Department of Neurobiology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Department of Neurobiology, Weizmann Institute of Science, Rehovot 7610001, Israel.
Trends Immunol. 2016 Mar;37(3):181-192. doi: 10.1016/j.it.2016.01.006. Epub 2016 Feb 11.
Recent findings have revealed distinct roles for type I and II interferons (IFN-I and IFN-γ) in the recruitment of immune cells to the central nervous system (CNS) and highlighted the importance of this process for brain maintenance and protection/repair. Furthermore, manipulation of IFN-I and IFN-γ pathways in pathological contexts has yielded conflicting results. We discuss these findings, focusing on two distinct conditions; relapsing remitting multiple sclerosis (RRMS) and brain aging. Using these examples, we propose that regulation of immune cell entry to the CNS is a mechanism through which interaction between IFN-I and -II can affect brain function from its anatomical borders. Deviation from homeostatic IFN-I/-II balance may contribute to distinct brain pathologies, resulting from either insufficient immune surveillance of the CNS and loss of immune-dependent protection, or overwhelming leukocyte entry and immune-mediated destruction.
最近的研究结果揭示了 I 型和 II 型干扰素（IFN-I 和 IFN-γ）在免疫细胞募集到中枢神经系统（CNS）中的独特作用，并强调了这一过程对于大脑维持和保护/修复的重要性。此外，在病理情况下对 IFN-I 和 IFN-γ途径的操作产生了相互矛盾的结果。我们讨论了这些发现，重点关注两种不同的情况：复发缓解型多发性硬化症（RRMS）和大脑衰老。使用这些例子，我们提出免疫细胞进入中枢神经系统的调节是一种机制，通过这种机制，IFN-I 和 -II 之间的相互作用可以从其解剖边界影响大脑功能。IFN-I/-II 平衡的偏离可能导致不同的脑病理学，这可能是由于对中枢神经系统的免疫监视不足和免疫依赖的保护丧失，或者是由于白细胞过度进入和免疫介导的破坏。
