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Immune system receptors recognizing house dust mite (HDM) allergens comprise a diverse group of pattern recognition receptors (PRRs) and cell surface proteins that initiate the allergic immune response. Key members include Toll-like receptor 4 (TLR4), which is activated by the major allergen Der p 2 through molecular mimicry of the MD-2 co-receptor (PubMed: 19322190, 26315357), and Protease-activated receptor 2 (PAR2), which is triggered by the proteolytic activity of Der p 1 (PMC: 3214062, 4130634). Additionally, C-type lectin receptors such as Dectin-2 (CLEC6A) and the Mannose Receptor (CD206) recognize glycan structures on HDM allergens to promote the production of cysteinyl leukotrienes and Th2-polarizing cytokines (PubMed: 19144989, 24129160). These receptors are primarily expressed on airway epithelial cells and dendritic cells, where their activation leads to the release of alarmins like IL-33 and TSLP, driving the pathogenesis of asthma and allergic rhinitis (PMC: 2727593, 3261116). Therapeutic strategies targeting these receptors, such as TLR4 antagonists (e.g., TAK-242) or experimental PAR2 inhibitors, aim to prevent the initial sensitization and subsequent inflammatory flares associated with HDM exposure (Frontiers: 2018, 2021).
Inhibition of allergen-induced innate immune signaling through the blockade of pattern recognition receptors (TLR4, Dectin-2) or protease-activated receptors (PAR2), preventing the release of pro-Th2 cytokines and alarmins.
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