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Neuro-immune crosstalk in CNS diseases.

机译:中枢神经系统疾病的神经免疫串扰。

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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 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.
机译:免疫细胞以原发性或继发性炎性成分渗透到许多神经系统疾病中。在中枢神经系统中,免疫细胞利用共享的介质来促进与神经元细胞的串扰。这种神经免疫串扰的净效应主要取决于相互作用的背景。早已确定,在许多实验范例中,CNS中的炎症反应可引起或加剧组织损伤。然而,新兴证据表明,在其他范例中,炎症细胞可以促进神经保护和修复。随着越来越清楚的是免疫细胞可以在CNS病变中释放神经破坏性分子和神经保护性分子,CNS炎症的双重作用也反映在分子水平上。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。

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