Rheumatoid arthritis (RA) is one of the most common systemic autoimmune diseases, and one of the least understood. Smoking is the major known environmental risk factor for RA, though little is known about the mechanisms involved. HLA-DR shared epitope (SE) genes are a widely recognized genetic risk factor for RA, though little is known about how these genes affect autoimmune reactions that lead to chronic inflammation and progressive joint and organ damage.

To better understand the interactions between smoking and HLA-DR SE genes in RA, a team of researchers in Sweden focused on the disease's distinctive autoimmune hallmark: citrulline, an amino acid not normally present in protein. While extremely rare in healthy individuals and relatively rare in other inflammatory conditions, citrulline-modified proteins are common in about two-thirds of RA patients and may be an underlying factor in the development of the disease. To investigate whether smoking and SE genes trigger immune reactions to citrullinated proteins, the team conducted a case-control study involving patients with recent-onset RA. The results, featured in the January 2006 issue of Arthritis & Rheumatism (http://www.interscience.wiley.com/journal/arthritis), suggest that smokers with SE genes are more susceptible to anticitrulline antibody-positive RA.

The study's 930 early RA patients, drawn from the Epidemiological Investigation of Rheumatoid Arthritis Study Group, ranged in age from 18 to 70 years. 383 healthy controls, drawn from the blood bank of northern Sweden, were matched for age, gender, and residential area. All participants completed questionnaires about their past and present smoking habits, as well as genotyping profiles. In addition, bronchial fluid was obtained from a representative sample of RA patients, including both current heavy smokers and lifelong non-smokers, and tested with immunosta
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Contact: Amy Molnar
amolnar@wiley.com
John Wiley & Sons, Inc.
3-Jan-2006

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