Johns T G, Kerlero de Rosbo N, Menon K K, Abo S, Gonzales M F, Bernard C C
Neuroimmunology Laboratory, La Trobe University, Bundoora, Victoria, Australia.
J Immunol. 1995 May 15;154(10):5536-41.
Chronic relapsing experimental autoimmune encephalomyelitis, a demyelinating disease induced by injection of central nervous system (CNS) tissue, is widely used as a model for multiple sclerosis. However, it is unclear which Ag or combination of Ags in the CNS induce the demyelinating immune response. We now show in Lewis rats that a single injection of myelin oligodendrocyte glycoprotein, a specific CNS myelin component, or an appropriately derived myelin oligodendrocyte glycoprotein peptide produces a relapsing remitting neurologic disease with extensive plaque-like demyelination. Igs from affected animals reacted specifically with myelin oligodendrocyte glycoprotein and stimulated a myelin protease activity, leading to myelin basic protein degradation. The demonstrated involvement of myelin oligodendrocyte glycoprotein as a new demyelinating neural Ag may provide a deeper insight into the pathogenesis of multiple sclerosis and its treatment.
慢性复发性实验性自身免疫性脑脊髓炎是一种通过注射中枢神经系统(CNS)组织诱导的脱髓鞘疾病,被广泛用作多发性硬化症的模型。然而,目前尚不清楚中枢神经系统中的哪种抗原或抗原组合会引发脱髓鞘免疫反应。我们现在在Lewis大鼠中发现,单次注射髓鞘少突胶质细胞糖蛋白(一种特定的中枢神经系统髓鞘成分)或适当衍生的髓鞘少突胶质细胞糖蛋白肽会产生一种复发缓解型神经疾病,并伴有广泛的斑块状脱髓鞘。患病动物的免疫球蛋白与髓鞘少突胶质细胞糖蛋白发生特异性反应,并刺激髓鞘蛋白酶活性,导致髓鞘碱性蛋白降解。髓鞘少突胶质细胞糖蛋白作为一种新的脱髓鞘神经抗原的参与,可能为深入了解多发性硬化症的发病机制及其治疗提供帮助。