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Allergen-specific Immunoglobulin E (IgE) and B-cell receptors (BCRs) are the primary immunological components responsible for recognizing grass pollen allergens and mediating allergic disease. In sensitized individuals, IgE antibodies bound to mast cells and basophils recognize grass pollen proteins, triggering the release of inflammatory mediators that cause symptoms of hay fever and asthma (Akdis & Akdis, 2014). Grass pollen allergoids are chemically modified allergens, often polymerized with glutaraldehyde or formaldehyde, designed to have significantly reduced IgE-binding capacity to improve safety during immunotherapy (Zidarn et al., 2022). Despite this modification, allergoids retain the ability to bind to B-cell receptors and present T-cell epitopes, which is critical for inducing immune tolerance (Pfaar et al., 2019). Therapeutic intervention with these allergoids aims to desensitize the patient by promoting the expansion of regulatory T and B cells and stimulating the production of protective IgG4 antibodies. These IgG4 antibodies act as 'blocking' agents that compete with IgE for allergen binding, thereby preventing the allergic cascade upon natural exposure to grass pollen (Klimek et al., 2022).
Induction of immune tolerance through desensitization, shifting the immune response from Th2-mediated inflammation to Th1/Treg-mediated regulation, and increasing allergen-specific IgG4 levels to block IgE-mediated mast cell activation.
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