髓鞘少突胶质细胞糖蛋白
脑脊髓炎
表位
髓鞘
脊髓
免疫学
病理
实验性自身免疫性脑脊髓炎
医学
多发性硬化
少突胶质细胞
蛋白脂蛋白1
小胶质细胞
中枢神经系统
髓鞘碱性蛋白
抗体
炎症
内科学
精神科
作者
Sandra Amor,NP Groome,Christopher Linington,Michael Morris,Klaus Dornmair,Minnetta V. Gardinier,Jean-Marie Matthieu,David Baker
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:1994-11-15
卷期号:153 (10): 4349-4356
被引量:283
标识
DOI:10.4049/jimmunol.153.10.4349
摘要
Abstract A recombinant protein corresponding to the Ig-like domain of myelin oligodendrocyte glycoprotein (MOG) and synthetic 15-mer peptides of the whole MOG molecule with eight amino acid overlaps were screened for their ability to induce experimental allergic encephalomyelitis (EAE) in Biozzi AB/H (H-2dq1) and SJL (H-2S) mice. Clinical and histologic evidence of EAE developed after sensitization with the recombinant MOG protein in both AB/H and SJL mice. In AB/H mice at least three MOG epitopes within residues 1-22, 43-57, and 134-148 induced clinical and histologic EAE, whereas only the sequence 92-106 was encephalitogenic in SJL mice. Histologically, the inflammatory response in the central nervous system consisted of perivascular accumulations of CD5+ T cells and F4/80+ macrophage/microglia cells equally distributed in the brain and spinal cord. The subpial/meningeal infiltration, characteristic of mouse EAE induced with spinal cord homogenate, was only observed in cases of severe clinical disease in SJL mice in which the cellular infiltrates predominated in the spinal cord. In spite of the presence of histologic lesions in AB/H mice immunized with MOG, clinical disease either rapidly resolved or was clinically silent. In contrast to immunization of SJL mice with recombinant MOG, sensitization to MOG 92-106 induced severe clinical paralysis. After recovery these animals relapsed and exhibited demyelinated lesions. This study is the first to describe encephalitogenic epitopes of MOG that induce both clinical and histologic signs of EAE in mice. These and previous findings implicating MOG as a target Ag for Ab-mediated attack in EAE suggest that such autoreactivity to MOG may be significant in the development of human demyelinating diseases such as multiple sclerosis.
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