Interleukin (IL)-6 has a variety of biological functions. For example, it 
stimulates the production of acute-phase reactants (C-reactive protein and serum 
amyloid A) and hepcidin which interferes with iron recycling and absorption, 
causing iron-deficient anemia, and augments expression of vascular endothelial 
growth factor and receptor activator of nuclear factor-κB ligand in synovial 
cells, leading to neovascularization and osteoclast formation. IL-6 also acts on 
lymphocytes, not only on B cells to stimulate autoantibody production, but also 
on naïve T helper cells to promote Th17 cell differentiation. Thus, an imbalance 
between T cell subsets possibly contributes to development of rheumatoid 
arthritis. Several clinical studies have demonstrated that a humanized anti-IL-6 
receptor antibody, tocilizumab, improves clinical symptoms in rheumatoid 
arthritis. Tocilizumab prevented radiographic progression of joint destruction 
by inhibiting cartilage/bone resorption. Tocilizumab also improved hematological 
abnormalities, including hypergammaglobulinemia, high levels of autoantibodies, 
and elevation of erythrocyte sedimentation rate and acute-phase proteins. 
Importantly, tocilizumab improved quality of life by reducing systemic symptoms, 
including fatigue, anemia, anorexia, and fever. These findings have confirmed 
that hyperproduction of IL-6 is responsible for the above clinical symptoms, 
including joint destruction. Many patients treated with tocilizumab achieved 
clinical remission associated with decreased serum IL-6, suggesting that IL-6 
enhances autoimmunity. Tocilizumab is a new therapeutic option for rheumatoid 
arthritis.