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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >The murine gammaherpesvirus-68 chemokine-binding protein M3 inhibits experimental autoimmune encephalomyelitis.
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The murine gammaherpesvirus-68 chemokine-binding protein M3 inhibits experimental autoimmune encephalomyelitis.

机译:鼠γ疱疹病毒68趋化因子结合蛋白M3抑制实验性自身免疫性脑脊髓炎。

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摘要

Chemokines are critical mediators of immune cell entry into the central nervous system (CNS), as occurs in neuroinflammatory disease such as multiple sclerosis. Chemokines are also implicated in the immune response to viral infections. Many viruses encode proteins that mimic or block chemokine actions, in order to evade host immune responses. The murine gammaherpesvirus-68 encodes a chemokine-binding protein called M3, which has unique biochemical features that enable it to bind to and inhibit an unusually broad range of chemokines. We applied a replication-defective adenoviral vector encoding M3 (AdM3) directly to the CNS to evaluate the capacity of this protein to inhibit neuroinflammation using the experimental autoimmune encephalomyelitis (EAE) model. Treatment with the AdM3 vector significantly reduced the clinical severity of EAE, attenuated CNS histopathology, and reduced numbers of immune cells infiltrating the CNS. These results suggest that M3 may represent a novel therapeutic approach to neuroinflammatory disease.
机译:趋化因子是免疫细胞进入中枢神经系统(CNS)的关键介质,正如神经炎性疾病(如多发性硬化症)中所发生的那样。趋化因子也参与了对病毒感染的免疫反应。许多病毒编码模仿或阻断趋化因子作用的蛋白质,从而逃避宿主的免疫反应。鼠丙种疱疹病毒68编码一种称为M3的趋化因子结合蛋白,它具有独特的生化特征,使其能够结合并抑制异常广泛的趋化因子。我们将编码M3(AdM3)的复制缺陷型腺病毒载体直接应用于中枢神经系统,以使用实验性自身免疫性脑脊髓炎(EAE)模型评估该蛋白抑制神经炎症的能力。用AdM3载体进行治疗可显着降低EAE的临床严重性,减弱CNS的组织病理学和减少渗透到CNS的免疫细胞的数量。这些结果表明,M3可能代表一种新的神经炎性疾病的治疗方法。

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