Centre for Neuroscience and Trauma, Barts and the Blizard Institute, London, School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Department of Pathology, VU University Medical Centre, Amsterdam, the Netherlands.
Immunology. 2018 Jun;154(2):204-219. doi: 10.1111/imm.12922. Epub 2018 Apr 17.
Neurodegenerative diseases, the leading cause of morbidity and disability, are gaining increased attention as they impose a considerable socioeconomic impact, due in part to the ageing community. Neuronal damage is a pathological hallmark of Alzheimer's and Parkinson's diseases, amyotrophic lateral sclerosis, Huntington's disease, spinocerebellar ataxia and multiple sclerosis, although such damage is also observed following neurotropic viral infections, stroke, genetic white matter diseases and paraneoplastic disorders. Despite the different aetiologies, for example, infections, genetic mutations, trauma and protein aggregations, neuronal damage is frequently associated with chronic activation of an innate immune response in the CNS. The growing awareness that the immune system is inextricably involved in shaping the brain during development as well as mediating damage, but also regeneration and repair, has stimulated therapeutic approaches to modulate the immune system in neurodegenerative diseases. Here, we review the current understanding of how astrocytes and microglia, as well as neurons and oligodendrocytes, shape the neuroimmune response during development, and how aberrant responses that arise due to genetic or environmental triggers may predispose the CNS to neurodegenerative diseases. We discuss the known interactions between the peripheral immune system and the brain, and review the current concepts on how immune cells enter and leave the CNS. A better understanding of neuroimmune interactions during development and disease will be key to further manipulating these responses and the development of effective therapies to improve quality of life, and reduce the impact of neuroinflammatory and degenerative diseases.
神经退行性疾病是发病率和致残率的主要原因,由于老龄化社会的影响,它们造成了相当大的社会经济负担,因此越来越受到关注。神经元损伤是阿尔茨海默病和帕金森病、肌萎缩侧索硬化症、亨廷顿病、脊髓小脑共济失调和多发性硬化症的病理标志,尽管神经毒性病毒感染、中风、遗传性脑白质疾病和副肿瘤性疾病也观察到这种损伤。尽管病因不同,例如感染、基因突变、创伤和蛋白质聚集,但神经元损伤通常与中枢神经系统固有免疫反应的慢性激活有关。人们越来越意识到免疫系统在大脑发育过程中以及在介导损伤、再生和修复方面都不可分割地参与其中,这激发了调节神经退行性疾病中免疫系统的治疗方法。在这里,我们回顾了目前对星形胶质细胞和小胶质细胞以及神经元和少突胶质细胞如何在发育过程中塑造神经免疫反应的理解,以及由于遗传或环境触发因素引起的异常反应如何使中枢神经系统易患神经退行性疾病。我们讨论了外周免疫系统与大脑之间的已知相互作用,并回顾了关于免疫细胞如何进入和离开中枢神经系统的当前概念。更好地了解发育和疾病过程中的神经免疫相互作用将是进一步操纵这些反应和开发有效治疗方法以提高生活质量、减轻神经炎症和退行性疾病影响的关键。