Systemic lupus erythematosus is a chronic autoimmune disease in which the immune system confuses infections with its own healthy body tissue. The condition can harm multiple organs and tissues including skin, joints and kidneys. The disease is also categorized by elevated levels of type I interferon, a substance secreted by immune cells in response to viral infections. Little is known about the molecular mechanisms of this aspect of the condition.
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While examining the type I interferon signature, researchers at the University of Vermont’s Larner College of Medicine in Burlington identified a protein spontaneously active in lupus patients that normally signals an immune system activation during viral infections. Further investigation revealed the protein — mitochondrial antiviral signaling — was driving the type I interferon production. Researchers were able to inhibit this process in the laboratory setting by introducing an antioxidant to the MAVS, which prevented the subsequent production of interferon.
“[This is the] first paper showing that the interferon pathway can be activated by something other than viral infection or nucleic acids,” said Iwona Buskiewicz, PhD, an assistant professor in the department of pathology and laboratory medicine at the university. “A more focused antioxidant therapy targeting the particular organelle may have more efficacy.”
An estimated 1.5 million people in the U.S. have lupus. Only one new drug has become available for the condition in the past 50 years.
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