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The Antigen-MHC-TCR complex is the fundamental molecular unit of the adaptive immune response, consisting of a peptide antigen (allergen) bound to a Major Histocompatibility Complex (MHC) molecule on an antigen-presenting cell (APC) and recognized by a specific T-cell receptor (TCR) [1]. In allergic diseases, this interaction typically involves Th2-polarized T cells responding to environmental allergens, leading to IgE production and allergic inflammation [2]. Therapeutic strategies, such as allergen immunotherapy (AIT) and peptide-based vaccines, target this interaction to reprogram the immune system. By delivering the antigen in a controlled manner, these therapies aim to induce T-cell anergy, deletion, or the differentiation of regulatory T cells (Tregs) that secrete suppressive cytokines like IL-10 and TGF-beta [3]. This shift from a pro-allergic Th2 response to a tolerant state reduces the clinical symptoms of allergic rhinitis, asthma, and food allergies [1, 3]. (Citations: [1] Akdis & Akdis, J Allergy Clin Immunol 2014; [2] Larche et al., Nat Rev Immunol 2006; [3] Shamji & Durham, J Allergy Clin Immunol 2017).
Induction of peripheral T-cell tolerance through anergy, clonal deletion, and the generation of regulatory T cells (Tregs) that suppress Th2-mediated allergic inflammation [1, 2].
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