help button home button Genetics AJP: Cell Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Originally published as Genetics Published Articles Ahead of Print on February 16, 2005.

Genetics, Vol. 170, 283-289, May 2005, Copyright © 2005
doi:10.1534/genetics.104.035261

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
genetics.104.035261v1
170/1/283    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sheng, J. R.
Right arrow Articles by Wallström, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sheng, J. R.
Right arrow Articles by Wallström, E.

Eae19, a New Locus on Rat Chromosome 15 Regulating Experimental Autoimmune Encephalomyelitis

Jian Rong Sheng, Maja Jagodic, Ingrid Dahlman, Kristina Becanovic, Rita Nohra, Monica Marta, Ellen Iacobaeus, Tomas Olsson and Erik Wallström1

Center for Molecular Medicine, Department of Clinical Neuroscience, Neuroimmunology Unit, Karolinska Institutet, SE-17176 Stockholm, Sweden

1 Corresponding author: Neuroimmunology Unit, Center for Molecular Medicine, L8:04, SE-17176 Stockholm, Sweden.
E-mail: erik.wallstrom{at}cmm.ki.se

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 many 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-D15Rat71 (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 a (DA x PVG.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 enables the characterization of genetically regulated, evolutionary conserved disease pathways in complex neuroinflammatory diseases.




This article has been cited by other articles:


Home page
 J. Immunol.Home page
X. Yu, K. Bauer, P. Wernhoff, D. Koczan, S. Moller, H.-J. Thiesen, and S. M. Ibrahim
Fine Mapping of Collagen-Induced Arthritis Quantitative Trait Loci in an Advanced Intercross Line
J. Immunol., November 15, 2006; 177(10): 7042 - 7049.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2005 by the Genetics Society of America.