LAUSR

Rheumatoid arthritis (RA) is an autoimmune disease associated with chronic inflammation of joints. Abnormally activated cells such as synovial macrophages and synovial fibroblasts induce RA pathogenesis and ultimately joint destruction. Since macrophages can change their own characteristics depending on the microenvironmental condition, it has been suggested that activation and remission of RA are regulated by crosstalk between synovial macrophages and other cells. Moreover, recent findings of heterogeneity of synovial macrophages and fibroblasts support the idea that complex interactions regulate RA from its onset to remission. Importantly, an understanding of the intercellular crosstalk in RA is far from complete. Here, we summarize the molecular mechanisms underlying the pathological development of RA with particular reference to the crosstalk between synovial macrophages and fibroblasts.