Racke M K, Martin R, McFarland H, Fritz R B
Neuroimmunology Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MD 20892.
J Neuroimmunol. 1992 Mar;37(1-2):75-84. doi: 10.1016/0165-5728(92)90157-g.
Copolymer-1 (Cop-1) has been shown to inhibit in vivo development of experimental allergic encephalomyelitis (EAE) in animals and has been reported to have some therapeutic benefit in relapsing/remitting multiple sclerosis (MS). The mechanism by which Cop-1 acts in vivo is not known. The present study demonstrates that Cop-1 inhibits the in vitro response of several antigen-specific murine T cell hybridomas restricted to I-A, and to a lesser extent, I-E. The ability of human myelin basic protein (MBP)-specific T cell lines (TCL) to lyse targets in the context of three HLA-DR types associated with MS was also impaired by Cop-1. The results suggest that the observed inhibition was due to competition between Cop-1 and nominal antigen for the class II major histocompatibility complex (MHC) peptide binding site.
共聚物-1（Cop-1）已被证明可抑制动物实验性变应性脑脊髓炎（EAE）的体内发展，并且据报道在复发/缓解型多发性硬化症（MS）中具有一定的治疗益处。Cop-1在体内发挥作用的机制尚不清楚。本研究表明，Cop-1可抑制几种受I-A限制且在较小程度上受I-E限制的抗原特异性小鼠T细胞杂交瘤的体外反应。Cop-1还损害了人髓鞘碱性蛋白（MBP）特异性T细胞系（TCL）在与MS相关的三种HLA-DR类型背景下裂解靶标的能力。结果表明，观察到的抑制作用是由于Cop-1与名义抗原竞争II类主要组织相容性复合体（MHC）肽结合位点所致。
