Researchers at Yale University have linked SLE in mice to a genetic mutation. The mutation, which causes DNA repair to slow down, was shown to lead to lupus symptoms. 

The research team focused on a gene known as POL B, which functions to repair breaks in DNA. Decreased POL B expression, which results in weakened DNA repair, has been linked to SLE.

 

To test whether this was true, researchers constructed mouse models with mutated POL B. They exhibited decreased expression and much slower DNA synthesis. The mice subsequently developed disease characteristics that strongly resemble SLE, including dermatitis and renal disease.

 

"This finding implicates abnormal DNA repair as one of the causes of lupus in people," said senior author Joann Sweasy, professor of therapeutic radiology and genetics at Yale School of Medicine and member of Yale Cancer Center. "This mouse model of SLE will be useful to study how abnormal DNA repair is linked to lupus and to identify new drugs to treat this disease."

If a similar connection is found in humans, this link could potentially lead to breakthroughs in lupus treatment, at least in certain cases of lupus. Read more about the study here.