CD134 plays a crucial role in the pathogenesis of EAE and is upregulated in the CNS of patients with multiple sclerosis
CD134 plays a crucial role in the pathogenesis of EAE and is upregulated in the CNS of patients with multiple sclerosis
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DOI：
10.1016/j.jneuroim.2003.07.001
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发表时间：
2003-12-01
影响因子：
3.3
通讯作者：
Peña-Rossi, C
中科院分区：
文献类型：
--
作者：
Carboni, S;Aboul-Enein, F;Peña-Rossi, C
我们研究了CD 134（也称为OX 40）分子在实验性变态反应性脑脊髓炎（EAE）和多发性硬化（MS）中的作用。我们研究了Cd 134（-/-）小鼠对EAE的易感性，EAE是一种依赖于对髓鞘蛋白反应的浸润性CD 4 + T淋巴细胞的自身免疫小鼠模型。在Cd 134（-/-）小鼠中注射髓鞘少突胶质细胞糖蛋白（MOG）诱导的EAE显示出较不严重的疾病临床体征，并显着减少中枢神经系统（CNS）内的炎性浸润。耐药性与CD 134（-/-）小鼠CNS中浸润的致病性IFN γ产生T细胞的大幅减少有关。此外，对EAE动物和MS患者的CNS组织切片的分析显示，CD 134（+）细胞存在于活动性病变中，主要是血管周围浸润。MS患者和EAE受影响小鼠的脑组织中存在表达CD 134的T细胞，以及在CD 134（-/-）小鼠中获得的疾病评分显著降低提供的功能证据表明，干扰T细胞中的CD 134分子可能是活动性MS治疗干预的适当靶点。（C）2003 Elsevier B. V.保留所有权利。
We investigated the role of the CD134 (also named OX40) molecule in experimental allergic encephalomyelitis (EAE) and multiple sclerosis (MS). We examined the susceptibility of Cd134(-/-) mice to EAE, an autoimmune murine model that is dependent on infiltrating CD4+ T lymphocytes reactive to myelin proteins. EAE induced by myelin oligodendrocyte glycoprotein (MOG) injection in Cd134(-/-) mice showed less severe clinical signs of disease and markedly reduced inflammatory infiltrates within the central nervous system (CNS). Resistance was associated with a strong reduction of pathogenic IFNgamma-producing T cells infiltrating the CNS of Cd134(-/-) mice. Furthermore, analysis of CNS tissue sections from EAE animals and MS patients revealed the presence of CD134(+) cells that were localized in active lesions, mainly in perivascular infiltrates. The presence of CD134-expressing T cells in brain tissue of MS patients and EAE affected mice, together with the functional evidence provided by the significant decrease in disease score obtained in Cd134(-/-) mice, indicate that interfering with the CD134 molecule in T cells may be an appropriate target for therapeutic intervention in active MS. (C) 2003 Elsevier B.V. All rights reserved.