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环孢素增强病毒诱导的T细胞介导的脱髓鞘。环孢素对脱髓鞘病毒感染的影响。

Cyclosporine enhances virally induced T-cell-mediated demyelination. The effect of cyclosporine on a demyelinating virus infection.

作者信息

Fazakerley J K, Webb H E

出版信息

J Neurol Sci. 1987 Mar;78(1):35-50. doi: 10.1016/0022-510x(87)90076-1.

Abstract

Semliki Forest virus infection of adult mice results in a demyelinating meningoencephalomyelitis. Demyelination does not result from direct viral damage but from the activity of T lymphocytes. We have studied the effect of the immunosuppressant cyclosporine (Cs) on the outcome of this infection. Cs had no effect when given 5 days after the infection, and little effect when given 4 h after infection. When the Cs was given 48 h before infection there was a prolongation of the blood and brain virus titres, and a reduction in some mice of serum IgG anti-viral antibody synthesis, but an increase in the severity of the CNS inflammatory response and the demyelination. Consideration of these findings along with measurement of Cs levels in the serum and cerebrospinal fluid suggests that this drug does not cross the blood brain barrier.

摘要

成年小鼠感染Semliki森林病毒会导致脱髓鞘性脑膜脑脊髓炎。脱髓鞘并非由病毒直接损伤所致,而是由T淋巴细胞的活性引起。我们研究了免疫抑制剂环孢素(Cs)对这种感染结果的影响。感染后5天给予Cs没有效果,感染后4小时给予Cs效果甚微。当在感染前48小时给予Cs时,血液和脑内病毒滴度延长,一些小鼠血清IgG抗病毒抗体合成减少,但中枢神经系统炎症反应和脱髓鞘的严重程度增加。结合血清和脑脊液中Cs水平的测量来考虑这些发现表明,这种药物不能穿过血脑屏障。

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Pathogenesis of virus-induced demyelination.病毒诱导的脱髓鞘病变的发病机制。
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