| T细胞共刺激分子在重症肌无力发病机制中的作用 |
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| 引用本文： | 吴怀国,任明山.T细胞共刺激分子在重症肌无力发病机制中的作用[J].国际免疫学杂志,2007,30(1):31-35. |
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| 作者姓名： | 吴怀国 任明山 |
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| 作者单位： | 230001,合肥,安徽医科大学附属省立医院;230001,合肥,安徽医科大学附属省立医院 |
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| 基金项目： | 安徽省教育厅自然科学基金重点资助（2005KJ343ZC）;安徽省人才开发基金重点资助（20052041） |
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| 摘 要： | 重症肌无力（MG）是由乙酰胆碱受体抗体介导的细胞免疫依赖性和补体参与的神经肌接头部位的自身免疫性疾病，免疫应答异常是其发病本质。近年研究发现CD28：CTLA4／87和CD154／CD40是最重要的共刺激分子，对T和B淋巴细胞的增殖、活化、抗体和细胞因子的分泌均具有重要作用，其对重症肌无力的发生和发展也具有十分关键的作用。
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| 关 键 词： | 共刺激分子 重症肌无力 发病机制 |
| 修稿时间： | 2005-12-30 |
The role of T cell co-stimulatory molecules in the pathogenesis of MG |
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| WU Huai-guo,REN Ming-shan.The role of T cell co-stimulatory molecules in the pathogenesis of MG[J].International Journal of Immunology,2007,30(1):31-35. |
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| Authors: | WU Huai-guo REN Ming-shan |
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| Institution: | Department of Neurology, Affiliated Provincial Hospital, Anhui Medical University, Hefei 230001, China |
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| Abstract: | Myasthenia gravis(MG) is cell immune-dependent and complement-participative autoimmune neuromuscular disease mediated by antibodies against the nicotinic acetylcholine receptor(AChR),Its essential pathogenesis is immune response dysfunction.Recent researches show that CD28:CTLA4/B7 and CD154/CD40 are major co-stimulatory molecules which play important roles in the activation,proliferation, antibody secretion of B cells and the activation and cytokine production of T cells,they also play a critical role in the occurrence and development of MG. |
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| Keywords: | Co-stimulatory molecule Myasthenia gravis Pathogenesis |
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