Roos R P, Firestone S, Wollmann R, Variakojis D, Arnason B G
J Neuroimmunol. 1982 Jun;2(3-4):223-34. doi: 10.1016/0165-5728(82)90057-1.
Theiler's virus (TV)-infected mice were treated with antithymocyte serum (ATS), cyclophosphamide or pepstatin (a protease inhibitor) to determine the effect on demyelination. When ATS and cyclophosphamide were begun at the time of infection there was significantly less demyelination at 2.5-3.5 weeks than in pepstatin or non-treated infected controls. When immunosuppression was continued for 5 weeks, or when it was not started until 5 weeks post-infection, no significant decrease in demyelination was seen compared to controls. The findings indicate that timing of immunosuppression is critical in determining the extent of TV demyelination. Such demyelination may occur by different mechanisms that are active at different times. The "bystander effect' may be important in early demyelination, but late demyelination may be due to other causes, such as oligodendrocyte lytic infection.
用抗胸腺细胞血清(ATS)、环磷酰胺或胃蛋白酶抑制剂(一种蛋白酶抑制剂)处理感染泰勒病毒(TV)的小鼠,以确定其对脱髓鞘的影响。在感染时开始使用ATS和环磷酰胺,2.5 - 3.5周时的脱髓鞘程度明显低于使用胃蛋白酶抑制剂或未处理的感染对照组。当免疫抑制持续5周,或直到感染后5周才开始免疫抑制时,与对照组相比,脱髓鞘程度没有显著降低。研究结果表明,免疫抑制的时机对于确定TV脱髓鞘的程度至关重要。这种脱髓鞘可能通过在不同时间活跃的不同机制发生。“旁观者效应”可能在早期脱髓鞘中起重要作用,但晚期脱髓鞘可能是由于其他原因,如少突胶质细胞溶解性感染。