title: A murine model of peanut anaphylaxis: T- and B-cell responses to a major peanut allergen mimic human responses.
abstract: BACKGROUND
  Peanut allergy affects 0.6% of the US population. At the present time, allergen avoidance is the only therapeutic option. Animal models of food-induced anaphylaxis would facilitate attempts to design novel immunotherapeutic strategies for the treatment of peanut allergy.
  
  
  OBJECTIVE
  The purpose of this study was to develop a murine model of IgE-mediated peanut hypersensitivity that closely mimics human peanut allergy.
  
  
  METHODS
  C3H/HeJ mice sensitized orally with freshly ground whole peanut and cholera toxin as adjuvant were challenged orally 3 and 5 weeks later with crude peanut extract. Anaphylactic reactions were determined. T- and B-cell responses to Ara h 1 and Ara h 2, the major peanut allergens, were characterized by evaluating splenocyte proliferative responses and IgE antibody concentrations. Furthermore, IgE antibodies in the sera of patients with peanut 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 mice. 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 allergy. Furthermore, these Ara h 2-specific IgE antibodies bound the same Ara h 2 isoforms and major allergenic epitopes as antibodies in the sera of human subjects with peanut allergy. Splenocytes from mice with peanut allergy exhibited proliferative responses to Ara h 1 and Ara h 2.
  
  
  CONCLUSIONS
  This murine model of peanut allergy mimics the clinical and immunologic characteristics of peanut allergy in human subjects and should be a useful tool for developing immunotherapeutic approaches for the treatment of peanut allergy.
authors.affiliation: Department of Pediatrics, Mount Sinai School of Medicine, New York, USA.
authors.forename: X M
authors.initials: XM
authors.lastname: Li
authors.forename: D
authors.initials: D
authors.lastname: Serebrisky
authors.forename: S Y
authors.initials: SY
authors.lastname: Lee
authors.forename: C K
authors.initials: CK
authors.lastname: Huang
authors.forename: L
authors.initials: L
authors.lastname: Bardina
authors.forename: B H
authors.initials: BH
authors.lastname: Schofield
authors.forename: J S
authors.initials: JS
authors.lastname: Stanley
authors.forename: A W
authors.initials: AW
authors.lastname: Burks
authors.forename: G A
authors.initials: GA
authors.lastname: Bannon
authors.forename: H A
authors.initials: HA
authors.lastname: Sampson
mesh_terms: D055516:2S Albumins, Plant; D000485:Allergens / Q000009:adverse effects* / Q000276:immunology; D000707:Anaphylaxis / Q000139:chemically induced* / Q000276:immunology; D000818:Animals; D052179:Antigens, Plant; D010367:Arachis / Q000009:adverse effects* / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology*; D004195:Disease Models, Animal; D005260:Female; D005512:Food Hypersensitivity / Q000276:immunology; D006023:Glycoproteins / Q000009:adverse effects / Q000276:immunology; D006801:Humans; D007073:Immunoglobulin E / Q000276:immunology; D008565:Membrane Proteins; D051379:Mice; D008809:Mice, Inbred C3H; D010940:Plant Proteins / Q000009:adverse effects / Q000276:immunology; D012882:Skin Tests; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D055516:2S Albumins, Plant; D000485:Allergens; D052179:Antigens, Plant; C500889:Ara h 1 protein, Arachis hypogaea; C078642:Ara h II protein, Arachis hypogaea; D006023:Glycoproteins; D008565:Membrane Proteins; D010940:Plant Proteins; D007073:Immunoglobulin E