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Grass-pollen allergen-specific immune system components refer to the collective immunological elements—including specific IgE antibodies, T-helper 2 (Th2) cells, and effector cells like mast cells—that mediate hypersensitivity to proteins found in grass pollen. In sensitized individuals, exposure to allergens such as Phl p 1 and Phl p 5 triggers the cross-linking of IgE on mast cells, resulting in the release of inflammatory mediators like histamine and leukotrienes. This complex of components is the primary target of allergen-specific immunotherapy (AIT), which aims to modify the underlying disease process rather than just managing symptoms. By administering controlled doses of grass pollen extracts, AIT promotes the expansion of T-regulatory (Treg) cells and the secretion of IL-10 and TGF-beta, which suppress the allergic cascade. This therapeutic approach induces long-term tolerance, reduces the risk of developing asthma, and provides sustained relief from allergic rhinitis and conjunctivitis [1][3][5].
Allergen-specific immunotherapy (AIT) works by inducing peripheral immune tolerance through the administration of gradually increasing doses of allergens. This process shifts the immune response from a Th2-dominated allergic profile to a T-regulatory (Treg) and Th1-weighted profile, leading to the production of 'blocking' IgG4 antibodies and a reduction in allergen-specific IgE-mediated mast cell and basophil activation [1][4].
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