Kerschensteiner M, Meinl E, Hohlfeld R
Institute of Clinical Neuroimmunology, Ludwig-Maximilians University Munich, Marchioninistr. 17, 81377 Munich, Germany.
Neuroscience. 2009 Feb 6;158(3):1122-32. doi: 10.1016/j.neuroscience.2008.09.009. Epub 2008 Sep 13.
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 becoming 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.
在许多具有原发性或继发性炎症成分的神经疾病中，免疫细胞会浸润中枢神经系统（CNS）。在中枢神经系统中，免疫细胞利用共享介质促进与神经元细胞的相互作用。这种神经免疫相互作用的最终效果关键取决于相互作用的背景。长期以来人们已经确定，在许多实验模型中，中枢神经系统的炎症反应会导致或加剧组织损伤。然而，新出现的证据表明，在其他模型中，炎症细胞可有助于神经保护和修复。中枢神经系统炎症的这种双重作用在分子水平上也有所体现，因为越来越清楚的是，免疫细胞在中枢神经系统损伤中可释放神经破坏性和神经保护性分子。因此，破坏性和保护性因素之间的平衡最终决定了神经免疫相互作用的最终结果。
