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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 effect of immunosuppressive protocols on spontaneous CNS remyelination following toxin-induced demyelination.
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The effect of immunosuppressive protocols on spontaneous CNS remyelination following toxin-induced demyelination.

机译：免疫抑制方案对毒素诱导的脱髓鞘后自发中枢神经系统髓鞘再生的影响。

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Glial cell transplantation is a potential therapy for human demyelinating disease, though obtaining large numbers of human myelinating cells for transplantation remains a major stumbling block. Autologous transplantation is currently not possible, since the adult human CNS is not a good source of oligodendrocyte precursors, and long-term immunosuppression of engrafted allogeneic or xenogeneic cells is therefore likely to be necessary. Immunosuppressive drugs may need to be used in situations where more recent, active areas of demyelination are undergoing endogenous remyelination. It is therefore pertinent to establish the extent to which immunosuppressive protocols will suppress spontaneous remyelination. In order to investigate this issue, we created demyelinating lesions in the spinal cord of adult rats and compared the extent of remyelination in animals receiving different immunosuppressive treatments. In animals given only cyclosporin A, there was no difference in the extent of either Schwann cell or oligodendrocyte remyelination of ethidium bromide-induced demyelinating lesions. However, in animals given cyclophosphamide, either alone or in combination with cyclosporin, there was a significant reduction in the extent of oligodendrocyte-mediated remyelination. These results demonstrate that cyclophosphamide is deleterious to oligodendrocyte remyelination and for this reason should be used with caution in patients with demyelinating disease.
机译：胶质细胞移植是治疗人脱髓鞘疾病的一种潜在疗法，尽管获得大量用于移植的人髓鞘细胞仍然是主要的绊脚石。由于成年人类CNS不是少突胶质细胞前体的良好来源，因此目前不可能进行自体移植，因此可能有必要对移植的同种异体或异种细胞进行长期的免疫抑制。在较新的活跃的脱髓鞘区域正在进行内源性髓鞘再生的情况下，可能需要使用免疫抑制药物。因此，确定免疫抑制方案抑制自发性髓鞘再生的程度是相关的。为了调查此问题，我们在成年大鼠的脊髓中产生了脱髓鞘病变，并比较了接受不同免疫抑制治疗的动物的髓鞘再生程度。在仅给予环孢菌素A的动物中，溴化乙锭诱导的脱髓鞘性病变的雪旺氏细胞或少突胶质细胞再髓鞘化的程度没有差异。然而，在单独或与环孢菌素联合给予环磷酰胺的动物中，少突胶质细胞介导的髓鞘再生程度显着降低。这些结果表明，环磷酰胺对少突胶质细胞的髓鞘再生有害，因此在脱髓鞘疾病患者中应谨慎使用。

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