TNF superfamily member TWEAK exacerbates inflammation and demyelination in the cuprizone-induced model
TNF superfamily member TWEAK exacerbates inflammation and demyelination in the cuprizone-induced model
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DOI：
10.1016/j.jneuroim.2007.12.003
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发表时间：
2008-02-01
影响因子：
3.3
通讯作者：
Ting, Jenny P-Y.
中科院分区：
文献类型：
--
作者：
Iocca, Heather A.;Plant, Sheila R.;Ting, Jenny P-Y.
炎性细胞因子与包括多发性硬化症在内的多种神经系统疾病的病理学有关。我们研究了TNF家族成员TWEAK在神经炎症中的作用。喂食铜腙的小鼠在大脑中经历神经炎症和脱髓鞘，但是在从饮食中去除铜腙后，炎症消退并发生髓鞘再生。使用这个模型，我们证明了缺乏TWEAK的小鼠在脱髓鞘和小胶质细胞浸润方面表现出显著的延迟。在髓鞘再生过程中，缺乏TWEAK基因的小鼠仅表现出髓鞘再生的轻微延迟。因此，本研究确定了TWEAK在促进神经炎症和加剧脱髓鞘铜蛋白引起的损伤过程中的主要作用。(C)2007 Elsevier B.V.保留所有权利。
Inflammatory cytokines have been implicated in the pathology of multiple neurologic diseases, including multiple sclerosis. We examined the role of the TNF family member TWEAK in neuroinflammation. Cuprizone-fed mice undergo neuroinflammation and demyelination in the brain, but upon removal of cuprizone from the diet, inflammation is resolved and remyelination occurs. Using this model, we demonstrate that mice lacking TWEAK exhibit a significant delay in demyelination and microglial infiltration. During remyelination, mice lacking the TWEAK gene demonstrate only a marginal delay in remyelination. Thus, this study identifies a primary role of TWEAK in promoting neuroinflammation and exacerbating demyelination during cuprizone-induced damage. (C) 2007 Elsevier B.V. All rights reserved.