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The T-cell receptor (TCR) recognizing hazel allergen-derived peptides presented by MHC class II is a critical mediator in the pathogenesis of hazelnut allergy. This receptor, typically found on CD4+ T helper cells, specifically binds to immunodominant epitopes derived from hazelnut proteins such as Cor a 1, the major allergen in hazelnut pollen and nuts. Upon recognition of these peptides presented by Major Histocompatibility Complex (MHC) class II molecules on antigen-presenting cells, the TCR triggers a signaling cascade that leads to the activation of Th2-polarized immune responses. This activation results in the production of pro-allergic cytokines like IL-4 and IL-13, which drive B-cell isotype switching to IgE and subsequent mast cell degranulation. In a therapeutic context, this TCR is the primary target for allergen-specific immunotherapy (ASIT) and peptide-based vaccines, which seek to desensitize the immune system or induce peripheral tolerance. By modulating the interaction between the TCR and the hazelnut peptide-MHC complex, clinicians aim to shift the immune response from a Th2-mediated allergic state to a Th1 or regulatory T-cell (Treg) dominated state, thereby reducing clinical sensitivity to hazelnut exposure.
Antigen-specific immunotherapy (ASIT) or peptide-based immunotherapy aims to induce immune tolerance by repeatedly exposing the T-cell receptor to specific allergen-derived peptides, leading to T-cell anergy, deletion, or the induction of regulatory T cells (Tregs).
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