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The interaction between antigen-presenting cells (APCs) and T cells via processed mite-derived peptides presented on MHC molecules is the central mechanism of house dust mite (HDM) allergy and its treatment through immunotherapy [1]. HDM allergens, such as Der p 1 and Der f 2, are captured by APCs, proteolytically processed into peptides, and displayed on MHC Class II molecules [2]. These complexes are recognized by the T cell receptor (TCR) on CD4+ T cells, which in allergic individuals typically triggers a Th2-polarized response characterized by IgE production and eosinophilic inflammation [3]. Therapeutic interventions, specifically allergen-specific immunotherapy (AIT), utilize this pathway to desensitize the immune system by promoting the development of regulatory T cells (Tregs) and shifting the cytokine profile toward immune tolerance [4]. This target is critical for managing HDM-induced allergic rhinitis and asthma, aiming to provide long-term relief by modifying the underlying disease pathology rather than just treating symptoms [5]. Drugs targeting this complex, such as HDM allergen extracts, work by modulating the T cell response to favor protective immunity over allergic hypersensitivity [6].
Allergen-specific immunotherapy (AIT) involves the administration of mite-derived peptides to induce immunological tolerance. These peptides are processed by antigen-presenting cells (APCs) and presented on Major Histocompatibility Complex (MHC) molecules to T cells. This interaction leads to a shift from a Th2-mediated allergic response to a Th1 or regulatory T cell (Treg) response, reducing the production of IgE and increasing the production of IgG4 and inhibitory cytokines like IL-10 [1][2].
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