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Human T-cell receptors (TCRs) that recognize peptides derived from Poa annua (annual bluegrass) pollen are central to the pathogenesis of grass pollen allergy. These TCRs, primarily expressed on CD4+ T helper 2 (Th2) cells, bind to specific allergenic peptides—most notably from the Poa a 1 and Poa a 5 proteins—when they are presented by Major Histocompatibility Complex (MHC) class II molecules on the surface of antigen-presenting cells (Würtzen et al., 2005). This molecular interaction initiates a signaling cascade that promotes the production of pro-inflammatory cytokines such as IL-4 and IL-13, which drive B-cell class switching to IgE and subsequent mast cell degranulation (Larche et al., 2006). In clinical practice, these TCRs are the primary targets of allergen-specific immunotherapy (AIT), which seeks to modify the immune response by inducing peripheral T-cell tolerance or shifting the T-cell profile toward a regulatory phenotype (Akdis & Akdis, 2014). Successful modulation of these TCR-mediated pathways can lead to long-term desensitization and a reduction in symptoms of allergic rhinitis and asthma. Understanding the specific TCR repertoires involved in Poa annua sensitivity is crucial for developing personalized peptide-based vaccines and improving the efficacy of existing immunotherapies.
Induction of peripheral T-cell tolerance, anergy, or differentiation into regulatory T cells (Tregs) through controlled, repeated exposure to specific allergenic peptides presented by MHC class II molecules.
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