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Human Molecular Genetics Advance Access originally published online on July 8, 2003
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Human Molecular Genetics, 2003, Vol. 12, No. 17 2191-2199
DOI: 10.1093/hmg/ddg221
© 2003 Oxford University Press

Gene expression profile in multiple sclerosis patients and healthy controls: identifying pathways relevant to disease

Roberto Bomprezzi1,*, Markus Ringnér1,2, Seungchan Kim1,3, Michael L. Bittner1,3, Javed Khan4, Yidong Chen1, Abdel Elkahloun1, Aimee Yu5, Bibiana Bielekova5, Paul S. Meltzer1, Roland Martin5, Henry F. McFarland5 and Jeffrey M. Trent3

1Cancer Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA, 2Department of Theoretical Physics, Lund University, SE-223 62 Lund, Sweden, 3Translational Genomics Research Institute, Phoenix, AZ 85004, USA, 4Advanced Technology Center, National Cancer Institute, National Institutes of Health, Gaithersburg, MD 20877, USA and 5Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA

Received May 3, 2003; Revised June 12, 2003; Accepted June 26, 2003

Multiple sclerosis (MS) and other T cell-mediated autoimmune diseases develop in individuals carrying a complex susceptibility trait, probably following exposure to various environmental triggers. Owing to the presumed weak influence of single genes on disease predisposition and the recognized genetic heterogeneity of autoimmune disorders in humans, candidate gene searches in MS have been difficult. In an attempt to identify molecular markers indicative of disease status rather than susceptibility genes for MS, we show that gene expression profiling of peripheral blood mononuclear cells by cDNA microarrays can distinguish MS patients from healthy controls. Our findings support the concept that the activation of autoreactive T cells is of primary importance for this complex organ-specific disorder and prompt further investigations on gene expression in peripheral blood cells aimed at characterizing disease phenotypes.

* To whom correspondence should be addressed at: Cancer Genetics Branch, National Human Genome Research Institute, National Institutes of Health, 50 South Drive, Bldg 50 Room 5150, Bethesda, MD 20892-8000, USA. Tel: +1 3014964655; Fax: +1 3014023241; Email: rbomprez{at}nhgri.nih.gov


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