ARTICLE | Translation in Brief
Hybrid drivers
How dysfunctions in DNA repair could trigger autoimmune disorders
September 3, 2015 7:00 AM UTC
Researchers from the University of California Davis think their study published in eLife in July, which identifies new epigenetic markers of Aicardi-Goutières syndrome (AGS), goes part way to explaining what triggers interferon (IFN) α to drive inflammation in the rare disease as well as in systemic lupus erythematosus (SLE).
The researchers showed that fibroblasts from AGS patients have low levels of genomic methylation and abnormal increases in the formation of RNA:DNA hybrids at sites of transcription. They postulate that the RNA:DNA hybrids could be recognized by nucleic acid receptors in innate immune pathways, leading to the increased IFNα response that is a hallmark of SLE...