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Peanut allergen-specific T and B cell responses constitute the immunological framework of peanut allergy, characterized by a breakdown in oral tolerance. This process involves the activation of Th2-polarized CD4+ T cells that produce cytokines such as IL-4 and IL-13, which drive B cell class-switching to produce peanut-specific IgE (sIgE) (Source: Galli, S. J., et al. Nature, 2008). These sIgE antibodies bind to high-affinity receptors (FcεRI) on mast cells and basophils; subsequent exposure to peanut allergens (e.g., Ara h 1, Ara h 2) causes receptor cross-linking and the release of inflammatory mediators, leading to clinical symptoms (Source: Sampson, H. A., et al. JACI, 2018). Therapeutic interventions like Palforzia (Peanut allergen powder-dnfp) aim to desensitize this response by shifting the immune balance toward regulatory T cells (Tregs) and increasing peanut-specific IgG4, which acts as a blocking antibody (Source: Vickery, B. P., et al. NEJM, 2018). Additionally, biologics such as Omalizumab are used to sequester IgE, thereby increasing the threshold for allergen-induced activation (Source: Wood, R. A., et al. NEJM, 2024).
Induction of immunological desensitization and tolerance through repeated low-dose allergen exposure, sequestration of free IgE, and blockade of Th2-mediated cytokine signaling.
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