Hoffman P M, Cimino E F, Robbins D S
Retrovirus Research Center, Department of Veterans Affairs Medical Center, Baltimore, MD 21218.
J Neuroimmunol. 1991 Aug;33(2):157-65. doi: 10.1016/0165-5728(91)90059-g.
A dose and time related effect on neurologic disease expression followed transfer of viral specific cytotoxic T lymphocytes (CTL) to recipient NFS/N mice previously infected at 2 days of age with Cas-Br-M murine leukemia virus. Cas-Br-M MuLV gp70 was expressed in spleen and capillary endothelial cells in the brain and spinal cord of CTL recipients, but the progression of gliosis, vacuolation, and cell death that followed endothelial cell MuLV gp70 expression in unprotected Cas-Br-M MuLV infected mice was interrupted in protected CTL recipients. A direct cytotoxic effect of CTL on infected brain capillary endothelial or neural cells could not be demonstrated. Reduced levels of infectious MuLV and MuLV gp70 expression in brain following syngeneic CTL transfer early in the course of disease suggest that CTL may function by preventing a time-limited interaction of Cas-Br-M MuLV with a susceptible target cell or receptor critical for neurologic disease induction during the perinatal period.
在将病毒特异性细胞毒性T淋巴细胞（CTL）转移到2日龄时曾感染Cas-Br-M小鼠白血病病毒的受体NFS/N小鼠后，对神经疾病表达出现了剂量和时间相关效应。Cas-Br-M MuLV gp70在CTL受体的脾脏以及脑和脊髓的毛细血管内皮细胞中表达，但在未受保护的感染Cas-Br-M MuLV小鼠中，内皮细胞MuLV gp70表达后随之发生的胶质细胞增生、空泡形成和细胞死亡进程在受保护的CTL受体中被中断。无法证明CTL对受感染的脑毛细血管内皮细胞或神经细胞有直接细胞毒性作用。在疾病早期进行同基因CTL转移后，脑中传染性MuLV和MuLV gp70表达水平降低，这表明CTL可能通过阻止Cas-Br-M MuLV在围产期与对神经疾病诱导至关重要的易感靶细胞或受体进行有时间限制的相互作用来发挥作用。
