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Demyelination induced by Theiler's virus: influence of the H-2 haplotype.
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Abstract
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.
Title: Demyelination induced by Theiler's virus: influence of the H-2 haplotype.
Description:
Abstract
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.
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