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House dust mite–specific immune receptors are a diverse group of host proteins that recognize and initiate immune responses to allergens from house dust mites (HDM), such as Dermatophagoides pteronyssinus and Dermatophagoides farinae [7, 12, 15]. This category includes innate pattern recognition receptors (PRRs) like Dectin-2 (CLEC6A), which senses HDM glycans, and Toll-like receptor 4 (TLR4), which is activated by the MD-2-mimicking allergen Der p 2 [1, 2, 5, 11]. Other innate receptors involved include the Mannose Receptor (CD206) and DC-SIGN (CD209), which bind glycosylated allergens, and Protease-Activated Receptor 2 (PAR2), which is triggered by HDM proteases like Der p 1 [12, 14, 15]. The group also encompasses adaptive immune receptors, primarily the high-affinity IgE receptor (FcεRI) on mast cells and basophils—which binds HDM-specific IgE—and T-cell receptors (TCRs) that recognize HDM-derived peptides presented on MHC molecules [7, 12]. Activation of these receptors leads to the production of pro-inflammatory mediators like cysteinyl leukotrienes and Th2 cytokines (IL-4, IL-5, IL-13), driving the pathogenesis of allergic asthma, rhinitis, and atopic dermatitis [3, 6, 9]. Therapeutic interventions include allergen-specific immunotherapy (AIT) to induce immune tolerance, monoclonal antibodies like omalizumab to block the IgE-mediated pathway, and various inhibitors targeting downstream signaling or specific innate sensing mechanisms [2, 12, 13].
Neutralization of allergen-specific IgE, induction of immune tolerance through allergen-specific immunotherapy, and blockade of innate sensing pathways.
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