Lin Tao

An iguratimod prodrug reduces RA-FLS invasiveness by disrupting STAT1–C3–TNFα-mediated crosstalk between fibroblast-like synoviocytes and macrophages

Background Rheumatoid arthritis (RA) is driven in part by hyperactivated fibroblast-like synoviocytes (FLS) that invade articular structures. Iguratimod (IGU), a conventional synthetic DMARD, is clinically effective, but its direct molecular target and impact on synovial cell-cel...