Benveniste E N
Department of Cell Biology, University of Alabama at Birmingham 35294-0005, USA.
J Mol Med (Berl). 1997 Mar;75(3):165-73. doi: 10.1007/s001090050101.
One of the characteristic features of microglia is their rapid activation in response to injury, inflammation, neurodegeneration, infection, and brain tumors. This review focuses on the role of the microglia in multiple sclerosis (MS), a chronic inflammatory demyelinating disease of the central nervous system (CNS), and in the animal model of MS, experimental allergic encephalomyelitis (EAE). Microglial activation in MS and EAE is thought to contribute directly to CNS damage through several mechanisms, including production of proinflammatory cytokines, matrix metalloproteinases, and free radicals. In addition, activated microglia serve as the major antigen-presenting cell in the CNS, likely contributing to aberrant immune reactivity at this site. A mechanistic understanding of the way in which microglia are activated and ultimately inhibited is crucial for the formulation of therapeutic modalities to treat MS and other CNS autoimmune disease.
小胶质细胞的特征之一是它们会在受到损伤、炎症、神经退行性变、感染和脑肿瘤刺激时迅速激活。本综述聚焦于小胶质细胞在多发性硬化症(MS)(一种中枢神经系统(CNS)的慢性炎性脱髓鞘疾病)以及MS动物模型——实验性自身免疫性脑脊髓炎(EAE)中的作用。MS和EAE中的小胶质细胞激活被认为通过多种机制直接导致CNS损伤,这些机制包括促炎细胞因子、基质金属蛋白酶和自由基的产生。此外,活化的小胶质细胞是CNS中的主要抗原呈递细胞,可能导致该部位异常的免疫反应。对小胶质细胞激活及最终被抑制方式的机制性理解对于制定治疗MS和其他CNS自身免疫性疾病的治疗方案至关重要。