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T-cell receptors (TCRs) specific for Parietaria judaica T-cell epitopes are the key molecular components on the surface of CD4+ T-lymphocytes that recognize allergens from the wall pellitory plant (NIH, 1996). These TCRs interact with peptide fragments derived from major allergens, such as Par j 1 and Par j 2, which are presented by Major Histocompatibility Complex (MHC) Class II molecules—primarily HLA-DR and HLA-DQ—on antigen-presenting cells (Karger, 2003; NIH, 2019). This interaction is central to the pathogenesis of Parietaria allergy, as it initiates the Th2-mediated immune cascade that leads to IgE production and allergic symptoms like rhinitis and asthma (NIH, 2019; MDPI, 2021). In allergic individuals, the recognition of these epitopes triggers the release of pro-inflammatory cytokines such as IL-4 and IL-5 (NIH, 1996). Therapeutic interventions, such as allergen-specific immunotherapy (AIT), target these TCR-mediated pathways to induce immunological tolerance (NIH, 2006; MDPI, 2021). By administering controlled doses of the allergen or its epitopes, AIT aims to reprogram the T-cell response toward a regulatory or Th1 phenotype (NIH, 1994; NIH, 2003). This reprogramming often involves the induction of regulatory T-cells (Tregs) that produce suppressive cytokines like IL-10 and TGF-beta (MDPI, 2021). Modern approaches also explore the use of hypoallergenic recombinant allergens or T-cell epitope peptides to minimize the risk of IgE-mediated systemic reactions while effectively modulating the T-cell response (NIH, 2000; Karger, 2003). These strategies are designed to desensitize the immune system and provide long-term relief from allergic symptoms (NIH, 2006). Understanding the specific TCR-MHC-peptide interactions is crucial for developing precision medicine approaches in allergy treatment (MDPI, 2021).
Induction of immunological tolerance through allergen-specific immunotherapy (AIT), which involves shifting the T-cell response from a Th2-polarized state to a regulatory (Treg) or Th1-polarized state, leading to reduced IgE production and suppressed allergic inflammation.
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