中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (1): 90-91.doi: 10.4103/1673-5374.175050

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

间充质干细胞调节免疫功能促进多发性硬化症的髓鞘再生

  

  • 收稿日期:2015-11-06 出版日期:2016-01-15 发布日期:2016-01-15

Mesenchymal stem cells require the peripheral immune system for immunomodulating effects in animal models of multiple sclerosis

Laura Salinas Tejedor, Thomas Skripuletz, Martin Stangel,Viktoria Gudi   

  1. Clinical Neuroimmunology and Neurochemistry, Department of Neurology, Hannover Medical School, Hanover, Germany(Salinas Tejedor L, Skripuletz T, Stangel M, Gudi V)
    Center for Systems Neuroscience, Hannover, Germany(Salinas Tejedor L, Stangel M)
  • Received:2015-11-06 Online:2016-01-15 Published:2016-01-15
  • Contact: Martin Stangel, M.D.,stangel.martin@MH-Hannover.de.
  • Supported by:

    This research on MSC was supported by the German Research Foundation (DFG, FOR 1103, TP1b, STA 518/4-1) All authors contributed to the writing and editing of this paper.

摘要:

多发性硬化症是中枢神经系统的慢性炎症疾病,并且会影响少突胶质细胞和髓磷脂。髓鞘丢失会导致渐进性轴突损伤和神经元死亡,进而导致神经退变和功能障碍。目前已证实有几种炎症因素会影响此类神经性紊乱的发展,研究者们普遍认为自身反应性T淋巴细胞向中枢神经系统迁移会发生免疫反应,随后触发特定髓鞘抗原。众所周知,髓鞘再生是天然的修复机制,对快速跳跃式神经传导的恢复也尤为重要。此外,其可修复轴突髓鞘单元,因此可以保护继发性轴突退变。这种再生过程意味着少突胶质前体细胞向脱髓鞘区域迁移,并分化为成熟的少突胶质细胞髓鞘。遗憾的是,这一过程对多发性硬化症患者来说通常是无法完全完成的,而目前的治疗方法多为基于使用免疫调节药物来减少炎症反应,但这种干预方法不能修复现有损伤。出于这个原因,广泛的研究正在髓鞘再生治疗领域展开,意图停止疾病进展并能够修复神经功能障碍。

Abstract:

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) that affects oligodendrocytes and myelin. Loss of myelin leads to progressive axonal damage and neuronal death resulting in neurodenegeration and functional disability. Several inflammatory factors influence the development of this neurological disorder. It is generally accepted that autoreactive T lymphocytes migrate towards the CNS then initiating an immune reaction upon encountering the specific myelin antigen. Remyelination is the natural repair mechanism and is important to restore the fast saltatory nerve conduction. In addition it restores the axon-myelin unit and may thus preserve the axon from secondary degeneration. This regenerative process implies the migration of oligodendroglial precursors cells (OPC) towards demyelinated regions and their differentiation into mature myelinating oligodendrocytes. Unfortunately, this process is often incomplete in MS patients and current treatments are based on the use of immunomodulatory drugs, which diminish the inflammatory reaction, but they do not repair existing damage.  For this reason, extensive research is being conducted in the area of remyelinating therapies in order to stop disease progression and restore neurological disabilities.