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Human class I major histocompatibility complex transgene prevents virus‐induced demyelination in susceptible mutant B 10.d2 dml mice
Author(s) -
Rodriguez M.,
Pedrinaci S.,
David C. S.
Publication year - 1993
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410330211
Subject(s) - transgene , mutant , major histocompatibility complex , virology , biology , genetically modified mouse , virus , immunology , genetics , gene
Abstract Theiler's murine encephalomyelitis virus (TMEV) induces immune‐mediated demyelination in susceptible strains of mice, providing an excellent model for multiple sclerosis. Class I genes within the major histocompatibility complex locus (H‐2D region)play a major role in determining whether strains of mice develop chronic in determining whether strains of mice develop chronic demyelination and TMEV persistence. B 10.D2 dml mice with deletion in the 3′ end of D d and the 5′ end of L d genes develop the most prominent demyelination in comparison with resistant B10. D2 mice normal complementation of H‐2D region genes. We tested whether expression of a class I human transgene (HLA‐B27) would modulate virus‐induced demyelination in mutant B10.D2 dml mice. Transgenic B10.D2 dml (HLA‐B27 + ) mice infected with virus showed dramatic decrease in the extent of demyelination ( p < 0.0001) and virus antigen expression in spinal cord compared with littermate controls without the human class I transgene. These experiments demonstrate that transgenic expression of a human class I major histocompatibility complex locus molecule can prevent demyelination induced by a virus in mutant mice.