Yu Xiao-Hua, Jiang Na, Zheng Xi-Long, Cayabyab Francisco S, Tang Zhi-Bin, Tang Chao-Ke
Life Science Research Center, Key Laboratory for Atherosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, China.
Department of Electrocardiogram, the Second Affiliated Hospital, University of South China, Hengyang, Hunan 421001, China.
Clin Chim Acta. 2014 Apr 20;431:33-9. doi: 10.1016/j.cca.2014.01.012. Epub 2014 Feb 6.
Interleukin-17 (IL-17) A, the most important cytokine of the IL-17 family predominantly secreted by T helper 17 (Th17) cells, plays a critical role in the development of inflammatory diseases. Its receptor is an obligate heterodimer composed of IL-17 receptor (IL-17R) A and C, the main members of the IL-17R family. Binding of IL-17A to the IL-17RA/C complex can activate a variety of downstream signaling pathways such as nuclear factor kappa-B (NF-κB), activator protein 1 (AP1) and CCAAT/enhancer-binding protein (C/EBP) to induce the expression of proinflammatory cytokines and chemokines. IL-17A also promotes mRNA stability. Growing evidence shows that IL-17A is involved in lipid metabolism and the pathogenesis of atherosclerosis, a chronic inflammatory arterial disease driven by both innate and adaptive immune responses to modified lipoproteins. In the current review, we describe recent progress on regulation and signaling of IL-17A, and highlight its impacts on lipid metabolism and atherosclerosis.
白细胞介素-17（IL-17）A是IL-17家族中最重要的细胞因子，主要由辅助性T细胞17（Th17）分泌，在炎症性疾病的发展中起关键作用。其受体是一种由IL-17受体（IL-17R）A和C组成的必需异二聚体，IL-17R家族的主要成员。IL-17A与IL-17RA/C复合物结合可激活多种下游信号通路，如核因子κB（NF-κB）、活化蛋白1（AP1）和CCAAT/增强子结合蛋白（C/EBP），以诱导促炎细胞因子和趋化因子的表达。IL-17A还可促进mRNA稳定性。越来越多的证据表明，IL-17A参与脂质代谢和动脉粥样硬化的发病机制，动脉粥样硬化是一种由对修饰脂蛋白的固有免疫和适应性免疫反应驱动的慢性炎症性动脉疾病。在本综述中，我们描述了IL-17A调控和信号传导方面的最新进展，并强调了其对脂质代谢和动脉粥样硬化的影响。
