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Polyclonal IgE antibodies and T-cell receptors (TCRs) specific to Dactylis glomerata (orchard grass) pollen allergens are the primary immunological components responsible for orchard grass-induced Type I hypersensitivity. IgE antibodies specific for allergens such as Dac g 1 and Dac g 5 bind to high-affinity FcεRI receptors on mast cells and basophils; upon allergen exposure, cross-linking of these IgE-receptor complexes triggers the release of inflammatory mediators like histamine (WHO/IUIS, 2024). TCRs on allergen-specific CD4+ T cells recognize peptide fragments of these allergens presented by MHC class II molecules, driving a Th2-biased immune response characterized by the production of cytokines such as IL-4, IL-5, and IL-13 (Bousquet et al., 2008). These interactions underlie the pathophysiology of allergic rhinitis, conjunctivitis, and seasonal asthma. Therapeutic strategies targeting these components include the monoclonal antibody omalizumab, which sequesters circulating IgE, and allergen-specific immunotherapy (AIT). AIT aims to desensitize the immune system by inducing T-cell anergy or shifting the response toward a regulatory phenotype, thereby reducing the clinical severity of the allergic response (Akdis & Akdis, 2014).
Omalizumab inhibits the binding of IgE to the high-affinity IgE receptor (FcεRI) on the surface of mast cells and basophils, thereby limiting the release of allergic mediators (FDA, 2023). Allergen-specific immunotherapy (AIT) using Dactylis glomerata extracts works by inducing peripheral T-cell tolerance, increasing the production of IL-10 and TGF-beta by regulatory T cells, and promoting the synthesis of allergen-specific IgG4 antibodies which act as blocking antibodies to prevent IgE-mediated mast cell activation (Akdis & Akdis, 2014; Larche et al., 2006).
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