Food allergy is defined as an adverse reaction to food proteins caused by immunologic mechanisms and is now estimated to affect over 11 million Americans. The disorder affects approximately 6% of children and appears to be increasing in prevalence despite efforts at prevention through dietary means. Milk or egg allergy in infants/young children are most common (-2.5%) but are likely to resolve (-50-85%) by age 5 years. Peanut allergy now affects 0.8% of young children, is often severe, sometimes fatal and in contrast to milk and egg allergy, peanut allergy resolves only in about 20% of patients. Previous studies have shown that genetics play a role in peanut allergy, but it is clear that environmental influences account for the startling, recently documented, doubling in incidence in young children in the US. There is only a limited understanding of the mechanisms involved in the developmental course of food allergies. For peanut allergy in particular, it is not known why only certain atopic individuals acquire this allergy, or what mechanisms are responsible for its permanence. To effectively prevent or reverse the progression of food allergy, immune interventions will be needed. Furthermore, it is likely that successful strategies will need to be directed to those persons at identifiable risk (e.g., who have biomarkers associated with development of peanut allergy). This observational study will investigate the developmental immunology of peanut, egg and milk allergy. We will enroll a cohort of 400 children age 3-12 months with atopic dermatitis and allergy to egg and/or milk and follow them over a 4-year period. During this time we predict that approximately 20% will develop clinical peanut allergy and 25-50% will experience resolution of egg or milk allergy. This strategy should enable us to delineate, compare and contrast biological markers and immunologic changes associated with the development of peanut allergy and loss of egg and milk allergy, while simultaneously evaluating important genetic and environmental influences. The results should form a basis for improved prevention and treatment. We will address hypotheses associated with the following specific aims: 1) To evaluate immune (T cell, humoral) and genetic (Toll-like receptor polymorphisms) parameters associated with the occurrence of peanut allergy and clinical outcomes; 2): To evaluate environmental (diet, hygiene-related) and clinical genetic (atopic dermatitis) factors that may influence occurrence of peanut allergy and clinical outcomes.
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