Lee JY, et al. - Researchers identified the ligands of enolase-1 (ENO1) that might promote inflammatory loops in vitro and increase the severity of arthritis in vivo. A key component of atherogenic lipids, apolipoprotein B (Apo B), interacting with ENO1 (which is expressed on the surface of immune cells) aggravated arthritis due to potentiated inflammatory response. A novel mechanism by which lipid metabolism regulates chronic inflammation in RA was suggested by this. They identified the apoB in the synovid fluid of patients with RA as a specific ligand to ENO1 with a higher affinity than plasminogen, a known ENO1 ligand.