Role of interleukin-17 in cartilage and bone destruction in rheumatoid arthritis

Interleukin 17 is a newly discovered inflammatory cytokine produced by T cells. Although pathogenesis of rheumatoid arthritis is still unknown more and more data show that IL-17 has an influence in this process. The concentration of this interleukin is very high locally in the joint fluid and synovium of the patients with rheumatoid arthritis. The most recent studies show, that IL-17 is situated at the top of inflammatory cascade and stimulates fibroblasts, synovial cells and macrophages to higher production of proinflammatory cytokines. Moreover IL-17 initiates the loss of proteoglycans and stimulates increased production of enzymes in chondrocytes causing degradation of collagen. Rheumatoidal synovial fibroblasts produce metalloproteinases, which can be regulated by IL-17 in the presence of proinflammatory cytokines. It is suggested, that IL-17 stimulates osteoblasts to synthesis of prostaglandin E2 (PGE2) and expression of receptor gene NF - kappa ss (RANK), which induces osteclastogenesis. Probably IL-17 is responsible for intensive resorption of bone tissue in rheumatoid arthritis. It seems, that IL-17 plays an important role in the immunological response and in the destruction of cartilage and bone tissue in rheumatoid arthritis. The deeper understanding of the mechanism of IL-17 action on the cartilage and bone cells may help to introduce the new methods of treatment in rheumatoid arthritis.