IL-27/IL-27R诱发的失控性炎症反应在川崎病发病中的作用及机制研究

川崎病(KD)的病因及发病机制至今不明，其危害在于引起冠脉损伤，而失控性炎症反应可能是KD发病的重要机制之一。IL-27是新近发现的细胞因子，参与了多种失控性免疫炎性疾病的发生，IL-27与其受体(IL-27R)结合能产生强大的免疫调节作用,发挥促炎及抑炎双重效应。本研究拟采用人冠状动脉内皮细胞,利用表达谱芯片、多重蛋白检测技术、siRNA等技术，探究KD发病及冠脉损伤机制中是否与IL-27及其受体的异常表达相关、IL-27是否通过JAK/STATs、PI3K/Akt、ERK1/2信号转导途径触发失控性炎症反应参与KD发病及冠脉损伤,具有重要理论价值和临床意义。

The etiology and pathogenesis of Kawasaki disease (KD) is still unknown, and the prognosis of KD depends on the degree of coronary artery lesion (CAL). Uncontrolled inflammatory reaction may be one of the important mechanisms in the pathogenesis of KD. IL-27 is a newly found cytokine, involved in a variety of uncontrolled immune inflammatory disease. IL-27 and its receptor (IL-27R) binding can have a powerful role in immune regulation and exert proinflammatory and anti-inflammatory double effect. We will apply the human coronary artery endothelial cells(HCAECs),expression microarray, detection of multiple protein, siRNA and Flow cytometry technology to explore whether uncontrolled inflammatory response associated with the abnormal expression of IL-27 involved in the pathogenesis of KD, and to analysis whether IL-27 though activated JAK/STATs、PI3K/Akt、ERK1/2 etc signal transduction pathways to trigger uncontrolled inflammatory response involved in the pathogenesis of KD, so as to provide a theoretical basis for the pathogenesis of KD.