may experience more severe symptoms.