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Human Molecular Genetics Advance Access published online on April 6, 2005
Human Molecular Genetics, doi:10.1093/hmg/ddi141
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© The Author 2005. Published by Oxford University Press. All rights reserved

Article

Shared gene expression profiles in individuals with autoimmune disease and unaffected first-degree relatives of individuals with autoimmune disease

Kevin Maas 1, Heidi Chen 2, Yu Shyr 2, Nancy J. Olsen 1, and Thomas Aune 3*

1 Division of Rheumatology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232, USA; Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
2 Deparment of Biostatistics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
3 Division of Rheumatology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232, USA; Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA; MCN T3219, Vanderbilt University Medical Center, 1161 21st Ave. S, Nashville, TN 37232

* To whom correspondence should be addressed.
Thomas Aune, E-mail: thomas.aune{at}vanderbilt.edu


  Abstract

Patients with autoimmune disorders exhibit highly reproducible gene expression profiles in their peripheral blood mononuclear cells. These signatures may result from chronic inflammation, other disease manifestations, or may reflect family resemblance. To test the latter hypothesis, we determined gene expression profiles in unaffected first-degree relatives of individuals with autoimmune disease. Gene expression profiles in unaffected first-degree relatives resembled the profiles found in individuals with autoimmune diseases. A high percentage of differentially expressed genes in unaffected first-degree relatives were previously identified autoimmune signature genes. Examination of the linear regression relationship of gene transcript levels between parent-offspring pairs revealed that autoimmune signature genes display high levels of family resemblance. Taken together, these results support the hypothesis that these variations in gene transcript levels are associated with family resemblance rather than clinical manifestations of disease.


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