The synovial membrane of rheumatoid arthritis (RA) is characterized by an infiltrate of a variety of inflammatory cells, such as lymphocytes, macrophages, and dendritic cells, together with proliferation of synovial fibroblast-like cells. Numerous cytokines are overproduced in the inflamed joint, and macrophages and synovial fibroblasts are an important source of proinflammatory cytokines. Tumor necrosis factor alpha (TNF-α) and IL-1, two major macrophage products, are crucial in the process of chronic inflammation and joint destruction, and they give rise to effector components, including other inflammatory cytokines, chemokines, growth factors, matrix proteases, nitric oxide, and reactive oxygen species [10]. IL-6 is a pleiotropic cytokine produced substantially by activated fibroblasts, and its proinflammatory actions include simulating the acute-phase response, B-cell maturation into plasma cells, T-cell functions, and hematopoietic precursor cell differentiation [11].