The investigators then turned their attention to lupus-prone mice. When they treated these mice with a mitochondrial ROS scavenger, the mice displayed decreased autoimmunity, decreased type I IFN responses and an improved clinical phenotype. The results were consistent with the hypothesis that mitochondrial ROS promotes lupus-like disease. Thus, the researchers concluded that mitochondria play a role in autoimmune disease via contribution to the generation of NETs, as well as by contributing pro-inflammatory oxidized mitochondrial DNA.
Lara C. Pullen, PhD, is a medical writer based in the Chicago area.
Reference
- Lood C, Blanco LP, Purmalek MM, et al. Neutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease. Nat Med. 2016 Feb;22(2):146–153. doi: 10.1038/nm.4027. Epub 2016 Jan 18.
Editor’s note: The research team for this study is from the University of Washington in Seattle and the NIH’s National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). It was jointly led by Keith B. Elkon, University of Washington professor of Rheumatology, and Mariana J. Kaplan, chief of the NIAMS Systemic Autoimmunity Branch.
