Lipton H L, Canto C D
Infect Immun. 1977 Mar;15(3):903-9. doi: 10.1128/iai.15.3.903-909.1977.
In the present study, cyclophosphamide and rabbit anti-mouse thymocyte serum were used to immunosuppress SJL/J mice infected with Theiler's mouse encephalomyelitis virus (TMEV) in order to delineate the potential mechanism(s) of virus-induced cellular injury in this infection. Whereas both immunosuppressive agents produced a significant increase in mortality, this treatment had differing effects on the pathological involvement of gray and white-matter structures in the central nervous system. The central nervous system of immunosuppressed TMEV-infected mice had increased microglial cell proliferation and neuronal necrosis, longer maintenance of high virus levels and spread of virus antigen to involve the neocortex and hippocampal complex. These observations indicate that TMEV causes a cytolotic infection of neurons and possibly other cells in gray matter. In contrast, immunosuppression produced a dramatic reduction in mononuclear inflammatory cells in the leptomeninges and spinal cord white matter of infected mice and prevented demyelination. Further, virus antigen was not detected in the leptomeninges and white matter of immunosuppressed and infected mice. These findings suggest that demyelination of TMEV infection is immune mediated.
在本研究中,使用环磷酰胺和兔抗小鼠胸腺细胞血清对感染泰勒氏小鼠脑脊髓炎病毒(TMEV)的SJL/J小鼠进行免疫抑制,以阐明该感染中病毒诱导细胞损伤的潜在机制。虽然两种免疫抑制剂均导致死亡率显著增加,但这种治疗对中枢神经系统灰质和白质结构的病理累及有不同影响。免疫抑制的TMEV感染小鼠的中枢神经系统有小胶质细胞增殖增加和神经元坏死,高病毒水平维持时间更长,且病毒抗原扩散至累及新皮层和海马复合体。这些观察结果表明,TMEV引起灰质中神经元以及可能其他细胞的溶细胞性感染。相比之下,免疫抑制使感染小鼠软脑膜和脊髓白质中的单核炎性细胞显著减少,并防止了脱髓鞘。此外,在免疫抑制的感染小鼠的软脑膜和白质中未检测到病毒抗原。这些发现提示,TMEV感染的脱髓鞘是免疫介导的。