Kohanawa M, Asano M, Minagawa T, Nakane A
Department of Microbiology, Hokkaido University School of Medicine, Kita-ku, Sapporo, Japan.
Microb Pathog. 1997 Jul;23(1):33-8. doi: 10.1006/mpat.1996.0125.
Acute encephalomyelitis caused by Theiler's virus strain GD VII resembles human poliomyelitis, and T cells are essential in eliminating the virus from the brain, though not from the spinal cord. We speculated that macrophage-lineage cells might play a crucial role in eliminating the virus from the spinal cord. To analyse the role of macrophage-lineage cells in the infection, antibodies specific for beta2 integrin, as well as an anti-leukocyte function antigen 1 (LFA-1) monoclonal antibody (MAb) and an anti-complement receptor type 3 (CR3) MAb were used to deplete the corresponding cell populations in Theiler's virus-infected mice. Infiltration of CD8+ T cells into the brain and spinal cord was inhibited by the administration of the anti-LFA-1 MAb, and viral replication was augmented only in the brain. The number of CD4+ T cells and macrophage antigen-1 (Mac-1[+]) cells in the brain and spinal cord were not decreased by anti-LFA-1 MAb treatment. Anti-CR3 MAb treatment led to decrease of Mac-1(+) cells in the brain and spinal cord. The viral replication in the spinal cord of anti-CR3 MAb treated mice was augmented, but not that in the brain. These results indicate that the defense mechanism against Theiler's virus strain GD VII is dependent on Mac-1(+) cells in the spinal cord.
泰勒氏病毒株GD VII引起的急性脑脊髓炎类似于人类脊髓灰质炎,T细胞对于从脑中清除病毒至关重要,尽管不能从脊髓中清除病毒。我们推测巨噬细胞系细胞可能在从脊髓中清除病毒方面发挥关键作用。为了分析巨噬细胞系细胞在感染中的作用,使用针对β2整合素的特异性抗体,以及抗白细胞功能抗原1(LFA-1)单克隆抗体(MAb)和抗补体受体3(CR3)MAb来耗尽泰勒氏病毒感染小鼠中的相应细胞群体。给予抗LFA-1 MAb可抑制CD8 + T细胞向脑和脊髓的浸润,并且病毒复制仅在脑中增加。抗LFA-1 MAb处理并未降低脑和脊髓中CD4 + T细胞和巨噬细胞抗原1(Mac-1[+])细胞的数量。抗CR3 MAb处理导致脑和脊髓中Mac-1(+)细胞减少。抗CR3 MAb处理的小鼠脊髓中的病毒复制增加,但脑中的病毒复制未增加。这些结果表明,针对泰勒氏病毒株GD VII 的防御机制依赖于脊髓中的Mac-1(+)细胞。