A murine model of peanut anaphylaxis: T- and B-cell responses to a major peanut allergen mimic human responses

Background: Peanut allergy affects 0.6% of the US population. At the presen t time, allergen avoidance is the only therapeutic option. Animal models of Toed-induced anaphylaxis would Facilitate attempts to design novel immunot herapeutic strategies for the treatment of peanut allergy. Objective: The purpose of this study was to develop a murine model of IgE-m ediated peanut hypersensitivity that closely mimics human peanut allergy. Methods: C3H/HeJ mice sensitized orally with freshly ground whole peanut an d cholera toxin as adjuvant were challenged orally 3 and 5 weeks later with crude peanut extract. Anaphylactic reactions were determined. T- and B-cel l responses to Ara h 1 and Ara h 2, the major peanut allergens, were charac terized by evaluating splenocyte proliferative responses and IgE antibody c oncentrations. Furthermore, IgE antibodies in the sera of patients with pea nut allergy and mice were compared for antibody binding to Ara h 2 isoforms and allergenic epitopes, Results: Peanut-specific IgE was induced by oral peanut sensitization, and hypersensitivity reactions were provoked by feeding peanut to sensitized mi ce. The symptoms were similar to those seen in human subjects. Ara h 1- and Ara h 2-specific antibodies were present in the sera of mice with peanut a llergy. Furthermore, these Ara h 2-specific IgE antibodies bound the same A ra h 2 isoforms and major allergenic epitopes as antibodies in the sera of human subjects with peanut allergy. Splenocytes from mice with peanut aller gy exhibited proliferative responses to Ara h 1 and Ara h 2, Conclusion: This murine model of peanut allergy mimics the clinical and imm unologic characteristics of peanut allergy in human subjects and should be a useful tool for developing immunotherapeutic approaches for the treatment of peanut allergy.