Kerschensteiner Martin, Meinl Edgar, Hohlfeld Reinhard
Institute of Clinical Neuroimmunology, Ludwig-Maximilians University Munich, Marchioninistr, 17, 81377 Munich, Germany.
Results Probl Cell Differ. 2010;51:197-216. doi: 10.1007/400_2009_6.
Immune cells infiltrate the central nervous system (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 into CNS lesions. It is thus the balance between destructive and protective factors that ultimately determines the net result of the neuro-immune interaction.
在许多神经系统疾病中,免疫细胞会浸润中枢神经系统(CNS),这些疾病具有原发性或继发性炎症成分。在中枢神经系统中,免疫细胞利用共同的介质来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,炎症细胞可以促进神经保护和修复。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,免疫细胞可以向中枢神经系统病变部位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。