Role of nuclear factor κB in multiple sclerosis and experimental autoimmune encephalomyelitis.
Role of nuclear factor κB in multiple sclerosis and experimental autoimmune encephalomyelitis.
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核因子 κB 在多发性硬化症和实验性自身免疫性脑脊髓炎中的作用。
DOI:
10.4103/1673-5374.237109
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发表时间:
2018-09
影响因子:
6.1
通讯作者:
Lin W
中科院分区:
文献类型:
--
作者:
Yue Y;Stone S;Lin W
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, 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 experimental autoimmune encephalomyelitis.
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