Burt R K, Burns W, Ruvolo P, Fischer A, Shiao C, Guimaraes A, Barrett J, Hess A
National Institutes of Health, National Heart Lung and Blood Institute, Clinical Hematology Branch, Bethesda, Maryland.
J Neurosci Res. 1995 Jul 1;41(4):526-31. doi: 10.1002/jnr.490410412.
Experimental allergic encephalomyelitis (EAE), an animal model for multiple sclerosis (MS), is a paralytic disease of the central nervous system (CNS) mediated by T-lymphocytes reactive to myelin basic protein (MBP). Lewis rats actively immunized with fragment 68 to 82 of guinea pig MBP develop a monophasic disease with spontaneous recovery. Lymphocyte recognition of the primary encephalitogenic sequence of MBP (fragment 68 to 82) is V beta 8.2 T cell receptor (TCR) skewed [1-3]. Lewis rats in clinical remission at 1 month and 3 months after spontaneous resolution of EAE retain V beta 8.2 T-lymphocytes in the CNS when analyzed by reverse transcriptase polymerase chain reaction or in situ hybridization. In contrast, 1 and 3 months after clinical remission from syngeneic bone marrow transplantation, V beta 8.2 T lymphocytes are absent from the CNS. During clinically active EAE and inflammatory breakdown of the blood-brain barrier, immune ablation and reconstitution with syngeneic bone marrow results in clinical tolerance of the new immune system to myelin.
实验性自身免疫性脑脊髓炎（EAE）是多发性硬化症（MS）的动物模型，是一种由对髓鞘碱性蛋白（MBP）产生反应的T淋巴细胞介导的中枢神经系统（CNS）麻痹性疾病。用豚鼠MBP的68至82片段主动免疫的Lewis大鼠会发展为单相疾病并自发恢复。淋巴细胞对MBP主要致脑炎序列（68至82片段）的识别是Vβ8.2 T细胞受体（TCR）偏向性的[1-3]。通过逆转录酶聚合酶链反应或原位杂交分析，在EAE自发消退后1个月和3个月处于临床缓解期的Lewis大鼠，其CNS中保留有Vβ8.2 T淋巴细胞。相比之下，在同基因骨髓移植临床缓解1个月和3个月后，CNS中不存在Vβ8.2 T淋巴细胞。在临床活动期EAE以及血脑屏障发生炎性破坏期间，用同基因骨髓进行免疫消融和重建会导致新免疫系统对髓鞘产生临床耐受性。
