Abstract:Serum amyloid A1(SAA1)-FPR2 interaction initiates type 2 immunity against group 13 mite aeroallergens. Saa −/− mice are protected from house dust mite (HDM)-induced airway hyperresponsiveness. HDM induces dissociation of SAA1 into monomers, which signal through formyl peptide receptor 2 (FPR2) to cause IL-33 release and allergic sensitization. Patients with chronic rhinosinusitis, who are commonly sensitized to HDM, have increased SAA1 and FPR2 expression in their nasal epithelial cells
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