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The T-cell receptor (TCR) recognizing allergen–major histocompatibility complex II (MHC II) is a critical molecular assembly that dictates the specificity of the adaptive immune response to environmental allergens [1]. These receptors are expressed on CD4+ T lymphocytes and bind to specific peptide fragments derived from allergens, such as pollen or dust mites, when presented by MHC II molecules on antigen-presenting cells [2]. In allergic individuals, this recognition event typically triggers a Th2-polarized immune response, leading to the production of IgE antibodies and the recruitment of inflammatory cells [3]. Consequently, these TCRs are the primary focus of allergen immunotherapy (AIT), which seeks to modify the immune system's sensitivity by repeatedly exposing it to the target antigen [2,4]. Successful therapeutic intervention through these receptors results in the induction of peripheral tolerance, characterized by T-cell anergy or the expansion of IL-10-producing regulatory T cells [3]. Monitoring the frequency and phenotype of T cells bearing these specific receptors using MHC II tetramers has become a vital tool for assessing the efficacy of desensitization treatments [1].
Induction of immune tolerance by modulating TCR signaling to promote T-cell anergy, clonal deletion, or the differentiation of regulatory T cells (Tregs) [2,3].
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