A newly identified genetic variation increases the risk of two chronic, auto-immune inflammatory diseases: rheumatoid arthritis and systemic lupus erythematosus. These research findings result from a long-time collaboration between the Intramural Research Program of the National Institute of Arthritis and Musculoskeletal and Skin Diseases, or NIAMS, and other organizations, including the UC Davis Health System. NIAMS is part of the National Institutes of Health.

The research findings were published in the Sept. 6 issue of the New England Journal of Medicine.

Michael Seldin, chair of the Rowe Program in Genetics and a professor in the UC Davis Department of Biochemistry and Molecular Medicine, assisted in both the design and analysis of the study. The work was an outgrowth of previous collaborations conducted by the North American Rheumatoid Arthritis Consortium, of which Seldin is a founding investigator.

"This study has broad implications for both understanding the genetic variations that predispose toward autoimmune disease, and providing insight into critical steps that determine abnormal T-cell responses," Seldin said. "This research could lead to earlier diagnosis and treatment approaches to certain subgroups of subjects with either rheumatoid arthritis or systemic lupus."

Both rheumatoid arthritis and lupus are considered autoimmune diseases, or diseases in which the body's immune system attacks healthy tissue.

In rheumatoid arthritis, the immune system attacks the linings of the joints and sometimes other organs. In lupus, it attacks the internal organs, joints and skin. If not well controlled, both diseases can lead to significant disability.

-- David Ong, UC Davis Health System