Topham D J, Adesina A, Shenoy M, Craighead J E, Sriram S
Department of Pathology, College of Medicine, University of Vermont, Burlington 05405.
J Virol. 1991 Jun;65(6):3238-45. doi: 10.1128/JVI.65.6.3238-3245.1991.
Infection of female BALB/c mice with encephalomyocarditis virus results in the development of a paralytic syndrome in 7 to 10 days postinoculation. Previous studies had suggested the involvement of an immune component in the development of central nervous system pathology. We have examined the effects of T-cell depletion on the development of polioencephalitis (neuronal necrosis and inflammation of the brain and brain stem) and the relative contribution of the CD4+ and CD8+ subsets following the establishment of viremia. We show that monoclonal antibody depletion of T cells is effective in the reduction of polioencephalitis when given prior to viral inoculation. However, administration of the antibodies 12 h or more after viral inoculation failed to alter the development of polioencephalitis or encephalomyelitis. We conclude that T cells are involved in the development of central nervous system disease during the initial stages of infection but are not responsible for the later progression of disease.
用脑心肌炎病毒感染雌性BALB/c小鼠，在接种后7至10天会导致麻痹综合征的出现。先前的研究表明免疫成分参与了中枢神经系统病理学的发展。我们研究了T细胞耗竭对脑灰质炎（神经元坏死以及大脑和脑干炎症）发展的影响，以及病毒血症确立后CD4+和CD8+亚群的相对作用。我们发现，在病毒接种前给予单克隆抗体耗竭T细胞可有效减少脑灰质炎。然而，在病毒接种12小时或更长时间后给予抗体并不能改变脑灰质炎或脑脊髓炎的发展。我们得出结论，T细胞在感染初期参与中枢神经系统疾病的发展，但对疾病的后期进展并无责任。
