Martin R, Bielekova B, Gran B, McFarland H F
Neuroimmunology Branch, NINDS, National Institutes of Health, Bethesda, MD 20892-1400, USA.
J Neural Transm Suppl. 2000(60):361-73. doi: 10.1007/978-3-7091-6301-6_26.
Multiple Sclerosis (MS) is considered a T cell-mediated autoimmune disease of central nervous system myelin. Based on elegant experiments in an animal model of MS, experimental allergic encephalomyelitis (EAE), a number of myelin proteins and peptides derived from these can induce inflammatory demyelinating lesions. Recent studies with transgenic mice expressing human HLA-DR molecules and a myelin basic protein (MBP)-specific T cell receptor as well as data from a phase II clinical trial with an altered peptide ligand based on MBP peptide (83-99) provide convincing evidence that the pathogenetic concepts which largely stem from the above EAE studies are valid in MS, too.
多发性硬化症（MS）被认为是一种由T细胞介导的中枢神经系统髓鞘自身免疫性疾病。基于在MS动物模型实验性自身免疫性脑脊髓炎（EAE）中的精密实验，多种髓鞘蛋白及其衍生肽可诱发炎性脱髓鞘病变。近期对表达人类HLA-DR分子和髓鞘碱性蛋白（MBP）特异性T细胞受体的转基因小鼠的研究，以及一项基于MBP肽（83-99）的改变肽配体的II期临床试验数据，均提供了令人信服的证据，表明主要源于上述EAE研究的发病机制概念在MS中同样有效。
