原标题：小屋尘螨变应原Der p 13是一种脂肪酸结合蛋白并且是TLR2介导免疫应答的催化剂
① 屋尘螨（HDM）变应原Der p 13可能是一种脂结合蛋白，能够激活启动变应反应的关键先天信号通路；② 纯化的rDer p 13通过质谱、圆二色性、基于荧光的脂质结合分析和硅结构预测等方法来进行表征分析；③ 采用ELISA、嗜碱性粒细胞脱颗粒试验和体外气道上皮细胞活化试验检测Der p 13的IgE结合活性和致敏活性；④ 荧光脂质结合试验证实，该蛋白质对配体具有高度选择性，并且它与脂肪酸结合具有典型的脂质转运蛋白解离常数；⑤ Der p 13 通过其脂质结合能力，并由TLR2激活，然后在HDM过敏反应中起作用。
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
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 the allergic response. We investigated the IgE reactivity of recombinant Der p 13 (rDer p 13), its lipid-binding activities, and its capacity to stimulate airway epithelium cells.
Methods: Purified rDer p 13 was characterized by mass spectrometry, circular dichroism, fluorescence-based lipid-binding assays, and in silico structural prediction. IgE-binding activity and allergenic potential of Der p 13 were examined by ELISA,basophil degranulation assays, and in vitro airway epithelial cell activation assays.
Results: Protein modeling and biophysical analysis indicated that Der p 13 adopts a b-barrel structure with a predominately apolar pocket representing a potential binding site for hydrophobic ligands. Fluorescent lipid-binding assays confirmed that the protein is highly selective for ligands and that it binds a fatty acid with a dissociation constant typical of lipid transporter proteins. The low IgE-binding frequency (7%, n = 224) in Thai HDM-allergic patients as well as the limited propensity to activate basophil degranulation classifies Der p 13 as a minor HDM allergen. Nevertheless, the protein with its presumptively associated lipid(s) triggered the production of IL-8 and GM-CSF in respiratory epithelial cells through a TLR2-, MyD88-, NF-kB-, and MAPK-dependent signaling pathway.
Conclusions: Although a minor allergen, Der p 13 may, through its lipid-binding capacity, play a role in the initiation of the HDM-allergic response through TLR2 activation.
Assoc. Prof. Dr. Alain Jacquet, Department of Medicine, Faculty of Medicine, Chulalongkorn University
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.