• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

多发性硬化症中抗髓鞘少突胶质细胞糖蛋白(MOG)抗体的免疫致病机制及临床相关性

Immunopathogenic and clinical relevance of antibodies against myelin oligodendrocyte glycoprotein (MOG) in Multiple Sclerosis.

作者信息

Berger T, Reindl M

机构信息

Department of Neurology, University of Innsbruck, Austria.

出版信息

J Neural Transm Suppl. 2000(60):351-60. doi: 10.1007/978-3-7091-6301-6_25.

DOI:10.1007/978-3-7091-6301-6_25
PMID:11205153
Abstract

Recent neuropathological findings identified four distinct immunopathogenic pathways of demyelination and tissue destruction in the most common inflammatory demyelinating central nervous system disorder, Multiple Sclerosis. One of this neuropathological subtypes is characterised by features of antibody-mediated demyelination. A role of anti-myelin antibodies in the disease evolution of multiple sclerosis has been suggested already for a long time, however, their pathogenetic and clinical relevance is not understood yet. This present article will discuss recently published and some preliminary data on the immunopathogenic role of antibodies against myelin oligodendrocyte glycoprotein (MOG) and other myelin/nonmyelin targets in multiple sclerosis, as well as possible clinical implications for prognosis and therapy in the future.

摘要

最近的神经病理学研究结果表明,在最常见的炎症性脱髓鞘中枢神经系统疾病——多发性硬化症中,存在四种不同的免疫致病途径导致脱髓鞘和组织破坏。这种神经病理学亚型之一的特征是抗体介导的脱髓鞘。抗髓鞘抗体在多发性硬化症疾病演变中的作用早已被提出,然而,它们的发病机制和临床相关性尚不清楚。本文将讨论最近发表的以及一些关于抗髓鞘少突胶质细胞糖蛋白(MOG)和其他髓鞘/非髓鞘靶点抗体在多发性硬化症中的免疫致病作用的初步数据,以及未来对预后和治疗可能的临床意义。

相似文献

1
Immunopathogenic and clinical relevance of antibodies against myelin oligodendrocyte glycoprotein (MOG) in Multiple Sclerosis.多发性硬化症中抗髓鞘少突胶质细胞糖蛋白(MOG)抗体的免疫致病机制及临床相关性
J Neural Transm Suppl. 2000(60):351-60. doi: 10.1007/978-3-7091-6301-6_25.
2
The myelin oligodendrocyte glycoprotein (MOG): a model for antibody-mediated demyelination in experimental autoimmune encephalomyelitis and multiple sclerosis.髓鞘少突胶质细胞糖蛋白(MOG):实验性自身免疫性脑脊髓炎和多发性硬化中抗体介导的脱髓鞘模型。
J Neural Transm Suppl. 2000(58):123-33. doi: 10.1007/978-3-7091-6284-2_10.
3
Antibodies from inflamed central nervous system tissue recognize myelin oligodendrocyte glycoprotein.来自炎症性中枢神经系统组织的抗体可识别髓鞘少突胶质细胞糖蛋白。
J Immunol. 2005 Aug 1;175(3):1974-82. doi: 10.4049/jimmunol.175.3.1974.
4
Identification of a pathogenic antibody response to native myelin oligodendrocyte glycoprotein in multiple sclerosis.在多发性硬化症中鉴定针对天然髓鞘少突胶质细胞糖蛋白的致病性抗体反应。
Proc Natl Acad Sci U S A. 2006 Dec 12;103(50):19057-62. doi: 10.1073/pnas.0607242103. Epub 2006 Dec 1.
5
Antibodies against the myelin oligodendrocyte glycoprotein and the myelin basic protein in multiple sclerosis and other neurological diseases: a comparative study.多发性硬化症及其他神经疾病中抗髓鞘少突胶质细胞糖蛋白和髓鞘碱性蛋白抗体的比较研究
Brain. 1999 Nov;122 ( Pt 11):2047-56. doi: 10.1093/brain/122.11.2047.
6
Antibodies against glycosylated native MOG are elevated in patients with multiple sclerosis.多发性硬化症患者体内针对糖基化天然髓鞘少突胶质细胞糖蛋白的抗体水平升高。
Neurology. 2005 Sep 13;65(5):781-2; author reply 781-2. doi: 10.1212/wnl.65.5.781-b.
7
Immune responses against the myelin/oligodendrocyte glycoprotein in experimental autoimmune demyelination.实验性自身免疫性脱髓鞘中针对髓鞘/少突胶质细胞糖蛋白的免疫反应。
J Clin Immunol. 2001 May;21(3):155-70. doi: 10.1023/a:1011031014433.
8
Anti-MOG autoantibodies in Italian multiple sclerosis patients: specificity, sensitivity and clinical association.意大利多发性硬化症患者中的抗髓鞘少突胶质细胞糖蛋白自身抗体:特异性、敏感性及临床关联
Int Immunol. 2004 Apr;16(4):559-65. doi: 10.1093/intimm/dxh056.
9
Signaling cascades activated upon antibody cross-linking of myelin oligodendrocyte glycoprotein: potential implications for multiple sclerosis.髓鞘少突胶质细胞糖蛋白抗体交联后激活的信号级联反应:对多发性硬化症的潜在影响。
J Biol Chem. 2005 Mar 11;280(10):8985-93. doi: 10.1074/jbc.M413174200. Epub 2005 Jan 4.
10
Commentary: Sorting the wheat from the chaff: identifying demyelinating components of the myelin oligodendrocyte glycoprotein (MOG)-specific autoantibody repertoire.述评:去伪存真:鉴定髓鞘少突胶质细胞糖蛋白(MOG)特异性自身抗体库中的脱髓鞘成分
Eur J Immunol. 2004 Aug;34(8):2065-71. doi: 10.1002/eji.200425291.

