The study identifies a new animal model for human SLE and implicates for the first time that deficiency in a single gene, Aiolos, can cause the autoimmune disease.

Lead author Dr. Sun Jian, a Chinese scientist who works with Dr. Patrick Matthias at the Friedrich Miescher Institute for Biomedical Research (FMI) in Basel, Switzerland, said the finding "offers a potential new approach for treating this class of diseases."

Their study shows that mice deficient in zine finger transcription factor Aiolos develop characteristics of human SLE. These mice produce anti-dsDNA and other autoantibodies, a hallmark of SLE, which form an immune complex resulting in tissue damage and glomerulonephritis, eventually leading to chronic renal failure.

The results also provide evidence that the lack of another transcription factor, OBF-1, can prevent the development of autoimmunity and SLE in Aiolos mutant mice.

SLE is a complex autoimmune disease involving multiple organs. It affects about one million people in the United States, 90 percent of whom are women. The incidence of SLE is even higher in Asia.

Previously, it was assumed that multiple genes contributed to human SLE.

"However, our results show that a single gene defect can cause SLE, indicating that the transcription factor Aiolos could function as a 'master gene' in the development of SLE," said Sun.

Sun is currently setting up a project in China to investigate the expression and variation of the Aiolos gene in lupus patients.

(Xinhua News Agency February 17, 2003)