Nat Neurosci:上海交大自身免疫性脑脊髓炎新成果

2013-09-05 佚名 生物通

来自上海交通大学医学院、美国克利夫兰诊所(Cleveland Clinic)的研究人员,在新研究中证实在NG2+神经胶质细胞中的Act1选择性介导了IL-17诱导的实验性自身免疫性脑脊髓炎(EAE)发病。这一研究发现在线发表在9月1日的《自然神经科学》(Nature Neuroscience)杂志上。【原文下载】 论文的通讯作者是美国克利夫兰诊所的李晓霞(Xiaoxia Li,音译)博士

来自上海交通大学医学院、美国克利夫兰诊所(Cleveland Clinic)的研究人员,在新研究中证实在NG2+神经胶质细胞中的Act1选择性介导了IL-17诱导的实验性自身免疫性脑脊髓炎(EAE)发病。这一研究发现在线发表在9月1日的《自然神经科学》(Nature Neuroscience)杂志上。【原文下载

论文的通讯作者是美国克利夫兰诊所的李晓霞(Xiaoxia Li,音译)博士,实验设计和大部分实验工作、数据解析是由第一作者、上海交通大学医学院的康自珍(Zizhen Kang)博士完成。康自珍的主要研究方向为免疫与疾病,偏重于神经免疫学。

多发性硬化症是由T细胞介导的一种人类中枢神经系统炎症性脱髓鞘病,以炎症性脱髓鞘伴有神经退行性变为特征,但目前对于其确切的分子机制尚不清楚。将许多髓鞘的组件注入到动物体内可以诱导EAE。研究EAE模型可帮助确定自身免疫中枢神经系统炎症性疾病形成有关的免疫致病事件。在EAE的初期阶段,除了T细胞激活和扩增,还有抗原递呈细胞(APC)生成细胞因子调控效应CD4 + T细胞分化,其中包括Th1、TNFα和Th17 T细胞系。

值得注意的是,近期的一些研究表明Th1细胞和Th17细胞可以通过不同的机制各自诱导EAE。在缺失IL-17或IL-17R的小鼠中EAE受到显著抑制,IL-17特异性的抑制可减轻炎症,表明在EAE的效应阶段IL-17介导的信号极其重要。但目前并不清楚IL-17参与EAE形成及发病的确切机制。

Act1(NF-κB activator 1)是IL-17信号的一个重要的胞内接头蛋白(adaptor)。在以往的研究中该研究小组曾报道,除去小鼠神经外胚层谱系,包括神经元、少突神经胶质细胞和星形胶质细胞的IL-7受体信号关键转导子Act1,可减小EAE的严重程度。

在这篇新文章中,研究人员探讨了这一研究发现的细胞学基础。他们发现除去神经元或成熟少突胶质细胞中的Act1并不会影响EAE的疾病病程,在星形胶质细胞中除去Act1也只会轻微影响疾病病程。而在NG2+神经胶质细胞中除去Act1则会显著地减小EAE的严重程度。并且,研究人员证实在NG2+神经胶质细胞中IL-17诱导了特征性的炎症介质表达。IL-17还强有力地抑制了体外少突胶质细胞细胞系的成熟,降低了它们的存活。

这些数据确定了NG2+神经胶质细胞是EAE中IL-17主要的中枢神经系统细胞靶点。少突胶质细胞系对于IL-17介导的毒性作用敏感,进一步表明了炎症与多发性硬化症中神经退行性变之间的直接关联。

原文下载

Kang Z, Wang C, Zepp J, Wu L, Sun K, Zhao J, Chandrasekharan U, Dicorleto PE, Trapp BD, Ransohoff RM, Li X.Act1 mediates IL-17–induced EAE pathogenesis selectively in NG2+ glial cells.Nat Neurosci. 2013 Sep 1. 

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    2014-03-25 wgx306
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    2013-12-14 liye789132251
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    2013-09-07 lsndxfj
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