Interleukin 17 contributes to the chronicity of inflammatory diseases such as rheumatoid arthritis.

Rheumatoid arthritis (RA) is a chronic inflammatory disease leading to joint destruction and bone resorption. The proinflammatory cytokine interleukin 17 (IL-17), primarily produced by Th17 cells, has been shown to be involved in all stages of the disease and to be an important contributor of RA chronicity. Three major processes drive the IL-17-mediated chronicity. Several epigenetic events, enhanced in RA patients, lead to the increased production of IL-17 by Th17 cells. IL-17 then induces the production of several inflammatory mediators in the diseased synovium, which are further synergistically enhanced via combinations of IL-17 with other cytokines. IL-17 also promotes the survival of both the synoviocytes and inflammatory cells and promotes the maturation of these immune cells. This leads to an increased number of synoviocytes and inflammatory cells in the synovial fluid and in the synovium leading to the hyperplasia and exacerbated inflammation observed in joints of RA patients. Furthermore, these IL-17-driven events initiate several feedback-loop mechanisms leading to increased expansion of Th17 cells and thereby increased production of IL-17. In this review, we aim to depict a complete picture of the IL-17-driven vicious circle leading to RA chronicity and to pinpoint the key aspects that require further exploration.