Rodriguez M, Miller D J, Lennon V A
Department of Neurology, Mayo Medical School, Rochester, MN 55905, USA.
Neurology. 1996 Feb;46(2):538-45. doi: 10.1212/wnl.46.2.538.
We tested the hypothesis that immunoglobulins directed against a CNS autoantigen, myelin basic protein, may promote remyelination in the course of a chronic, immune-mediated demyelinating disease. SJL/J mice infected chronically with Daniel's strain of Theiler's virus served as an experimental model of MS. The spinal cords of these mice exhibit extensive primary demyelination and inflammation with minimal spontaneous remyelination. Treatment with whole antiserum or affinity-purified mouse immunoglobulins directed against rat or rabbit myelin basic protein increased new myelin synthesis as measured by quantitative morphometry. Electron microscopy revealed numerous oligodendrocytes in remyelinated CNS lesions and a relative lack of inflammatory cells. Viral antigen persisted in the spinal cord despite enhanced CNS-type remyelination. These findings indicate that immunoglobulins reactive with myelin autoantigens have the potential to promote myelin repair.
针对中枢神经系统自身抗原髓鞘碱性蛋白的免疫球蛋白,可能在慢性免疫介导的脱髓鞘疾病过程中促进髓鞘再生。长期感染丹尼尔株泰勒病毒的SJL/J小鼠作为多发性硬化症的实验模型。这些小鼠的脊髓表现出广泛的原发性脱髓鞘和炎症,自发髓鞘再生极少。用针对大鼠或兔髓鞘碱性蛋白的全抗血清或亲和纯化的小鼠免疫球蛋白治疗,通过定量形态学测量发现新的髓鞘合成增加。电子显微镜显示,在重新髓鞘化的中枢神经系统病变中有大量少突胶质细胞,且炎性细胞相对较少。尽管中枢神经系统型髓鞘再生增强,但病毒抗原仍持续存在于脊髓中。这些发现表明,与髓鞘自身抗原反应的免疫球蛋白具有促进髓鞘修复的潜力。