Cellular and molecular perspectives of macrophage in rheumatoid arthritis

Rheumatoid arthritis(RA)is a systemic,inflammatory autoimmune disease,which is still a significant unmet medical need despite significant therapeutic advances.The pathogenesis of RA involves many types of immune cells,such as T cells,B cells,macrophages and so on.It′s known that the synovial membrane contains two layers,the outer layer,or subintima and the inner layer,or intima.The intimal cells mainly include two types of cells,fibroblasts synoviocyte and macrophage-like synoviocyte.In the inflamed rheumatoid synovial tissues,there is a large number of macrophage-like synoviocytes.These cells can produce key pro-inflammatory cytokines,chemokines and growth factors and their signaling pathways,including nuclear factorκB,Janus kinase-signal transducer,are highly activated.It will trigger cartilage destruction and perpetuate inflammation.This review attempts to high-light some aberrations of macrophage in immunoreaction including the roles of genetic and environmental factors,cellular alterations,especially signaling pathways that are implicated in the pathogenesis of RA.

Rheumatoid arthritis （RA） is a systemic, inflammatory autoimmune disease, which is still a significant unmet medical need despite significant therapeutic advances. The pathogenesis of RA involves many types of immune cells, such as T cells, B cells, macrophages and so on. It＇s known that the synovial membrane contains two layers, the outer layer, or subintima and the inner layer, or intima. The intimal cells mainly include two types of cells, fibroblasts synoviocyte and macrophage-like synoviocyte. In the inflamed rheumatoid synovial tissues, there is a large number of macrophage-like synoviocytes. These cells can produce key pro-inflammatory cytokines, chemokines and growth factors and their signaling pathways, including nuclear factor KB, Janus kinase-signal transducer, are highly activated. It will trigger cartilage destruction and perpetuate inflammation. This review attempts to high-light some aberrations of macrophage in immunoreaction including the roles of genetic and environ- mental factors, cellular alterations, especially signaling pathways that are implicated in the pathogenesis of RA.