引用本文的文献

1
Prediction of Disordered Regions and Their Roles in the Anti-Pathogenic and Immunomodulatory Functions of Butyrophilins.预测无规则区域及其在丁酸素的抗病原体和免疫调节功能中的作用。
Molecules. 2018 Feb 4;23(2):328. doi: 10.3390/molecules23020328.
2
Upregulation of Myelin Gene Expression by a Physically-Modified Saline via Phosphatidylinositol 3-Kinase-Mediated Activation of CREB: Implications for Multiple Sclerosis.通过磷酯酰肌醇 3-激酶介导的 CREB 激活上调髓鞘基因表达:对多发性硬化症的影响。
Neurochem Res. 2018 Feb;43(2):407-419. doi: 10.1007/s11064-017-2435-1. Epub 2017 Nov 15.
3
Body fluid biomarkers in multiple sclerosis: how far we have come and how they could affect the clinic now and in the future.
多发性硬化症中的体液生物标志物:我们已经取得的进展以及它们如何在当下和未来影响临床实践。
Expert Rev Clin Immunol. 2015 Jan;11(1):69-91. doi: 10.1586/1744666X.2015.991315. Epub 2014 Dec 18.
4
Peptidome analysis of cerebrospinal fluid by LC-MALDI MS.LC-MALDI MS 分析脑脊液中的肽组
PLoS One. 2012;7(8):e42555. doi: 10.1371/journal.pone.0042555. Epub 2012 Aug 6.
5
Gemfibrozil, a lipid-lowering drug, increases myelin genes in human oligodendrocytes via peroxisome proliferator-activated receptor-β.吉非贝齐,一种降脂药物,通过过氧化物酶体增殖物激活受体-β增加人少突胶质细胞中的髓鞘基因。
J Biol Chem. 2012 Oct 5;287(41):34134-48. doi: 10.1074/jbc.M112.398552. Epub 2012 Aug 9.
6
Polyreactive myelin oligodendrocyte glycoprotein antibodies: Implications for systemic autoimmunity in progressive experimental autoimmune encephalomyelitis.多反应性髓鞘少突胶质细胞糖蛋白抗体:对进行性实验性自身免疫性脑脊髓炎中全身自身免疫的影响。
J Neuroimmunol. 2007 Feb;183(1-2):69-80. doi: 10.1016/j.jneuroim.2006.11.024. Epub 2007 Jan 2.
7
Massive apoptosis in lymphoid organs in animal models for primary and secondary progressive multiple sclerosis.原发性和继发性进行性多发性硬化症动物模型中淋巴器官的大量细胞凋亡。
Am J Pathol. 2005 Dec;167(6):1631-46. doi: 10.1016/S0002-9440(10)61247-3.