Your immune system may have more in common with a Corvette than you thought. When a virus or bacteria enters a human body, the immune system revs up to fight and expel the invader. Once the invader is gone, the body puts on the brakes to stop the immune response.
But a new study by Patrick Gaffney, M.D., and Kathy Moser, Ph.D., of the Oklahoma Medical Research Foundation shows that variation of a particular gene-known as TNFAIP3-may cause the immune system to keep going at full speed long after the threat is gone, causing damage to the body.
"TNFAIP3 can be thought of as a critical brake mechanism for the immune system," said Gaffney, the senior author on the study and associate member of OMRF's Arthritis and Immunology Research Program. "When the gene doesn't function properly, the immune system redlines."
The research, done in conjunction with David Altshuler, M.D., Ph.D., a researcher at the Broad Institute of Harvard University and the Massachusetts Institute of Technology, appears in the August edition of the journal Nature Genetics.
Lupus is a chronic "autoimmune" disease in which the body's immune system attacks healthy tissues and organs. Symptoms range from skin rashes and joint pain to strokes, seizures and organ failure. The Lupus Foundation of America estimates that as many as 2 million Americans suffer from the disease, which has no known cure and can be fatal.
In healthy individuals, normal versions of the TNFAIP3 gene produce a protein (called A20) that regulates and shuts off the immune response. In lupus patients with the gene variant, the immune system has trouble turning itself off, Gaffney said.