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Annals of the Rheumatic Diseases 2004;63:1387-1392; doi:10.1136/ard.2003.017194
Copyright © 2004 BMJ Publishing Group Ltd & European League Against Rheumatism.
Annals of the Rheumatic Diseases 2004;63:1387-1392
© 2004 by BMJ Publishing Group Ltd & European League Against Rheumatism

EXTENDED REPORT

A gene expression signature for recent onset rheumatoid arthritis in peripheral blood mononuclear cells

N Olsen1,2, T Sokka1,4, C L Seehorn1, B Kraft1,2, K Maas, J Moore3 and T M Aune2

1 Department of Medicine, Division of Rheumatology and Immunology, Vanderbilt University, Nashville TN 37232, USA
2 Department of Microbiology and Immunology, Vanderbilt University, Nashville TN 37232, USA
3 Program in Human Genetics and Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville TN 37232, USA
4 Jyväskylä Central Hospital, Jyväskylä, Finland

Correspondence to:
Correspondence to:
Dr N J Olsen
5323 Harry Hines Blvd, Dallas, TX 75390-8884, USA; nancy.olsen{at}UTSouthwestern.edu

Background: In previous studies the presence of a distinct gene expression pattern has been shown in peripheral blood cells from patients with autoimmune disease.

Objective: To determine whether other specific signatures might be used to identify subsets of these autoimmune diseases and whether gene expression patterns in early disease might identify pathogenetic factors.

Methods: Peripheral blood mononuclear cells were acquired from patients with rheumatoid arthritis (RA) and analysed by microarrays containing over 4300 named human genes. Patients with RA for <2 years were compared with subjects with longstanding RA (average duration 10 years) and with patients with other immune or autoimmune diagnoses.

Results: Cluster analyses permitted separation of the patients with early RA (ERA) from those with longstanding disease. Comparison with other patient groups suggested that the ERA signature showed some overlap with that seen in the normal immune response to viral antigen as well as with a subset of patients with systemic lupus erythematosus.

Conclusions: The ERA signature may reflect, in part, a response to an unknown infectious agent. Furthermore, shared features with some lupus patients suggest that common aetiological factors and pathogenetic pathways may be involved in these two autoimmune disorders.

Abbreviations: ERA, early rheumatoid arthritis; MHC, major histocompatibility complex; PBMC, peripheral blood mononuclear cell; PCR, polymerase chain reaction; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus; TGFß, transforming growth factor ß

Keywords: rheumatoid arthritis; gene expression; peripheral blood mononuclear cells; synovitis


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