Ann Rheum Dis 63:1387-1392 doi:10.1136/ard.2003.017194
  • Extended report

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

  1. N Olsen1,2,
  2. T Sokka1,4,
  3. C L Seehorn1,
  4. B Kraft1,2,
  5. K Maas,
  6. J Moore3,
  7. T M Aune2
  1. 1Department of Medicine, Division of Rheumatology and Immunology, Vanderbilt University, Nashville TN 37232, USA
  2. 2Department of Microbiology and Immunology, Vanderbilt University, Nashville TN 37232, USA
  3. 3Program in Human Genetics and Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville TN 37232, USA
  4. 4Jyväskylä Central Hospital, Jyväskylä, Finland
  1. Correspondence to:
    Dr N J Olsen
    5323 Harry Hines Blvd, Dallas, TX 75390-8884, USA;
  • Accepted 18 January 2004


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.