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Grass pollen-specific T-cell receptors (TCRs) are heterodimeric surface proteins on CD4+ T helper cells that mediate the recognition of grass pollen-derived peptides presented by Major Histocompatibility Complex class II (MHC II) molecules (Wambre et al., 2011, J Allergy Clin Immunol). In sensitized individuals, the interaction between these TCRs and allergen-MHC II complexes initiates a Th2-biased immune cascade, characterized by the release of cytokines like IL-4 and IL-13, which drive IgE production and allergic inflammation (Durham & Shamji, 2023, J Allergy Clin Immunol). These receptors are central to the pathogenesis of seasonal allergic rhinitis and asthma. Therapeutic strategies, such as allergen immunotherapy (AIT), specifically target this interaction to induce immunological tolerance (Larche et al., 2006, Nat Rev Immunol). By modulating TCR signaling through chronic or high-dose exposure, treatments aim to promote the development of regulatory T cells (Tregs) and suppress the pathogenic Th2 response, providing long-term relief from allergic symptoms (Akdis & Akdis, 2014, Nat Rev Drug Discov). Monitoring TCR repertoire and cytokine profiles, such as the reduction of Th2A cells, serves as a biomarker for treatment efficacy (Wambre et al., 2017, Sci Transl Med).
Allergen immunotherapy (AIT) targets these receptors by providing controlled exposure to allergens or peptides, leading to T-cell desensitization, induction of regulatory T cells (Tregs), and a shift from a Th2 to a Th1 or Treg immune profile (Durham & Shamji, 2023, J Allergy Clin Immunol).
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