Background Oral immunotherapy offers a promising therapeutic option for peanut allergy. Given that during oral immunotherapy an allergic patient ingests an allergen that could potentially cause a serious reaction, safety of oral immunotherapy is of particular concern. Objective The purpose of this study is to examine safety during the initial escalation day, build-up phase, and home dosing phase in subjects enrolled in a peanut oral immunotherapy study. Methods Skin, upper respiratory, chest and abdominal symptoms were recorded with initial escalation day and build-up phase dosings. Subjects also maintained daily diaries detailing symptoms after each home dosing. A statistical analysis of this data was performed. Results Twenty of 28 patients completed all phases of the study. During the initial escalation day, upper respiratory (79%) and abdominal (68%) symptoms were the most likely symptoms experienced. The risk of mild wheezing during the initial escalation day was 18%. The probability of having any symptoms after a build-up phase dose was 46%, with a risk of 29% for upper respiratory symptoms and 24% for skin symptoms. The risk of reaction with any home dose was 3.5%. Upper respiratory (1.2%) and skin (1.1%) were the most likely symptoms after home doses. Treatment was given with 0.7% of home doses. Two subjects received epinephrine after one home dose each. Conclusions Subjects were more likely to have significant allergic symptoms during the initial escalation day when they were in a closely monitored setting than during other phases of the study. Allergic reactions with home doses were rare.

Mast cells have primarily been associated with mediating the pathological secondary responses to allergens in sensitized hosts. In view of the recent evidence for a mast cell role in modulating primary immune responses to pathogens, the likelihood for a role of mast cells in influencing primary immune response to allergens has grown. New evidence suggests that mast cells drive the development of Th2 responses to allergens, particularly when allergen exposure occurs concomitantly with exposure to pathogen products present in the environment. These new roles for mast cells in allergy and infection suggest additional drug targets to prevent development of allergic disease and allergic exacerbations of established disease.

Pollen food syndrome results from cross-reactivity between pollen-specific IgE and homologous proteins found in fruits and vegetables. These proteins can be grouped into several categories based on structure and include profilins, pathogenesis-related proteins, and cross-reactive carbohydrate determinants. Although cooking the reactive fruits and vegetables has been shown to destroy IgE-binding epitopes, evidence suggests that the remaining linear epitopes can bind cross-reactive T cells and enhance T-cell activation in vitro. Several methods of diagnosing food allergies exist, including skin prick tests and double-blind food challenges; however, diagnosing pollen food syndrome depends almost exclusively on clinical history. Immunotherapy has been studied as a treatment for pollen food syndrome, with highly variable results.

To evaluate whether pertussis induces the development of allergy, a prospective study was performed in 25 children aged 0.8-12.2 years. The patients underwent allergy diagnostics during pertussis infection and at a follow-up visit 8-14 months later. Diagnostic criteria included the medical history of the patients and their families, a modified skin prick test, measurement of serum IgE and radio-allergosorbent test screening for specific sensitizations. At the time of pertussis, serum IgE concentration in the study group was 62 +/- 30 kU/ml. At the follow-up visit, there was a significant increase in serum IgE to 137 +/- 51 kU/ml, which was also significantly higher than IgE in an age-matched control group. Children at a significantly higher risk for developing IgE increase or new allergic sensitizations were those with a family history of allergy or potentially allergic disease in their personal history. Our results indicate that pertussis may induce IgE production in affected children.

The prevalence of food allergy appears to be increasing. Hypersensitivity reactions to foods account for significant morbidity and mortality. The current standard of care for treatment of food allergies is limited to diligent dietary avoidance and prompt pharmacotherapy should an unexpected ingestion result in a reaction. Complex interactions between dietary antigens, the gastrointestinal flora, and the gut associated mucosal system drive host immune responses towards oral tolerance or hypersensitivity. Oral tolerance is achieved by regulatory T cell suppression of immune responses and by clonal anergy. Many novel therapies to treat food allergies are currently under investigation. Most utilize antigen-specific strategies in an attempt to induce oral tolerance. Oral immunotherapy (OIT) has been the focus of much attention. Early studies had established the safety and efficacy of OIT, but its ability to induce long-term tolerance versus a state of desensitization remains to be firmly established. Nevertheless, recent advances in our understanding of oral tolerance induction has increased optimism that disease-modifying therapies for food allergies will soon be the standard of care.

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