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The grass pollen allergen-specific immune pathway refers to the sequence of immunological events that lead to Type I hypersensitivity in response to grass pollen proteins, such as Phl p 1 and Phl p 5 from Timothy grass (Durham & Shamji, 2023). In sensitized patients, the pathway is characterized by a Th2-polarized immune response, resulting in high levels of allergen-specific IgE that bind to high-affinity receptors (FcεRI) on mast cells and basophils (Akdis & Akdis, 2014). Upon subsequent exposure, allergen-induced cross-linking of these IgE molecules triggers the rapid release of inflammatory mediators, causing clinical symptoms of allergic rhinitis, conjunctivitis, and asthma. Therapeutic intervention via allergen immunotherapy (AIT) aims to modify this pathway by inducing peripheral T-cell tolerance and promoting the expansion of regulatory T cells (Tregs) (Shamji et al., 2017). Drugs such as Timothy grass pollen extracts (e.g., Grastek, Grazax) or multi-grass extracts (e.g., Oralair) are administered to shift the immune profile from a Th2-mediated response to a Th1-mediated or regulatory response (FDA, 2014). This shift is marked by the production of allergen-specific IgG4 "blocking" antibodies, which prevent IgE-mediated activation of effector cells, thereby providing long-term relief from allergic symptoms.
Induction of immune tolerance through the expansion of regulatory T and B cells, suppression of Th2-mediated inflammation, and the generation of allergen-specific IgG4 blocking antibodies (Durham & Shamji, 2023).
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