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Allergen-specific CD4+ T cells are a specialized subset of helper T cells that play a central role in the pathogenesis of IgE-mediated allergies, such as grass pollen allergy (J Allergy Clin Immunol. 2010 Jun;125(6):1407–1409). In sensitized individuals, these cells typically exhibit a Th2-polarized phenotype, producing pro-inflammatory cytokines like IL-4, IL-5, and IL-13 upon recognition of allergen-derived peptides presented by MHC class II molecules. This cytokine profile drives IgE production by B cells, eosinophil recruitment, and mast cell activation, leading to allergic symptoms (JAMA. 2017;317(6):615-625). Therapeutic strategies, collectively known as allergen immunotherapy (AIT), target these cells to restore immune tolerance. By administering controlled doses of allergens or specific peptides, AIT aims to induce T-cell anergy, clonal deletion, or a shift toward a regulatory phenotype (Treg or Tr1), which suppresses the allergic cascade (World Journal of Methodology 4(1):26-45). Monitoring these cells using pMHCII-tetramers and assessing the induction of IL-10-producing regulatory cells are key methods for evaluating the efficacy of such treatments.
Allergen immunotherapy (AIT) induces peripheral T-cell tolerance through mechanisms such as T-cell anergy, clonal deletion, or immune deviation from a Th2 to a Th1 or regulatory T-cell (Treg/Tr1) phenotype.
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