There is an unmet medical need for an effective food allergy therapy; thus, development of therapeutic interventions for food allergy is a top research priority. The food allergen-nonspecific therapies for food-induced anaphylaxis include monoclonal anti-IgE antibodies and Chinese herbs. The food allergen-specific therapies include oral, sublingual, and epicutaneous immunotherapy with native food allergens and mutated recombinant proteins. Diet containing heated milk and egg may represent an alternative approach to oral immunomodulation. Oral food immunotherapy remains an investigational treatment to be further studied before advancing into clinical practice.
Food allergy is a growing public health problem. In the United States, it is estimated that 3.9% of general population under 18 years of age is affected by food allergies; the prevalence increased by 18% from 1997 to 2007. Currently, the only treatment of food allergy relies on strict food avoidance, dietary management to avoid nutritional deficiencies, and prompt emergency treatment of acute reactions. There is an unmet medical need for an effective food allergy therapy; thus, development of therapeutic interventions for food allergy is a top research priority. Studies concentrate on the foods most commonly implicated in severe IgE-mediated anaphylactic reactions (peanut, tree nuts, and shellfish) and the most common food allergens, such as cow’s milk and hen’s egg. The promising therapies under investigation can be classified as food allergen-nonspecific and food allergen-specific. The food allergen-nonspecific therapies for food-induced anaphylaxis include monoclonal anti-IgE antibodies, which increase the threshold dose for peanut in peanut-allergic individuals, and Chinese herbs, which prevent peanut anaphylaxis in an animal model and are currently being evaluated in human studies ( Table 1 ). The food allergen-specific therapies include oral immunotherapy (OIT), sublingual immunotherapy (SLIT), and epicutaneous immunotherapy (EPIT) with native food allergens ( Table 2 ) and mutated recombinant proteins, which have decreased IgE-binding activity, coadministered within heat-killed Escherichia coli to generate maximum immune response ( Table 3 ).
| Therapy | Mechanism of Action | Effects | Comments |
|---|---|---|---|
| Monoclonal anti-IgE | Binds to circulating IgE, prevents IgE deposition on mast cells, and blocks degranulation. Interferes with the facilitated antigen presentation by B-cell and dendritic cells. | Improves symptoms of asthma and allergic rhinitis; provides protection against peanut anaphylaxis in 75% of treated patients. | Subcutaneous at monthly or 2-week intervals, unknown long-term consequences of IgE elimination; food nonspecific; ongoing studies of combined anti-IgE and milk OIT in children |
| Traditional TCM | Down-regulation of T H 2 cytokines (IL-4, IL-5, and IL-13), up-regulation of T H 1 cytokines (IFN-γ and IL-12), decreased allergen IgE, decreased T-cell proliferation to peanut. | Reverses allergic inflammation in the airways, affords prolonged protection from peanut anaphylaxis (for ∼half of mouse lifespan). | Oral, generally safe and well tolerated; current studies focus on identification of the crucial active herbal components in the multiherb formulas and establishing optimal dosing in phase I and II clinical trials |
| Therapy | Mechanism of Action | Effects | Comments |
|---|---|---|---|
| Subcutaneous | |||
| Conventional peanut immunotherapy | Altered T-cell responses, up-regulation of suppressor cells | Increased oral peanut tolerance | Subcutaneous injections of gradually increasing doses of allergen; unacceptably high rate of serious adverse events |
| Birch pollen immunotherapy for oral allergy to apple | Marked reduction in skin test reactivity to raw apple; effect of immunotherapy inversely correlated with baseline skin reactivity but not with serum apple or birch IgE | Significant reduction or total resolution of oral allergy symptoms to raw Golden Delicious apple in a subset of patients receiving immunotherapy for at least 12 months | Clinical effect lasting for up to 30 months after discontinuation in >50% of patients |
| Oral/Sublingual | |||
| OIT | Decreased: skin test reactivity, food IgE, and IL-4 production by food-specific PBMCs Increased: food IgG, IgA, CD4 + CD23 high T cells; IL-10 | Oral food desensitization or increased threshold dose of food for clinical reactions up to 6 months; short-term success rate approximately 75% | No long-term follow-up data; many patients experience recurrence of symptoms if food not ingested on a daily basis. Significant rate of moderate to severe adverse reactions; convenience of home administration of maintenance doses |
| SLIT | Serum hazelnut IgG4 and total IL-10 increased in treated group; no change in hazelnut IgE | Oral food desensitization or increased threshold dose on oral hazelnut challenge | Systemic side effects rate 0.2% during rush buildup phase; adverse reaction rate less than with OIT; no long-term follow-up |
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