Association between susceptibility to Theiler's virus-induced demyelination and T-cell receptor Jβ1-Cβ1 polymorphism rather than Vβ deletion

Yil Bahk Young Yil Bahk, C. A. Kappel, G. Rasmussen, B. S. Kim*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

18 Scopus citations

Abstract

Theiler's murine encephalomyelitis virus (TMEV) induces demyelinating disease in susceptible mouse strains after intracerebral inoculation. The clinical symptoms and histopathology of the central nervous system appear to be similar to those of human multiple sclerosis (MS), and thus, this system provides an excellent infectious animal model for studying MS. The virus- induced demyelination is immune mediated, and the genes involved in the immune response such as those for the T-cell receptor β-chain and major histocompatibility complex (MHC) haplotypes are known to influence disease susceptibility. To define whether the T-cell receptor Jβ-Cβ or Vβ genes are associated with susceptibility, we have analyzed F2 mice from crosses of susceptible SJL/J (Vβ(a)-JCβ(a)) mice and resistant C57L (Vβ(a)-JCβ(b)) mice. Our results indicate that susceptibility to TMEV-induced demyelination is associated with restriction fragment length polymorphism reflecting the T- cell receptorJβ1-Cβ1 region rather than the Vβ polymorphism. This association becomes stronger when the MHC haplotype is considered in the linkage analysis. However, differences in the T-cell receptor α-chain haplotype have no significant influence on the pathogenesis of TMEV-induced demyelination.

Original languageEnglish (US)
Pages (from-to)4181-4185
Number of pages5
JournalJournal of virology
Volume71
Issue number5
DOIs
StatePublished - 1997

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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