Yepes Manuel
Department of Neurology and Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
Front Biosci. 2007 May 1;12:2772-81. doi: 10.2741/2271.
The tumor necrosis factor superfamily (TNFSF) of cytokines comprises 19 ligands and 28 receptors (1). Ligand-mediated activation of TNFSF receptors plays a role in the pathogenesis of multiple central nervous system (CNS) diseases such as multiple sclerosis (2) and cerebral ischemia (3). Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a member of the TNFSF (4) that binds a small cell surface receptor known as fibroblast growth factor-inducible 14 (Fn14) (5-7). There is a growing body of evidence indicating that the interaction between TWEAK and Fn14 plays a role on cell death, regulation of the permeability of the neurovascular unit (NVU) and development of an inflammatory response in the CNS under physiological and pathological conditions (8, 9). Accordingly, here we will review the information available to this date on the role of this cytokine and its receptor in the CNS.
细胞因子的肿瘤坏死因子超家族（TNFSF）由19种配体和28种受体组成（1）。TNFSF受体的配体介导激活在多种中枢神经系统（CNS）疾病如多发性硬化症（2）和脑缺血（3）的发病机制中起作用。肿瘤坏死因子样凋亡弱诱导剂（TWEAK）是TNFSF的成员之一（4），它与一种称为成纤维细胞生长因子诱导14（Fn14）的小细胞表面受体结合（5 - 7）。越来越多的证据表明，在生理和病理条件下，TWEAK与Fn14之间的相互作用在细胞死亡、神经血管单元（NVU）通透性调节以及CNS炎症反应的发展中起作用（8, 9）。因此，在此我们将综述迄今为止关于这种细胞因子及其受体在CNS中的作用的现有信息。
