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首页> 外文期刊>Journal of neuroinflammation >Suppression of experimental autoimmune encephalomyelitis by interleukin-10 transduced neural stem/progenitor cells
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Suppression of experimental autoimmune encephalomyelitis by interleukin-10 transduced neural stem/progenitor cells

机译:白介素10转导的神经干/祖细胞抑制实验性自身免疫性脑脊髓炎

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Neural stem/progenitor cells (NSPCs) have the ability to migrate into the central nervous system (CNS) to replace damaged cells. In inflammatory CNS disease, cytokine transduced neural stem cells may be used as vehicles to specifically reduce inflammation and promote cell replacement. In this study, we used NSPCs overexpressing IL-10, an immunomodulatory cytokine, in an animal model for CNS inflammation and multiple sclerosis (MS). Intravenous injection of IL-10 transduced neural stem/progenitor cells (NSPCIL-10) suppressed myelin oligodendrocyte glycoprotein aa 35–55 (MOG35-55)- induced experimental autoimmune encephalomyelitis (EAE) and, following intravenous injection, NSPCIL-10 migrated to peripheral lymphoid organs and into the CNS. NSPCIL-10 suppressed antigen-specific proliferation and proinflammatory cytokine production of lymph node cells obtained from MOG35-55 peptide immunized mice. In this model, IL-10 producing NSPCs act via a peripheral immunosuppressive effect to attenuate EAE.
机译:神经干/祖细胞(NSPC)具有迁移到中枢神经系统(CNS)中以替换受损细胞的能力。在炎性CNS疾病中,细胞因子转导的神经干细胞可以用作媒介物以特异性减轻炎症并促进细胞置换。在这项研究中,我们在中枢神经系统炎症和多发性硬化症(MS)动物模型中使用了过表达IL-10(一种免疫调节细胞因子)的NSPC。静脉注射IL-10转导的神经干/祖细胞(NSPCIL-10)抑制了髓磷脂少突胶质细胞糖蛋白aa 35–55(MOG35-55)诱导的实验性自身免疫性脑脊髓炎(EAE),并且在静脉注射后,NSPCIL-10迁移至外周血淋巴器官进入中枢神经系统。 NSPCIL-10抑制了从MOG35-55肽免疫小鼠获得的淋巴结细胞的抗原特异性增殖和促炎细胞因子的产生。在该模型中,产生IL-10的NSPC通过外周免疫抑制作用来减弱EAE。

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