Dual role of inflammation in CNS disease

Dual role of inflammation in CNS disease
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DOI:
10.1212/01.wnl.0000275234.43506.9b
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发表时间:
2007-05-01
期刊:
影响因子:
9.9
通讯作者:
Meinl, Edgar
Meinl, Edgar
中科院分区:
医学1区
文献类型:
--
作者:
Hohlfeld, Reinhard;Kerschensteiner, Martin;Meinl, Edgar

文献摘要

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中枢神经系统的炎症反应通常被认为是导致或促成神经元损伤的原因。然而,新出现的证据表明,炎症反应也可以起到神经保护作用。神经系统和免疫系统采用重叠的机制和共享的介质来促进两个系统之间的串扰。例如,免疫细胞不仅产生神经破坏分子,而且产生支持神经轴突生长、存活和可塑性的因子。这也许可以解释为什么炎症反应可能有助于损伤和保护神经元。中枢神经系统炎症的双重作用也有重要的治疗意义,只是刚刚开始探索。
Inflammatory responses in the CNS have usually been perceived to cause or contribute to neuron injury. However, emerging evidence suggests that inflammatory reactions can also be neuroprotective. The nervous and immune systems employ overlapping mechanisms and shared mediators that promote cross-talk between the two systems. Immune cells, for example, produce not only neurodestructive molecules but also factors that can support neuroaxonal growth, survival, and plasticity. This might explain why inflammatory reactions may contribute to both injury and protection of neurons. The dual role of CNS inflammation also has important therapeutic implications that are only beginning to be explored.