The Role of Tocilizumab in the Treatment of Rheumatoid Arthritis

The characteristic pathophysiology in rheumatoid arthritis (RA) is the destruction of bone and cartilage due to persistent synovitis of unknown etiology. Pro-inflammatory cytokines, including tumor necrosis factor alpha (TNF┙), interleukin-1 (IL-1), and interleukin-6 (IL-6), are overproduced in inflamed synovial membranes, and are critically involved in the spread and persistence of the inflammation. IL-6, which was identified as a B-cell stimulatory factor in 1986, is a multifunctional cytokine (Hirano, 2010), and a key mediator in the pathological processes of RA, especially in the activation of immune cells and osteoclasts (Cronstein, 2007). For RA drug therapy, therefore, inhibition of IL-6 signaling is suitable for shutting down both inflammation and bone destruction. Tocilizumab (TCZ) is a humanized monoclonal antibody (human IgG1 κ subclass) against IL-6 receptor (IL-6R). The data from the recent clinical studies on TCZ suggests that TCZ has several advantages over other antirheumatic drugs (Bergman et al., 2010).