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The allergen-specific immune system refers to the complex network of adaptive and innate immune components that recognize and respond to environmental allergens. This system is characterized by a Th2-biased response, where B cells produce allergen-specific Immunoglobulin E (IgE) antibodies that sensitize mast cells and basophils by binding to high-affinity FcεRI receptors [3, 13]. Upon re-exposure, the allergen cross-links these IgE molecules, triggering the rapid release of inflammatory mediators such as histamine, leukotrienes, and cytokines, which drive the clinical symptoms of Type I hypersensitivity [12, 14]. This pathway is central to the pathogenesis of chronic conditions like allergic asthma, rhinitis, and life-threatening anaphylaxis [10, 11]. Therapeutic interventions target various nodes of this system, including the neutralization of IgE (e.g., omalizumab) and the inhibition of Th2-pathway signaling (e.g., dupilumab) [15, 18]. Additionally, allergen-specific immunotherapy (AIT) aims to modify the system's underlying biology by inducing long-term immune tolerance through the expansion of regulatory T cells (Tregs) and the production of protective IgG4 blocking antibodies [1, 16].
Modulation of the immune response through neutralization of allergen-specific IgE, blockade of Th2-type cytokines (IL-4, IL-5, IL-13), antagonism of histamine receptors, or induction of immune tolerance via regulatory T and B cell expansion.
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