A pathogenic hierarchy for synovial fibroblasts in rheumatoid arthritis

Rheumatoid arthritis (RA) is a chronic autoimmune disorder that affects 0.5–1% of the world’s population (1). It is characterized by inflammation and progressive destruction of joints (1). Synovial fibroblasts play important roles in initiating and driving RA by secreting inflammatory cytokines and chemokines, degrading cartilage, and stimulating osteoclasts that lead to bone erosion (2).