甘露聚糖结合凝集素
发病机制
川崎病
血管炎
凝集素
免疫学
系统性血管炎
补体系统
凝集素途径
生物
医学
疾病
病理
经典补体途径
内科学
免疫系统
动脉
作者
Akihiro Nakamura,Mitsuhiko Okigaki,Noriko N. Miura,Chinatsu Suzuki,Naohito Ohno,Fuyuki Kametani,Kenji Hamaoka
标识
DOI:10.1016/j.clim.2014.03.019
摘要
Kawasaki disease (KD) is a paediatric idiopathic vasculitis. In this study, on the basis of studies using an established animal model for KD, we report that mannose-binding lectin (MBL) is involved in the pathogenesis of the disease. KD-like experimental murine vasculitis was induced by intraperitoneally administering a Candida albicans water-soluble extract (CAWS). MBL-A gradually increased in the serum of the model mice treated with CAWS. Deposition of MBL-A and MBL-C was observed in the aortic root, including the coronary arteries, which is a predilection site in experimental vasculitis. Corresponding to the distribution patterns of MBLs, marked deposition of C3/C3-derived peptides was also observed. Regarding the self-reactivity of MBLs, we observed that MBLs interacted with core histones to activate the lectin pathway. These results suggest that some types of pathogens provoke the MBL-dependent complement pathway (lectin pathway) to cause and/or exacerbate KD-like vasculitis.
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