The minor house dust mite allergen Der p 13 is a fatty acid‐binding protein and an activator of a TLR2‐mediated innate immune response

• DOI: 10.1111/all.12899
• Publication Date: 2016-03-28T14:26:43Z
• Authors: P. Satitsuksanoa; M. Kennedy; D. Gilis; M. Le Mignon; N. Suratannon; W. T. Soh; J. Wongpiyabovorn; P. Chatchatee; M. Vangveravong; T. Rerkpattanapipat; A. Sangasapaviliya; S. Piboonpocanun; E. Nony; K. Ruxrungtham; A. Jacquet
• Keywords: Models, Molecular; 0301 basic medicine; Protein Conformation; Dermatophagoides pteronyssinus; Respiratory Mucosa; Allergens; Immunoglobulin E; Fatty Acid-Binding Proteins; Lipid Metabolism; Cell Degranulation; Immunity, Innate; Toll-Like Receptor 2; Basophils; 3. Good health; 03 medical and health sciences; Animals; Humans; Antigens, Dermatophagoides; Carrier Proteins; Protein Binding

Abstract Background The house dust mite (HDM ) allergen Der p 13 could be a lipid‐binding protein able to activate key innate signaling pathways in the initiation of allergic response. We investigated IgE reactivity recombinant (rDer 13), its activities, and capacity stimulate airway epithelium cells. Methods Purified rDer was characterized by mass spectrometry, circular dichroism, fluorescence‐based assays, silico structural prediction. IgE‐binding activity allergenic potential were examined ELISA, basophil degranulation vitro epithelial cell activation assays. Results Protein modeling biophysical analysis indicated that adopts β‐barrel structure with predominately apolar pocket representing binding site for hydrophobic ligands. Fluorescent assays confirmed is highly selective ligands it binds fatty acid dissociation constant typical lipid transporter proteins. low frequency (7%, n = 224) Thai HDM‐allergic patients as well limited propensity classifies minor HDM allergen. Nevertheless, presumptively associated lipid(s) triggered production IL‐8 GM‐CSF respiratory cells through TLR2‐, MyD88‐, NF‐kB‐, MAPK‐dependent pathway. Conclusions Although allergen, may, capacity, play role response TLR2 activation.