肿瘤坏死因子-α受体1缺陷小鼠实验性自身免疫性神经炎的加重
Aggravation of experimental autoimmune neuritis in TNF-alpha receptor 1 deficient mice.
作者信息
Lu Ming-Ou, Duan Rui-Sheng, Quezada Hernan Concha, Chen Zhi-Guo, Mix Eilhard, Jin Tao, Yang Xin, Ljunggren Hans-Gustaf, Zhu Jie
机构信息
Division of Neurodegeneration and Neuroinflammation, Karolinska Institute, Karolinska University Hospital Huddinge, Stockholm, Sweden.
出版信息
J Neuroimmunol. 2007 May;186(1-2):19-26. doi: 10.1016/j.jneuroim.2007.02.004. Epub 2007 Apr 10.
The role of tumor necrosis factor (TNF)-alpha and its receptors in the pathogenesis of experimental autoimmune neuritis (EAN) induced by P0 peptide 180-199 in TNFR1 (p55) deficient (TNFR1-/-) mice was investigated. Compared to wild type EAN mice, TNFR1-/- EAN mice developed significantly more severe clinical signs, in parallel with enhanced numbers of inflammatory infiltrating cells in peripheral nerves and splenic P0-reactive T cell proliferation, as well as increased obviously MHC class II and CCR3 expression on the macrophages in the cauda equina. Our data indicated that TNF-alpha might have anti-inflammatory effect preventing the development of EAN in this mouse model.
研究了肿瘤坏死因子（TNF）-α及其受体在P0肽180-199诱导的实验性自身免疫性神经炎（EAN）发病机制中，在肿瘤坏死因子受体1（TNFR1，p55）缺陷（TNFR1-/-）小鼠中的作用。与野生型EAN小鼠相比，TNFR1-/- EAN小鼠出现明显更严重的临床症状，同时外周神经中炎性浸润细胞数量增加、脾脏P0反应性T细胞增殖增强，以及马尾巨噬细胞上MHC II类分子和CCR3表达明显增加。我们的数据表明，在该小鼠模型中，TNF-α可能具有抗炎作用，可预防EAN的发展。
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