摘要
补体(C)5a与其受体(C5aR)结合后,可诱导中性粒细胞、巨噬细胞等向炎症部位聚集,诱导炎性递质的生成。CD88和C5L2为目前已知的两种C5aR,在中性粒细胞、巨噬细胞和不成熟树突细胞上都有表达,可能促进炎症反应的发生。C5a可能通过细胞外信号调节激酶1、2以及P38促丝裂原激活蛋白激酶通路抑制中性粒细胞程序性死亡发挥促炎作用。抑制C5a与C5aR之间的相互作用,在一定程度上可以抑制中性粒细胞的活化、活性氧的释放以及那基质金属蛋白酶的生成,从而减轻炎症和组织损伤。进一步了解C5a及其受体在牙周炎发生发展中的作用机制可为牙周炎的治疗提供又一新途径。
The binding of complement（C）5a and its receptors（C5aR） can stimulate the aggregation of neutrophils and macrophages and generate inflammatory mediators during inflammation. C5aR includes CD88 and C5L2, which are expressed on neutrophils, macrophages, and immature dendritic cells. These cells can initiate inflammation. CSa could inhibit the death of programmed neutrophils to promote inflammation through extracellular signal-regulated kinase l, 2 and P38 mitogen-activated protein kinase pathways. Restraining the interaction between C5a and CSaR can inhibit neutrophil activation and the generation of reactive oxygen and matrix metalloproteinase. This process reduces inflammation and tissue damage. Further understanding of the role of C5a and CSa receptors in the development of periodontitis may offer a new approach to treat periodontitis.
出处
《国际口腔医学杂志》
CAS
2014年第5期603-608,共6页
International Journal of Stomatology
基金
四川省科技支撑计划(2011FZ0044)
关键词
补体5a
补体5a受体
效应通路
牙周炎
complement 5a
complement 5a receptor
effect of pathway
periodontitis
