NEW YORK (Reuters Health) - Peripheral blood cells of patients with early-stage rheumatoid arthritis (RA) share a unique gene expression profile, according to researchers.
The findings could provide a way to identify patients in the early stages of RA, Dr. Nancy J. Olsen of Vanderbilt University, Nashville, Tennessee and colleagues report in the November issue of the Annals of the Rheumatic Disease.
“Although new treatments for RA have greatly improved outcomes for the disease,” they note, “early and accurate diagnosis remains of primary importance to avoid long-term disability. However, it is currently not easy to identify those patients, in part because the nature of the initial insult remains unidentified.”
Dr. Olsen and her team had previously found a distinct gene expression pattern in peripheral blood cells from patients with autoimmune disease. They conducted the current study to determine if specific autoimmune conditions might have their own genetic signatures.
The researchers used microarrays containing more than 4,300 genes to compare peripheral blood mononuclear cell gene expression patterns in patients with RA for two years or less, those with long-standing disease, normal individuals, and those with other autoimmune disorders. Patients with established RA had the condition for an average of 10 years.
Nine genes showed at least threefold increased activity in subjects with early RA compared to individuals with established RA and those without the disease. In addition, 44 genes were downregulated more than threefold.
Three of the upregulated genes had immune system activity, and two affected glucocorticoid levels or activity. Many of the downregulated genes produced proteins involved in immune or inflammatory function or neoplasia and cell proliferation.
The researchers identified overlap between the early RA gene expression patterns and patterns seen in normal individuals after influenza vaccination. Some systemic lupus erythematosus patients also had the early RA gene expression signature.
“The possibility that the ERA signature reflects, in part, an immune response to an unidentified infectious agent,” the team concludes, is worthy of further study.
Source: Ann Rheum Dis 2004;63:1387-1392. [ Google search on this article ]
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