NEURO-IMMUNE CROSSTALK IN CNS DISEASES

被引:132
作者
Kerschensteiner, M. [1 ]
Meinl, E. [1 ,2 ]
Hohlfeld, R. [1 ,2 ]
机构
[1] Univ Munich, Inst Clin Neuroimmunol, D-81377 Munich, Germany
[2] Max Planck Inst Neurobiol, Dept Neuroimmunol, D-813777 Munich, Germany
关键词
neuroinflammation; neurotrophic factors; cytokines; chemokines; NERVE GROWTH-FACTOR; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MYELIN OLIGODENDROCYTE GLYCOPROTEIN; INTERLEUKIN-1 RECEPTOR ANTAGONIST; STROKE-INDUCED IMMUNODEPRESSION; CEREBRAL-ARTERY OCCLUSION; LONG-TERM POTENTIATION; NECROSIS-FACTOR-ALPHA; SPINAL-CORD-INJURY; MULTIPLE-SCLEROSIS;
D O I
10.1016/j.neuroscience.2008.09.009
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Immune cells infiltrate the CNS in many neurological diseases with a primary or secondary inflammatory component. In the CNS, immune cells employ shared mediators to promote crosstalk with neuronal cells. The net effect of this neuro-immune crosstalk critically depends on the context of the interaction. It has long been established that inflammatory reactions in the CNS can cause or augment tissue injury in many experimental paradigms. However emerging evidence suggests that in other paradigms inflammatory cells can contribute to neuroprotection and repair. This dual role of CNS inflammation is also reflected on the molecular level as it is becomingly increasingly clear that immune cells can release both neurodestructive and neuroprotective molecules in CNS lesions. It is thus the balance between destructive and protective factors that ultimately determines the net result of the neuro-immune interaction. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:1122 / 1132
页数:11
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