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Allergen-specific CD4+ T-cell receptors (TCRs) are the primary mediators of the adaptive immune response to environmental allergens. These receptors recognize specific allergen-derived peptides presented by Major Histocompatibility Complex class II (MHC-II) molecules on antigen-presenting cells (Janeway's Immunobiology, 2016). In allergic individuals, this recognition typically leads to a Th2-polarized response characterized by the production of IL-4, IL-5, and IL-13, which drive IgE production and eosinophilic inflammation (Akdis & Akdis, 2014). Therapeutic targeting of these TCRs via allergen immunotherapy (AIT) aims to redirect this response toward a tolerogenic state. This is achieved through the induction of regulatory T cells (Tregs), such as IL-10-secreting Tr1 cells and Foxp3+ Tregs, which suppress allergic inflammation and promote the production of protective IgG4 antibodies (Larche et al., 2006). Modern pharmacological approaches include peptide-based vaccines and nanoparticle-delivered allergens designed to engage the TCR in a non-inflammatory context, thereby inducing long-term clinical tolerance (Shamji & Durham, 2017).
Induction of peripheral T-cell tolerance through anergy, deletion, or the generation of regulatory T cells (Tregs) that secrete suppressive cytokines like IL-10 and TGF-beta, leading to immune deviation from Th2 to Th1/Treg profiles.
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