中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2013, Vol. 8 ›› Issue (35): 3296-3305.doi: 10.3969/j.issn.1673-5374.2013.35.004

• 原著:退行性病与再生 • 上一篇    下一篇

多发性硬化发的治疗新靶点：负性协同刺激分子PD-L1

  

  • 收稿日期:2013-08-05 修回日期:2013-11-06 出版日期:2013-12-15 发布日期:2013-12-15

PD-L1 is increased in the spinal cord and infiltrating lymphocytes in experimental allergic encephalomyelitis

Min Li1, Jiandong Jiang1, Bing Fu1, Jiechun Chen1, Qun Xue2, 3, Wanli Dong2, 3, Yanzheng Gu3, Lingtao Tang4, Limin Xue2, Qi Fang2, Mingyuan Wang5, Xueguang Zhang3   

  1. 1 Department of Neurology, Second People’s Hospital of Lianyungang City, Lianyungang 222006, Jiangsu Province, China
    2 Department of Neurology, First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China
    3 Institute of Clinical Immunology, Soochow University, Suzhou 215006, Jiangsu Province, China
    4 Department of Neurology, Third Hospital of Xingtai City, Xingtai 054000, Hebei Province, China
    5 Red-Cross Blood Center of Suzhou City, Suzhou 215006, Jiangsu Province, China
  • Received:2013-08-05 Revised:2013-11-06 Online:2013-12-15 Published:2013-12-15
  • Contact: Qun Xue, M.D., Chief physician, Master’s supervisor and Wanli Dong, M.D., Chief physician, Master’s supervisor, Department of Neurology, First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China; Institute of Clinical Immunology, Soochow University, Suzhou 215006, Jiangsu Province, China, babinsking@163.com.
  • About author:Min Li, Master, Attending physician. Min Li and Jiandong Jiang contributed equally to this work.

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摘要：

人类多发性硬化的病理过程和发病机制与实验性变态反应性脑脊髓炎非常相似，而已知实验性变态反应性脑脊髓炎发病中Th1细胞扮演着重要角色。而验证PD-L1在多发性硬化发病的发病中也可能有作用的假设，实验采用腋下注射髓鞘少突胶质细胞糖蛋白和完全弗氏佐剂及百日咳杆菌毒素建立实验性变态反应性脑脊髓炎小鼠模型，脊髓组织病理切片苏木精-伊红染色显示明显的炎性改变，脊髓组织Luxol Fast-Blue髓鞘染色显示明显的脱髓鞘改变，临床表现也符合实验性变态反应性脑脊髓炎的表现，证实模型建立成功。通过免疫组化、流式细胞仪、Western-blot检测负性协同刺激分子PD-L1在实验性变态反应性脑脊髓炎小鼠中的表达，发现模型小鼠脾细胞上和脊髓上的PD-L1分子表达都较正常小鼠明显增加，结果为进一步探讨PD-L1在多发性硬化发病机制中的可能作用奠定了基础。

中国神经再生研究（英文版）杂志出版内容重点： 脑损伤；脊髓损伤；周围神经损伤；帕金森；神经影像；神经再生 

关键词: 神经再生, 实验性变态反应性脑脊髓炎, 多发性硬化, 动物模型, 自身免疫性疾病, 共刺激信号, 协同刺激分子, PD-L1分子, B7-CD28超家族, 基金资助文章