Crotti Andrea, Glass Christopher K
Biogen, Cambridge, MA, USA.
Department of Cellular and Molecular Medicine, University of California San Diego, CA, USA; Department of Medicine, University of California San Diego, CA, USA.
Trends Immunol. 2015 Jun;36(6):364-73. doi: 10.1016/j.it.2015.04.007. Epub 2015 May 20.
Currently, the concept of 'neuroinflammation' includes inflammation associated with neurodegenerative diseases, in which there is little or no infiltration of blood-derived immune cells into the brain. The roles of brain-resident and peripheral immune cells in these inflammatory settings are poorly understood, and it is unclear whether neuroinflammation results from immune reaction to neuronal dysfunction/degeneration, and/or represents cell-autonomous phenotypes of dysfunctional immune cells. Here, we review recent studies examining these questions in the context of Huntington's disease (HD), where mutant Huntingtin (HTT) is expressed in both neurons and glia. Insights into the cellular and molecular mechanisms underlying neuroinflammation in HD may provide a better understanding of inflammation in more complex neurodegenerative disorders, and of the contribution of the neuroinflammatory component to neurodegenerative disease pathogenesis.
目前,“神经炎症”的概念包括与神经退行性疾病相关的炎症,在这类疾病中,几乎没有或根本没有源自血液的免疫细胞浸润到大脑中。人们对脑内固有免疫细胞和外周免疫细胞在这些炎症环境中的作用了解甚少,并且尚不清楚神经炎症是由对神经元功能障碍/退化的免疫反应引起的,和/或是否代表功能失调的免疫细胞的细胞自主表型。在此,我们综述了最近在亨廷顿舞蹈症(HD)背景下研究这些问题的相关研究,在HD中,突变型亨廷顿蛋白(HTT)在神经元和神经胶质细胞中均有表达。深入了解HD中神经炎症背后的细胞和分子机制,可能有助于更好地理解更复杂的神经退行性疾病中的炎症,以及神经炎症成分对神经退行性疾病发病机制的作用。