Lin R F, Lin T S, Tilton R G, Cross A H
Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110.
J Exp Med. 1993 Aug 1;178(2):643-8. doi: 10.1084/jem.178.2.643.
Experimental allergic encephalomyelitis (EAE) is a demyelinating autoimmune disorder that can be induced in susceptible mice by T lymphocytes sensitized to central nervous system (CNS) myelin components and is a prime animal model for the human CNS demyelinating disorder, multiple sclerosis (MS). Although CNS inflammation in which T lymphocytes and activated macrophages are the predominant cell types is observed in mice with EAE and in humans with MS, the exact mechanisms underlying the CNS damage and demyelination are not understood. Nitric oxide (NO), a gaseous free radical, has recently been shown to be a cytolytic product of activated macrophages. Using electron paramagnetic resonance spectroscopy, the nitric oxide free radical complexed with iron-sulfur proteins has been identified in affected spinal cords of mice with EAE, concurrent with the diminution of iron-sulfur proteins. These results indicate NO may play a role in the disease process of EAE, and perhaps MS.
实验性变应性脑脊髓炎（EAE）是一种脱髓鞘自身免疫性疾病，可通过对中枢神经系统（CNS）髓鞘成分致敏的T淋巴细胞在易感小鼠中诱发，是人类CNS脱髓鞘疾病——多发性硬化症（MS）的主要动物模型。尽管在患有EAE的小鼠和患有MS的人类中都观察到以T淋巴细胞和活化巨噬细胞为主要细胞类型的CNS炎症，但CNS损伤和脱髓鞘的确切机制尚不清楚。一氧化氮（NO）是一种气态自由基，最近已被证明是活化巨噬细胞的细胞溶解产物。利用电子顺磁共振波谱，在患有EAE的小鼠受影响的脊髓中已鉴定出与铁硫蛋白复合的一氧化氮自由基，同时铁硫蛋白减少。这些结果表明NO可能在EAE的疾病过程中起作用，也许在MS中也起作用。
