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Allergen-specific B cells and T helper cells (primarily Th2 and Tfh subsets) constitute the fundamental cellular axis of the adaptive immune system responsible for allergic sensitization and chronic allergic inflammation (Akdis & Akdis, 2014). T helper cells provide essential signals, including cytokines like IL-4 and IL-13 and surface molecules like CD40 ligand, which trigger B cells to undergo class-switch recombination to produce immunoglobulin E (IgE) (Larche et al., 2006). This IgE then sensitizes mast cells and basophils, leading to the immediate hypersensitivity reactions characteristic of diseases such as allergic rhinitis, asthma, and food allergy (Galli et al., 2008). Therapeutic intervention, most notably allergen-specific immunotherapy (AIT), aims to reprogram this axis by inducing regulatory T (Treg) and B (Breg) cells that suppress Th2 activity and promote the production of “blocking” IgG4 antibodies (Shamji & Durham, 2017). Additionally, monoclonal antibodies targeting the signaling molecules or products of these cells, such as IL-4 receptors (Dupilumab) or IgE (Omalizumab), are used to disrupt the pathogenic cycle of this cellular interaction (Wenzel et al., 2013).
Induction of immune tolerance through regulatory T and B cell expansion, suppression of Th2 cytokines, and promotion of IgE-to-IgG4 class switching (Akdis & Akdis, 2014; Shamji & Durham, 2017).
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