Stohlman S A, Bergmann C C, Cua D J, Lin M T, Ho S, Wei W, Hinton D R
Department of Neurology, University of Southern California, Los Angeles 90033, USA.
Adv Exp Med Biol. 1998;440:425-30. doi: 10.1007/978-1-4615-5331-1_53.
The role of CD4+ T cells in altering the activity of cytotoxic T lymphocytes (CTL) during infection of the central nervous system (CNS) by the neuroptropic JHMV strain of mouse hepatitis virus was examined. Adoptive transfer of in vitro activated CTL into CD4-depleted and control recipients showed that CTL were not effective in reducing JHMV replication within the CNS. The distribution of CD4+ and CD8+ T cells within the CNS during JHMV infection showed that the CD4+ T cells remained in perivascular and subarachnoid spaces and few entered the parenchyma. By contrast approximately half of the CD8+ T cells entered the parenchyma. In CD4-depleted mice the trafficking of CD8+ T cells was not inhibited; however, the majority of the cells were found to be apoptotic. These data suggested that CD4+ T cells were not required for CTL induction but were required for the maintenance of CTL viability. The limited role of CD4+ T cells in CTL induction was confirmed by comparison of CTL activity from CD4-depleted and control mice.
研究了CD4 + T细胞在嗜神经小鼠肝炎病毒JHMV株感染中枢神经系统（CNS）期间改变细胞毒性T淋巴细胞（CTL）活性中的作用。将体外活化的CTL过继转移到CD4缺失的受体和对照受体中，结果显示CTL在降低CNS内JHMV复制方面无效。JHMV感染期间CNS内CD4 +和CD8 + T细胞的分布表明，CD4 + T细胞保留在血管周围和蛛网膜下腔，很少进入实质。相比之下，约一半的CD8 + T细胞进入实质。在CD4缺失的小鼠中，CD8 + T细胞的迁移未受抑制；然而，发现大多数细胞发生凋亡。这些数据表明，CTL诱导不需要CD4 + T细胞，但维持CTL活力需要CD4 + T细胞。通过比较CD4缺失小鼠和对照小鼠的CTL活性，证实了CD4 + T细胞在CTL诱导中的作用有限。
