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doi:10.1534/genetics.104.035261
A more recent version of this article appeared on May 1, 2005.
REGULAR RESEARCH PAPERS |
Eae19, a new locus on rat chromosome 15 regulating experimental autoimmune encephalomyelitis
JianRong Sheng 1, Maja Jagodic 1, Ingrid Dahlman 1, Kristina Becanovic 1, Rita Nohra 1, Monica Marta 1, Ellen Iacobaeus 1, Tomas Olsson 1 and Erik Wallström 1*
1 Karolinska Institutet
* To whom correspondence should be addressed. E-mail: erik.wallstrom{at}cmm.ki.se.
Submitted on September 7, 2004
Revised on December 31, 2004
Accepted on 14 January 2005
Multiple sclerosis (MS) and its animal model myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (MOG-EAE) share a complex genetic predisposition with contributions from the major histocompatibility complex class II genes and multiple other genes. Linkage mapping in F2 crosses between the susceptible DA rat strain and the resistant ACI or BN rat strains in various models of autoimmune neuroinflammation have repeatedly displayed suggestive linkage to a region on rat chromosome 15. A direct study of this region was undertaken in congenic strains by transferring resistant ACI alleles to the susceptible DA background. Phenotypic analysis demonstrated lower maximal and cumulative EAE scores in the DA.ACI-D15Rat6-D15Rat 71 (C15), DA.ACI-D15Rat6-D15Rat48, D15Rat126-D15Rat71 (C15R3b) and DA.ACI-D15Rat23-D15rat71 (C15R4) strains compared to the parental DA rat strain. Linkage analysis was then performed in an (DAxPVG.AV1)F7 advanced intercross line, resulting in a LOD score of 4.7 for the maximal EAE score phenotype at the peak marker D15Rat71 and a confidence interval of 13 Mb overlapping with the congenic fragment defined by the C15R3b and the C15R4 strains. Thus, a new MOG-EAE locus with the designation Eae19 is identified on rat chromosome 15. There are 32 confirmed or predicted genes in the confidence interval, including immune-responsive gene 1 and neuronal ceroid lipofuscinose gene 5. Definition of loci such as Eae19 enable the characterization of genetically regulated, evolutionary conserved, disease pathways in complex neuroinflammatory diseases.
Key Words: EAE, QTL, autoimmunity, gene regulation, rat
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