Yarom Y, Naparstek Y, Lev-Ram V, Holoshitz J, Ben-Nun A, Cohen I R
Nature. 1983;303(5914):246-7. doi: 10.1038/303246a0.
Experimental autoimmune encephalomyelitis (EAE) induced by immunization to the basic protein of central nervous system myelin (BP) is a paralytic disease in which T lymphocytes attack the individual's own central nervous system. As the target is in white matter, EAE has been considered an experimental model of some aspects of human disease such as multiple sclerosis. To investigate whether autoimmune T lymphocytes could produce paralysis, we studied the effects on the electrophysiology of isolated nerves produced by T-lymphocyte lines reactive specifically to BP or other antigens. We now report that propagation of action potentials evoked by electrical stimulation was blocked by incubating optic nerves with specific anti-BP T cells. This blockade could be reversed for up to two hours by removing the anti-BP line cells from the optic nerve. The anti-BP line cells had no effect on conduction along allogeneic optic nerves or syngeneic peripheral nerves. This indicates that disruption of the function of myelin in neuroimmunological disease may result from an immunologically specific interaction between autoimmune T lymphocytes and myelin antigens.
通过对中枢神经系统髓磷脂碱性蛋白（BP）进行免疫诱导的实验性自身免疫性脑脊髓炎（EAE）是一种麻痹性疾病，其中T淋巴细胞攻击个体自身的中枢神经系统。由于靶点位于白质，EAE被认为是人类疾病如多发性硬化症某些方面的实验模型。为了研究自身免疫性T淋巴细胞是否会导致麻痹，我们研究了对由特异性针对BP或其他抗原的T淋巴细胞系产生的离体神经电生理学的影响。我们现在报告，用特异性抗BP T细胞孵育视神经会阻断电刺激诱发的动作电位的传导。通过从视神经中去除抗BP细胞系，这种阻断在长达两小时内可以逆转。抗BP细胞系对同种异体视神经或同基因外周神经的传导没有影响。这表明神经免疫疾病中髓磷脂功能的破坏可能源于自身免疫性T淋巴细胞与髓磷脂抗原之间的免疫特异性相互作用。
