Ara H 2‐specific IgE Epitope‐like Peptides Inhibit the Binding of IgE to Ara H 2 and Suppress Lge‐dependent Effector Cell Activation

Clinical and experimental analyses indicate a pathognomonic role for allergen IgE crosslinking through epitope–paratope interactions as a major initial step in the cascade leading to effector cell activation and clinical manifestations of lgE‐mediated food allergies. We aimed to undertake the initial development and assessment of Ara h 2‐specific IgE epitope‐like peptides that can bind to allergen‐specific IgE paratopes and suppress effector cell activation.