Department of Neurology, Changhai Hospital, 168 Changhai Road, Shanghai 200433, PR China.
J Neuroimmunol. 2013 Feb 15;255(1-2):32-8. doi: 10.1016/j.jneuroim.2012.10.013. Epub 2012 Nov 27.
The abnormal proliferation and polarization of Th17/Th1 subsets are believed to contribute to the progression of multiple sclerosis. We demonstrated that neural stem cells (NSCs) could inhibit CD4(+)T cells from mice of experimental autoimmune encephalomyelitis to proliferate and polarize into Th17 but promote their apoptosis and to generate regulatory T cells in response to myelin antigen via releasing prostaglandin E2 by activated Th1-derived IFN-γ. The study indicated that NSCs play a negatively regulatory role in T cell responses and provided novel evidence for the therapeutic mechanisms underlying the usage of NSCs to treat autoimmune diseases of central nervous system.
Th17/Th1 亚群的异常增殖和极化被认为有助于多发性硬化症的进展。我们证明神经干细胞（NSCs）可以抑制实验性自身免疫性脑脊髓炎小鼠的 CD4+T 细胞增殖和极化成为 Th17，但通过激活的 Th1 来源的 IFN-γ释放前列腺素 E2，促进其凋亡并产生调节性 T 细胞，以响应髓鞘抗原。该研究表明 NSCs 在 T 细胞反应中起负调节作用，并为 NSCs 用于治疗中枢神经系统自身免疫性疾病的治疗机制提供了新的证据。
