Jin Xuemei, Yamashita Toshihide
Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan; and Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST), 5 Sanbancho, Chiyoda-ku, Tokyo, Japan.
Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan; and Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST), 5 Sanbancho, Chiyoda-ku, Tokyo, Japan
J Biochem. 2016 May;159(5):491-6. doi: 10.1093/jb/mvw009. Epub 2016 Feb 8.
Accumulating evidence suggests that immune cells perform crucial inflammation-related functions including clearing dead tissue and promoting wound healing. Thus, they provide a conducive environment for better neuronal regeneration and functional recovery after adult mammalian central nervous system (CNS) injury. However, activated immune cells can also induce secondary damage of intact tissue and inhibit post-injury CNS repair. The inflammation response is due to the microglial production of cytokines and chemokines for the recruitment of peripheral immune cell populations, such as monocytes, neutrophils, dendritic cells and T lymphocytes. Interestingly, microglia and T lymphocytes can be detected at the injured site in both the early and later stages after nerve injury, whereas other peripheral immune cells infiltrate the injured parenchyma of the brain and spinal cord only in the early post-injury phase, and subsequently disappear. This suggests that microglia and T cells may play crucial roles in the post-injury functional recovery of the CNS. In this review, we summarize the current studies on microglia that examined neuronal regeneration and the molecular signalling mechanisms in the injured CNS. Better understanding of the effects of microglia on neural regeneration will aid the development of therapy strategies to enhance CNS functional recovery after injury.
越来越多的证据表明,免疫细胞执行着与炎症相关的关键功能,包括清除坏死组织和促进伤口愈合。因此,它们为成年哺乳动物中枢神经系统(CNS)损伤后更好的神经元再生和功能恢复提供了有利环境。然而,活化的免疫细胞也会诱导完整组织的继发性损伤,并抑制损伤后CNS的修复。炎症反应是由于小胶质细胞产生细胞因子和趋化因子,以募集外周免疫细胞群体,如单核细胞、中性粒细胞、树突状细胞和T淋巴细胞。有趣的是,在神经损伤后的早期和晚期,均可在损伤部位检测到小胶质细胞和T淋巴细胞,而其他外周免疫细胞仅在损伤后早期浸润脑和脊髓的损伤实质,随后消失。这表明小胶质细胞和T细胞可能在CNS损伤后的功能恢复中发挥关键作用。在这篇综述中,我们总结了目前关于小胶质细胞的研究,这些研究探讨了神经元再生以及损伤CNS中的分子信号机制。更好地理解小胶质细胞对神经再生的影响将有助于开发治疗策略,以增强损伤后CNS的功能恢复。