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The T-cell receptor (TCR) recognizing Artemisia-derived peptides presented on MHC class II is a specialized immune receptor that plays a central role in the pathogenesis of mugwort pollen allergy. In sensitized individuals, these TCRs specifically bind to the immunodominant epitope of the major allergen Art v 1, typically the peptide fragment Art v 1(25-36), when it is presented by MHC class II molecules such as HLA-DRB1*01:01 (1.2.4, 1.3.1). This recognition event triggers the activation and proliferation of allergen-specific CD4+ T cells, which predominantly exhibit a Th2 phenotype (1.3.2, 1.3.3). These activated T cells drive the production of IgE and the recruitment of inflammatory cells like eosinophils and mast cells, leading to allergic symptoms (1.3.2). The resulting immune response manifests clinically as allergic rhinitis, conjunctivitis, and potentially asthma (1.3.2). These TCRs are the primary targets of allergen-specific immunotherapy (AIT), which utilizes controlled exposure to Artemisia extracts or specific peptides to modulate the immune response (1.2.4, 1.3.2). AIT aims to induce T-cell anergy or a shift toward regulatory T-cell (Treg) responses, thereby reducing allergic sensitivity (1.2.4). Therapeutic success is often monitored through biomarkers such as the reduction in allergen-specific IgE levels and the induction of IgG4 (1.2.4). However, targeting these receptors via immunotherapy carries a risk of systemic allergic reactions, including anaphylaxis, necessitating careful dose escalation (1.2.4). Research into these TCRs also involves the development of TCR-engineered T cells for studying immune tolerance and potential therapeutic applications (1.2.5, 1.3.1).
Induction of T-cell tolerance and immune deviation from a Th2 to a Th1 or regulatory T-cell (Treg) phenotype
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