**The Role of Tocilizumab in the Treatment of Rheumatoid Arthritis**

Yasuhiko Hirabayashi1,2

*1Hikarigaoka Spellman Hospital, 2Graduate School of Medicine, Tohoku University Japan* 

### **1. Introduction**

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 (TNFα), 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).
