Researchers at the University of California, San Diego—supported by the Alliance for Lupus Research and the National Institutes of Health—have for the first time described a method that Staphylococcus aureus (staph) infection uses to inactivate the body’s immune system. A protein produced by the staph bacteria causes previously healthy B cells—a specialized cell of the immune system—to commit suicide, a process called apoptosis. The research will be published in the May 5 issue of the Journal of Experimental Medicine.
In the new study, the researchers found that SpA, a staph protein, functions as a B cell toxin in mice. The protein attaches to a receptor on B cells, eventually causing the B cells to turn on themselves in a suicide process.
Researchers believe that B cells play a major role in tissue damage that occurs in lupus. “By the targeted elimination of disease-causing B cells, properly dosed injections of SpA may have the potential to control the over-activity of the immune system that causes damage in autoimmune diseases like lupus and in certain cancers,” said Gregg Silverman, M.D., UCSD professor of medicine and senior author of the paper.
“The significance of Dr. Silverman’s research is that the discovery that injections of SpA limit the activity of B cells in animals allows us to proceed to the next step, to test the protein’s usefulness in people,” said John H. Klippel, MD, scientific director of the Alliance for Lupus Research, which funded this study. “If results hold true for people, SpA may eventually prove to be an effective treatment for lupus.”
In addition to Silverman, the study was conducted by the paper’s co-author Carl S. Goodyear, Ph.D., a UCSD postdoctoral researcher.
The study was funded by the National Institutes of Health and the Alliance for Lupus Research.