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Grass pollen-specific Immunoglobulin E (IgE) and T-cell receptors (TCRs) are the primary molecular components of the adaptive immune system that mediate hypersensitivity to grass pollen allergens, such as those from the Poaceae family (Source: NIH, 2024). IgE antibodies, when cross-linked by allergens on the surface of mast cells and basophils via the FcεRI receptor, trigger the immediate release of histamine and other inflammatory mediators, causing symptoms of allergic rhinitis and asthma (Source: MDPI, 2024). Concurrently, allergen-specific TCRs on Th2 cells recognize allergen-derived peptides presented by MHC molecules, orchestrating the late-phase allergic response through the secretion of cytokines like IL-4 and IL-5 (Source: NIH, 2024). These receptors are the therapeutic targets of allergen immunotherapy (AIT), which utilizes grass pollen extracts or recombinant allergens to induce immunological tolerance. AIT promotes a shift from a Th2-dominated response to a regulatory T-cell (Treg) and Th1-mediated response, characterized by the production of allergen-specific IgG4 'blocking' antibodies that prevent IgE-allergen interaction (Source: Frontiers in Immunology, 2024). This disease-modifying approach aims to provide long-term relief from allergic symptoms by fundamentally altering the immune system's recognition of grass pollen.
Allergen immunotherapy (AIT) induces peripheral T-cell tolerance and shifts the immune response from a Th2 to a Th1/Treg profile, leading to the production of allergen-specific IgG4 blocking antibodies and suppression of IgE-mediated mast cell degranulation (Source: NIH, 2024; MDPI, 2024).
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