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The grass pollen-specific immune response is a pathological immunological process characterized by hypersensitivity to proteins found in grass pollen, such as Phl p 1 and Phl p 5 from Phleum pratense (Timothy grass) (Durham & Penagos, 2016). This response is primarily an IgE-mediated type I hypersensitivity reaction, where allergen-specific IgE antibodies bind to high-affinity receptors (FcεRI) on mast cells and basophils, leading to the release of inflammatory mediators like histamine upon re-exposure (Shamji et al., 2017). Clinically, this manifests as seasonal allergic rhinitis, conjunctivitis, and potentially allergic asthma. Therapeutic intervention typically involves allergen immunotherapy (AIT), which utilizes standardized grass pollen extracts to desensitize the immune system (FDA, 2014). These treatments, such as sublingual tablets (e.g., Grazax, Grastek), aim to induce long-term clinical tolerance by promoting the production of blocking antibodies (IgG4) and regulatory T cells, thereby shifting the immune profile away from an allergic Th2-driven state (Durham & Penagos, 2016).
Induction of immune tolerance through allergen immunotherapy (AIT), involving the modulation of T-cell responses (Th2 to Th1/Treg shift) and the production of allergen-specific IgG4 blocking antibodies (Durham & Penagos, 2016; Shamji et al., 2017).
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