从干细胞到少突胶质细胞:脑治疗的前景。

Cui P Chen, Mary E Kiel, Dorota Sadowski, Randall D McKinnon
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引用次数: 19

摘要

多发性硬化症是一种自身免疫性疾病,破坏中枢神经系统形成髓磷脂的少突胶质细胞。虽然使用抗炎细胞因子和类固醇可以部分控制损伤,但内源性修复不足以替代丢失的细胞。到目前为止,由于同种异体移植物在这种敏感的免疫环境中的排斥反应,细胞补充(移植治疗)被认为不太可能成功。然而,干细胞生物学的进步为获得患者特异性的自体少突胶质细胞带来了新的希望,这可能会打破平衡,有利于修复。挑战在于如何设计这些细胞,使其对能够靶向迁移到脑和脊髓损伤处的线索作出反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
From stem cells to oligodendrocytes: prospects for brain therapy.

Multiple sclerosis is an autoimmune disease that destroys myelin-forming oligodendrocytes of the CNS. While the damage can be partially controlled using anti-inflammatory cytokines and steroids, endogenous repair is insufficient to replace lost cells. Until now cell replenishment (transplant therapy) has been viewed as unlikely to succeed due to allograft rejection in this sensitized immune environment. However, advances in stem cell biology give new hope for deriving patient-specific, autologous oligodendrocytes which may tip the balance to favor repair. The challenge will be to engineer these cells to respond to cues that can target their migration into lesions for brain and spinal cord repair.

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