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The Major histocompatibility complex class II (MHC II)-Bet v 1 peptide complex is a molecular assembly on the surface of antigen-presenting cells (APCs) that plays a central role in the pathogenesis of birch pollen allergy [1]. Bet v 1, the primary allergen from Betula verrucosa, is processed by APCs into immunodominant peptides which are then loaded onto MHC II molecules, particularly HLA-DRB1 alleles [2]. This complex is recognized by specific T cell receptors (TCRs) on CD4+ T cells, initiating a Th2-polarized immune response characterized by the secretion of pro-inflammatory cytokines like IL-4 and IL-13 [3]. This signaling cascade ultimately leads to the production of allergen-specific IgE and the subsequent activation of mast cells and basophils [4]. Therapeutic interventions, such as allergen-specific immunotherapy (AIT), target this interaction to induce immunological tolerance [5]. By repeatedly exposing the immune system to the Bet v 1-MHC II complex under controlled conditions, AIT promotes the induction of regulatory T cells (Tregs) and a shift toward a Th1-type response, reducing allergic symptoms [6].
Induction of peripheral T cell tolerance (anergy or deletion) and the promotion of regulatory T cell (Treg) activity, leading to a shift from a Th2 to a Th1 immune profile [5, 6].
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