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Allergen-specific components from Dermatophagoides pteronyssinus and Lepidoglyphus destructor mites are the primary antigenic proteins responsible for triggering IgE-mediated hypersensitivity in sensitized individuals (Thomas et al., 2010 [1]). These components include major allergens such as Der p 1, a cysteine protease that disrupts epithelial tight junctions, and Der p 2 and Lep d 2, which belong to the NPC2 family and facilitate lipid-mediated immune signaling (Gafvelin et al., 2001 [2]). In clinical medicine, these allergens serve as the active pharmaceutical ingredients in allergen-specific immunotherapy (AIT), which is the only disease-modifying treatment for mite-induced respiratory allergies (Akdis & Akdis, 2014 [3]). The therapeutic goal of administering these components is to shift the immune response from a Th2-dominated inflammatory state to a state of immune tolerance. This is achieved through the induction of regulatory T cells (Tregs) and the production of allergen-specific IgG4 antibodies, which act as "blocking" antibodies to prevent IgE-mediated mast cell degranulation (Shamji & Durham, 2017 [4]). Monitoring the efficacy of treatments targeting these allergens typically involves assessing changes in allergen-specific IgE and IgG4 levels, as well as clinical improvements in symptoms of allergic rhinitis and asthma (Zidarn et al., 2012 [5]). Safety concerns during treatment include the risk of systemic allergic reactions or anaphylaxis, necessitating administration under medical supervision.
Induction of peripheral T-cell tolerance, promotion of regulatory T-cell (Treg) expansion, and stimulation of allergen-specific IgG4 blocking antibodies that inhibit IgE-mediated mast cell degranulation.
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