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T-cell receptors (TCRs) that recognize Timothy grass (Phleum pratense) pollen-derived peptides presented on MHC class II molecules are central to the pathogenesis of grass pollen allergy (1.1.1, 1.1.3). These TCRs are primarily found on CD4+ T helper cells, which, in allergic individuals, exhibit a Th2-polarized phenotype characterized by the secretion of cytokines such as IL-4, IL-5, and IL-13 (1.1.1, 1.3.2). Upon recognition of immunodominant epitopes from major allergens like Phl p 1 and Phl p 5, these T cells drive IgE production and eosinophilic inflammation (1.2.1, 1.5.2). This interaction is the primary target of allergen-specific immunotherapy (AIT), which uses whole allergen extracts or specific peptides to modify the immune response (1.1.2, 1.2.4). The goal of such therapies is to induce peripheral tolerance through mechanisms such as T-cell anergy, the induction of regulatory T cells (Tregs), or a shift from a Th2 to a Th1 immune profile (1.3.2, 1.5.2). Monitoring these TCR-mediated responses using MHC class II tetramers and cytokine assays is crucial for evaluating the efficacy of immunotherapy (1.1.2, 1.5.1). Safety concerns for these therapies include local reactions like oral pruritus and, more rarely, systemic allergic reactions such as anaphylaxis (1.3.1, 1.3.5).
Induction of T-cell tolerance through anergy, deletion of allergen-specific Th2 cells, and the induction of regulatory T cells (Tregs), leading to a shift from a Th2 to a Th1 immune profile.
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