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Immune system modulation via allergen-specific tolerance induction is an immunological approach (rather than a single molecular target) that aims to retrain the immune system to tolerate specific allergens, thus reducing allergic reactivity. This process is central to allergen-specific immunotherapy (AIT), in which repeated allergen exposure shifts the immune system from a pathogenic Th2 allergic response toward a regulatory phenotype dominated by Tregs that secrete immunosuppressive cytokines such as IL-10 and TGF-β[1][2][3][4][5]. Key mechanisms include the induction of both natural and inducible Treg subsets, increased generation of allergen-specific blocking antibodies (IgG4), decreased allergen-specific IgE production, and reprogramming of dendritic cells to promote tolerance. This mechanism addresses the fundamental pathology in allergy by restoring immune homeostasis, but is best considered an immunological pathway or therapeutic strategy, not a discrete molecule or receptor[1][2][3][4][5].
Induction of allergen-specific regulatory T cells (Tregs: including natural Tregs [nTregs], Tr1, Th3); Suppression of effector T cell responses (Th2, Th1) via IL-10, TGF-β, and other inhibitory signals[1][2][3][4]; Induction of IgG4 “blocking antibodies” by Breg cells, limiting IgE-mediated responses; Dendritic cell reprogramming to a tolerogenic phenotype, favoring Treg expansion[2][4][5]; Reduction of pro-inflammatory cytokines (e.g., IL-4); Increased secretion of anti-inflammatory cytokines (IL-10, TGF-β)
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