川崎病冠状动脉病变相关细胞因子基因多态性

Cytokine genetic polymorphisms in Kawasaki disease combined with coronary artery lesions

川崎病是好发于5岁以下儿童的急性全身性中小血管炎性综合征，以全身中小动脉急性炎症反应为主要病理改变，可导致冠状动脉扩张、心肌梗死及猝死。细胞因子是主要由免疫细胞分泌的、能调节细胞功能的小分子多肽。在免疫应答过程中，细胞因子对于炎症细胞间相互作用、细胞的生长和分化有重要调节作用。川崎病急性期超抗原激活自身免疫反应，大量细胞因子及炎症介质释放入血，参与川崎病的发生发展及血管病变。许多炎症反应细胞因子与川崎病并发冠状动脉损害有关。该文就多种细胞因子在川崎病合并冠状动脉病变中的作用机制进行综述。

Kawasaki disease（KD） is an acute febrile childhood inflammatory disease, characterized by systemic small artery inflammation as the main pathological changes that can lead to expansion of coronary artery,myocardial infarction and sudden cardiac death. Cytokines secreted by immune cells are small molecules, which can regulate the function of inflammatory cells, play important roles in the process of immune response, stimulate the proliferation and differentiation of cells, and regulate interactions between them. In the acute phase, super antigens activate immune responses. A large number of cytokines and inflammatory mediators are released into the blood, which participate in the occurrence and development of KD and the vascular disease. Many inflammatory cytokines are associated with coronary artery damages in KD patients. In this paper, the roles of various cytokines in the coronary artery lesions of KD are reviewed.