中国神经再生研究(英文版) ›› 2018, Vol. 13 ›› Issue (9): 1507-1515.doi: 10.4103/1673-5374.237109

• 综述:退行性病与再生 • 上一篇    下一篇

核因子κB在多发性硬化症中的作用

  

  • 收稿日期:2018-06-08 出版日期:2018-09-15 发布日期:2018-09-15

Role of nuclear factor κB in multiple sclerosis and experimental autoimmune encephalomyelitis

Yuan Yue1, 2, Sarrabeth Stone1, 2, Wensheng Lin1, 2   

  1. 1 Department of Neuroscience, University of Minnesota, Minneapolis, MN, USA
    2 Institute for Translational Neuroscience, University of Minnesota, Minneapolis, MN, USA
  • Received:2018-06-08 Online:2018-09-15 Published:2018-09-15
  • Contact: Wensheng Lin, M.D., Ph.D., linw@umn.edu
  • Supported by:

    This study was supported by grants from the National Institutes of Health (NS094151 and NS105689) and the National Multiple Sclerosis Society (RG5239-A-3) to WL.

摘要:

orcid:0000-0003-4931-7642(Wensheng Lin)

Abstract:

The transcription factor nuclear factor κB (NF-κB) plays major roles in inflammatory diseases through regulation of inflammation and cell viability. Multiple sclerosis (MS) is a chronic inflammatory demyelinating and neurodegenerative disease of the central nervous system (CNS). It has been shown that NF-κB is activated in multiple cell types in the CNS of MS patients, including T cells, microglia/macrophages, astrocytes, oligodendrocytes, and neurons. Interestingly, data from animal model studies, particularly studies of experimental autoimmune encephalomyelitis (EAE), have suggested that NF-κB activation in these individual cell types has distinct effects on the development of MS. In this review, we will cover the current literature on NF-κB and the evidence for its role in the development of MS and its animal model EAE.

Key words: multiple sclerosis, experimental autoimmune encephalomyelitis, nuclear-factor κB, T cell, macrophage, microglia, astrocyte, oligodendrocyte, neuron