NG2^+胶质细胞在Th1-EAE和Th17-EAE中的不同作用

Partial depletion of NG2^+ glia has differential roles on Th1-and Th17-induced EAE

NG2^+胶质细胞在EAE中的作用还不清楚。课题组应用PDGFRα-CreER特异地诱导白喉毒素在NG2^+胶质细胞中表达,成功地在小鼠中枢神经系统中部分剔除NG2^+胶质细胞。研究发现部分剔除NG2^+胶质细胞的小鼠CNS中在诱导Active-EAE和Th1-EAE的发病过程中,表现为临床症状减轻、髓鞘蛋白脱落减少以及炎症细胞浸润减少,说明NG2^+胶质细胞能够增强胶质细胞的作用以加重Active-EAE和Th1-EAE的发病程度。与此相反,在Th17-EAE小鼠中,NG2^+胶质细胞能够抑制EAE的发生。这些结果提示NG2^+胶质细胞在不同诱导方式EAE发生中的作用是不同的,因此在治疗方法上也应该区别对待。这一结果将帮助多发性硬化患者的治疗提供新的靶点。

NG2＋glial cells constitute a major cell population in central nervous system（CNS）,however,its role in neuroinflammation remains unclear.We used genetic approaches to specifically and partially deplete NG2＋glia in mouse CNS and subjected them to EAE（an animal model of multiple sclerosis）induction by active immunization or adoptive transfer of MOG35-55-specific Th1/Th17 cells.While NG2^＋glia promoted active-EAE and Th1-EAE,it protected mice from Th17-EAE.Our results thus suggest differential roles of NG2^＋glia in Th1-and Th17-EAE,and provide potential therapeutic significance by modulating NG2^＋glia in Th1-and Th17-EAE and multiple sclerosis.