Identification of susceptibility genes for experimental autoimmune encephalomyelitis that overcome the effect of protective alleles at the eae2 locus.

Research output: Contribution to journalArticle


We have previously identified a locus on mouse chromosome 15 (eae2) that regulates susceptibility to experimental autoimmune encephalomyelitis in a cross between the susceptible strain B10.RIII and the resistant strain RIIIS/J. In an effort to verify the protective effect from having two RIIIS/J alleles at eae2, the resistant locus was bred into the susceptible strain in homozygous form. However, the expected effect was not as clear as in the original study. This might be due to an epistatic effect conferred by several unidentified genes in the genome of the resistant strain or due to the environment by genotype interactions, possibly overcoming the effect of protective alleles at eae2. To further the genetic understanding in this disease, a genome-wide linkage screening approach was employed on an F(2) intercross that carried the protective allele at eae2in homozygous form while the rest of the genome segregated between the B10.RIII and RIIIS/J strains as in the original investigation. In the present study we find one region on chromosome 7, not previously identified in this strain combination, that affects the disease at significant logarithm of the odds score and six regions showing suggestive evidence for linkage to disease phenotypes.


  • Johan Jirholt
  • Anna-Karin Lindqvist
  • Jenny C Karlsson
  • Åsa Andersson
  • Rikard Holmdahl
Research areas and keywords

Subject classification (UKÄ) – MANDATORY

  • Immunology in the medical area


  • Mice Inbred Strains, Mice, Linkage (Genetics), Genetic Predisposition to Disease, Female, Chromosome Mapping, Encephalomyelitis Experimental Autoimmune : genetics, Multigene Family, Support Non-U.S. Gov't, Animal
Original languageEnglish
Pages (from-to)79-85
JournalInternational Immunology
Issue number1
Publication statusPublished - 2002
Publication categoryResearch

Bibliographic note

The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Medical Inflammation Research (013212019)