川崎病动物模型及其发病机制研究进展  

The Development and Researches of the Pathogenesis of Kawasaki Disease Animal Models

作　　者：张新艳[1] 卢慧玲[1] Xinyan Zhang;Huiling Lu(Department of Pediatrics,Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Wuhan Hubei)

机构地区：[1]华中科技大学同济医学院附属同济医院儿科,湖北武汉

出　　处：《生理学研究》2017年第1期1-11,共11页Journal of Physiology Studies

基　　金：国家自然科学基金支持(81270949)。

摘　　要：川崎病(KD)随着发病率逐年增高,已经成为取代类风湿成为儿童后天性心脏病的主要病因。建立川崎病动物模型,对于其冠脉损伤病因及发病机制的研究至关重要,目前研究较多的有小鼠模型、兔模型、幼猪和犬模型,在动物模型的研究中发现单核/巨噬细胞的免疫激活、TNF-α和IL-1等细胞因子、基质金属蛋白酶(MMP-9)、血管内皮生长因-A(VEGF-A)、转化生长因子、TLR-2和MyD88及Dectin-1/Syk信号通路,均与川崎病模型中以冠状动脉损伤为主的免疫性血管炎有关。本文就目前运用川崎病免疫性血管炎模型研究其发病机制的现状进行总结概括。With the increasing morbidity of Kawasaki disease year by year, KD has become the main cause of acquired heart disease, which has replaced the rheumatoid disease. It’s vital to explore the etiology and pathogenesis of coronary artery lesions through establishing animal models of Kawasaki disease. At present, most researches focus on the mouse model, the rabbit model of immune vasculitis, young pig model and dog model, through which they found monocyte/macrophage activation, cytokines including TNF-α and IL-1, matrix metalloproteinases (MMP-9), vascular endothelial growth-A growth factors (VEGF-A), TLR-2 and MyD88 and Dectin-1/Syk signal pathway were all closely involved in the development of immune vasculitis in the KD animal models. In this paper, we summarize the latest development and researches of the pathogenesis of Kawasaki disease by using animal models of immune vasculitis.

关 键 词：川崎病 动物模型 免疫性血管炎 发病机制 免疫激活 超抗原 细胞因子 

分 类 号：R73[医药卫生—肿瘤]