Adaptive immune response to peanut allergens

The adaptive immune response to peanut allergens is a pathological immune process characterized by a Type I hypersensitivity reaction against specific peanut proteins, most notably Ara h 1, Ara h 2, and Ara h 3 (Sampson et al., 2018, J Allergy Clin Immunol). This process begins with a sensitization phase where the immune system incorrectly identifies peanut proteins as harmful, leading to the production of allergen-specific IgE antibodies by B cells, a process driven by Th2 cytokines such as IL-4 and IL-13 (Akdis et al., 2020, Nat Rev Immunol). Upon subsequent exposure, these IgE antibodies, which are bound to high-affinity FcεRI receptors on mast cells and basophils, cross-link with the allergen, triggering the rapid release of inflammatory mediators like histamine and leukotrienes (Anagnostou, 2018, Paediatr Drugs). This cascade results in clinical symptoms that can range from mild cutaneous reactions to severe, life-threatening anaphylaxis. Current therapeutic approaches do not target a single molecule but rather modulate this complex pathway through IgE sequestration (e.g., Omalizumab), cytokine inhibition (e.g., Dupilumab), or oral immunotherapy (e.g., Palforzia) to induce desensitization and increase the threshold of allergen tolerated (Wood et al., 2024, N Engl J Med; FDA, 2020).

Other names

Peanut allergyType I hypersensitivity to peanutPeanut-induced immune responsePeanut-specific IgE-mediated hypersensitivity

Therapeutic intervention involves neutralizing circulating IgE antibodies to prevent mast cell activation, blocking Th2-related cytokine signaling (IL-4/IL-13) to reduce allergic inflammation, or utilizing oral immunotherapy (OIT) to induce desensitization by shifting the immune profile from Th2-biased to regulatory T cell (Treg) and IgG4-mediated tolerance.