Figure 1: Schematic overview of the pathological role of IL-17 in RA. Several cell types are affected by IL-17 in RA joints. IL-17 can induce migration of RA peripheral blood monocytes in to the inflamed joints where they differentiate to macrophages. RA synovial tissue macrophages and fibroblasts activated with IL-17 can produce a number of proinflammatory factors that can mediate inflammation and neutrophil recruitment. Angiogenesis mediated by IL-17 can provide the inflamed joint with nutrients and oxygen and thereby perpetuate the vicious inflammatory cycle. IL-17 can also play a role in RA bone destruction by enhancing RANKL production alone or in synergy with TNF-α.