Rodriguez M, David C S
J Immunol. 1985 Sep;135(3):2145-8.
Demyelination induced by Theiler's virus was examined in nonrecombinant H-2 congeneic strains of mice on common backgrounds expressing independent haplotypes. Light and electron microscopy of spinal cord sections from mice with s, f, p, r, v, or q haplotypes on a C57BL/10 background showed perivascular inflammation and multifocal areas of demyelination in the white matter. The demyelination in these mice was usually associated with clinical neurologic deficits. In contrast, mice with identical genetic backgrounds but b, k, or d haplotypes showed no pathologic or clinical abnormalities. Qa or Tla haplotypes did not appear to influence demyelination. The observations support the hypothesis that susceptibility to Theiler's murine encephalomyelitis virus-induced demyelination is influenced by genes that are linked to the H-2 complex. The findings suggest that the demyelination may be mediated by immune cells rather than being a direct cytolytic effect of virus on oligodendrocytes.
在表达独立单倍型的常见背景下的非重组H-2同类系小鼠中，研究了泰勒氏病毒诱导的脱髓鞘现象。对C57BL/10背景下具有s、f、p、r、v或q单倍型的小鼠脊髓切片进行光镜和电镜检查，结果显示白质中有血管周围炎症和多灶性脱髓鞘区域。这些小鼠的脱髓鞘通常与临床神经功能缺损相关。相比之下，具有相同遗传背景但为b、k或d单倍型的小鼠未出现病理或临床异常。Qa或Tla单倍型似乎不影响脱髓鞘。这些观察结果支持以下假说：对泰勒氏鼠脑脊髓炎病毒诱导的脱髓鞘的易感性受与H-2复合体连锁的基因影响。研究结果表明，脱髓鞘可能由免疫细胞介导，而非病毒对少突胶质细胞的直接溶细胞作用。
