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Allergen-specific T-cell receptors (TCRs) that recognize Hev b-derived peptides on MHC class II molecules are the central mediators of the adaptive immune response in natural rubber latex (NRL) allergy. These receptors, expressed on CD4+ T helper cells, specifically bind to peptide fragments derived from major latex allergens such as Hev b 1, Hev b 3, Hev b 5, and Hev b 6.02 when presented by Major Histocompatibility Complex (MHC) class II molecules like HLA-DR or HLA-DQ (Wagner et al., 2001; Möller et al., 2012). This recognition event triggers T-cell activation and the subsequent secretion of Th2-type cytokines (e.g., IL-4, IL-5, and IL-13), which facilitate IgE production and eosinophilic inflammation (Akdis & Akdis, 2011). In therapeutic development, these TCR-peptide-MHC complexes are the primary targets for allergen-specific immunotherapy (AIT), which aims to induce immunological tolerance through T-cell anergy or the induction of regulatory T cells (Tregs) (Karisola et al., 2004). While AIT is effective, it carries a risk of systemic allergic reactions or anaphylaxis, and clinicians must also consider the 'latex-fruit syndrome,' where TCRs may cross-react with homologous proteins in foods like bananas and avocados (Bernstein et al., 2021). Understanding the specific TCR repertoire and the dominant MHC-II restricted epitopes is crucial for developing safer, peptide-based vaccines that minimize the risk of IgE-mediated anaphylaxis while effectively desensitizing the patient.
Induction of peripheral T-cell tolerance, T-cell anergy, or regulatory T-cell (Treg) differentiation to suppress the Th2-mediated allergic response (Akdis & Akdis, 2011).
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