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The systemic adaptive immune response to peanut allergen is a complex physiological process involving the sensitization and subsequent reaction of the immune system to proteins such as Ara h 1 and Ara h 2. In allergic individuals, this response is characterized by a Th2-cell bias, leading to high levels of allergen-specific IgE that prime mast cells and basophils for degranulation upon exposure (Akdis et al., 2014, J Allergy Clin Immunol). Polyclonal immunologic tolerance mechanisms refer to the therapeutic induction of a shift in this response, typically through oral immunotherapy (OIT), which promotes the expansion of regulatory T cells (Tregs) and the production of protective IgG4 antibodies (Kulis et al., 2018, J Allergy Clin Immunol). These IgG4 antibodies act as “blocking” agents that compete with IgE for allergen binding, thereby preventing the activation of effector cells. Drugs like Palforzia (Peanut allergen powder-dnfp) utilize this mechanism by providing controlled, escalating doses of peanut protein to desensitize the patient (FDA, 2020). Additionally, adjunct therapies like Omalizumab (Xolair) can be used to sequester IgE and lower the risk of reactions during the tolerance-induction process (Wood et al., 2024, N Engl J Med). This systemic reprogramming is not a single molecular target but a coordinated immunological transition aimed at achieving sustained unresponsiveness to peanut allergens.
Induction of regulatory T cells (Tregs), allergen-specific IgG4 production, and Th2-to-Th1 cytokine shift to suppress IgE-mediated mast cell activation.
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