IRF1 is critical for the TNF-driven interferon response in rheumatoid fibroblast-like synoviocytes

Abstract

IRF-1: a key regulator in rheumatoid Arthritis Thomas Karonitsch at the Medical University of Vienna, Austria, and colleagues showed that activation of the protein interferon regulatory factor 1 (IRF-1) in human synoviocytes promoted the expression of genes that contribute to sustained synovial inflammation in rheumatoid Arthritis (RA). They found that the Januse kinase (JAK) inhibitors baricitinb and tofacitinib, which are both approved for the treatment of RA, prevented the activation of IRF1 regulated proinflammatory genes. Their findings unvover a potential role for IRF1 activated genes as a biomarker to predict the treatment response to RA therapies and moreover highlight the benefit of targeting inflammatory pathways in synoviocytes for the treatment of RA.