http://brain.oupjournals.org/cgi/content/abstract/124/10/1927

Brain, Vol. 124, No. 10, 1927-1938, October 2001
Saleh M. Ibrahim (1), Eilhard Mix (2), Tobias Böttcher (2), Dirk Koczan (1), Ralf Gold (3), Arndt Rolfs (2) and Hans-Jürgen Thiesen (1)
1 Departments of Immunology
2 Neurology, University of Rostock, Rostock
3 The Clinical Research Group for Multiple Sclerosis and Neuroimmunology, Department of Neurology, University of Würzburg, Germany

Correspondence to: Saleh M. Ibrahim, MD, Department of Immunology, University of Rostock, Schillingallee 70, 18055 Rostock, Germany E-mail: saleh.ibrahim@med.uni-rostock.de

Abstract

Multiple sclerosis is thought to be a polygenic disease driven by dysregulation of the immune system leading to an autoimmune response against one or several antigens of cerebral white matter tissue.

Experimental autoimmune encephalomyelitis (EAE) is a mouse model that is used to study the aetiology and pathogenesis of multiple sclerosis and new therapeutic approaches.

We used oligonucleotide microarrays to determine gene expression profiles of the inflamed spinal cords of EAE mice at the onset and at the peak of the disease. Of the ~11 000 genes studied, 213 were regulated differentially and 100 showed consistent differential regulation throughout the disease.

Inflammation resulted in a profile of increased gene expression of immune-related molecules, extracellular matrix and cell adhesion molecules and molecules involved in cell division and transcription, and differential regulation of molecules involved in signal transduction, protein synthesis and metabolism.

Of the 104 genes with defined chromosomal locations, 51 mapped to known EAE-linked quantitative trait loci and as such are putative candidate genes for susceptibility to EAE.
 

© 2001 Oxford University Press