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Lack of immune system protein prevents lupus-like condition in mice

St. Louis, July 8, 2004 -- Removal of an immune system signaling protein prevents the development of a lupus-like condition in mice, researchers at Washington University School of Medicine in St. Louis and the National Institutes of Health have found.

If additional studies in other animal models and humans confirm that SLAM-associated protein (SAP) is a primary contributor to lupus, it may be an ideal target for the development of new drug treatments, scientists said.

"What's perhaps most exciting is that normal immune system functions were still largely intact in the experimental mice that lacked SAP," says Stanford Peng, M.D., Ph.D., assistant professor of medicine in rheumatology and of pathology and immunology and lead investigator for the study. "Other immune system proteins are potential targets for new autoimmune disease treatments, but they all affect large portions of the immune system, making weakened immune function a potential side effect of any new drug. Targeting SAP for treatment may avoid that risk."

Scientists have used several animal models to study the immunological underpinnings of human lupus, a condition that afflicts approximately 1.5 million Americans with arthritis, prolonged fatigue, skin rashes, kidney damage, anemia and breathing pain.

In one of these models, exposing mice to a hydrocarbon oil known as pristane causes mice to develop a condition with many similarities to human lupus, including kidney disease and arthritis. But in the new study, available in the July 15 issue of the Journal of Experimental Medicine, a genetically modified line of mice continued to be fit even after pristane exposure. Created by National Institutes of Health researcher and coauthor Pamela L. Schwartzberg, the mice lack the SAP gene.

"The mice appear to be generally healthy," Peng says. "They have none of the lupus-like symptoms of the control group, and their immune systems generally respond to vaccinations like those
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Contact: Michael C. Purdy
purdym@wustl.edu
314-286-0122
Washington University School of Medicine
8-Jul-2004


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