Advances in research on Toll-like receptors involved in the pathogenesis of rheumatoid arthritis

Rheumatoid arthritis (RA), an autoimmune disorder with chronic and protracted course, is perhaps the most severe and disabling type of disease. Therefore, it is vital to clarify the etiology and pathogenesis of RA. Toll-like receptors (TLRs) have been proved to play important roles in pathogenesis of RA and experimental arthritis, thus attracting wide attention in recent years. It has been found that some TLR expressions are dramatically changed in synoviocytes and immune cells of RA patients. The upregulated TLRs can induce the production of cytokines, chemokines and metal matrix proteinases in fibroblast-like synoviocytes, participate in regulating the functions of immune cells such as macrophages, dentritic cells, T cells and B cells, and promote angiogenesis and cartilage destruction by regulating the functions of endothelial cells and chondrocytes. All these contribute to the progression of RA and experimental arthritis. In short, many TLRs of diverse cells exert their actions synergistically or antagonistically to influence the progression of arthritis. Related research will lay significant theoretical foundations for the prevention, diagnosis and therapy of RA and specific drug development.