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用脑内皮细胞膜免疫诱导恒河猴发生自身免疫性脑脊髓炎。

Autoimmune encephalomyelitis in rhesus monkeys induced by immunization with cerebral endothelial cell membrane.

作者信息

Tsukada N, Koh C S, Yanagisawa N, Okano A, Taketomi T

机构信息

Department of Medicine (Neurology), Shinshu University, School of Medicine, Matsumoto, Japan.

出版信息

Acta Neuropathol. 1988;77(1):39-46. doi: 10.1007/BF00688241.

Abstract

It is postulated that multiple sclerosis might be an autoimmune demyelinating disease of the central nervous system (CNS). The mechanisms involved are unknown but, since the blood-brain barrier (BBB) is damaged, injury to endothelial cells is likely to have occurred. Our previous studies have led us to investigate the autoimmune effect of injuring the blood-brain barrier by immunizing rhesus monkeys with an endothelial cell membrane from the same kind of animals. The immunized animals developed a chronic or a relapsing neurological illness. Histological and ultrastructural examinations of the brain in the acute stage showed infiltrates of mononuclear cells around the blood vessels of the white matter of cerebrum, cerebellum, pons and midbrain, while in the chronic phase, large areas of demyelination and remyelination, especially in the white matter regions, were present. The animals immunized with extraneural antigen, an endothelial cell membrane obtained from human umbilical cord, developed no neurological illness. This results indicate that the brain endothelial cell membrane has an inflammatory encephalitogenic activity which could produce widespread demyelination in animals. The animal model described here may prove to be useful in the pathogenetic investigation of human autoimmune demyelinating diseases.

摘要

据推测,多发性硬化症可能是一种中枢神经系统(CNS)的自身免疫性脱髓鞘疾病。其中涉及的机制尚不清楚,但由于血脑屏障(BBB)受损,内皮细胞很可能已受到损伤。我们之前的研究促使我们通过用同种动物的内皮细胞膜免疫恒河猴来研究损伤血脑屏障的自身免疫效应。免疫后的动物出现了慢性或复发性神经疾病。急性期大脑的组织学和超微结构检查显示,大脑、小脑、脑桥和中脑白质血管周围有单核细胞浸润,而在慢性期,出现了大面积的脱髓鞘和再髓鞘形成,尤其是在白质区域。用从人脐带获得的神经外抗原(一种内皮细胞膜)免疫的动物未出现神经疾病。这些结果表明,脑内皮细胞膜具有炎性致脑炎活性,可在动物体内产生广泛的脱髓鞘。这里描述的动物模型可能在人类自身免疫性脱髓鞘疾病的发病机制研究中证明是有用的。

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