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Human Molecular Genetics Advance Access originally published online on December 21, 2005
Human Molecular Genetics 2006 15(3):501-509; doi:10.1093/hmg/ddi466
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© The Author 2005. Published by Oxford University Press. All rights reserved.
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact: journals.permissions@oxfordjournals.org

Identification of gene expression signatures in autoimmune disease without the influence of familial resemblance

Zheng Liu1,2, Kevin Maas1,2 and Thomas M. Aune1,2,*

1Division of Rheumatology, Department of Medicine and 2Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA

* To whom correspondence should be addressed at: MCN T3219, Vanderbilt University Medical Center, 1161 21st Avenue S., Nashville, TN 37232, USA. Tel: +1 6153437353; Fax: +1 6153226248; Email: thomas.aune{at}vanderbilt.edu

Received October 19, 2005; Accepted December 19, 2005

Even though autoimmune diseases are heterogeneous, believed to result from the interaction between genetic and environmental components, patients with these disorders exhibit reproducible patterns of gene expression in their peripheral blood mononuclear cells. A portion of this gene expression profile is a property of familial resemblance rather than autoimmune disease. Here, we wanted to identify the portion of this gene expression profile that is independent of familial resemblance and determine whether it is a product of disease duration, disease onset or other factors. By employing supervised clustering algorithms, we identified 100 genes whose expression profiles are shared in individuals with various autoimmune diseases but are not shared by unaffected family members of individuals with autoimmune disease or by controls. Individuals with early disease (1 year after onset) and established disease (10 years after onset) exhibit a near-identical expression pattern, suggesting that this unique profile is a product of disease onset rather than disease duration.


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