Rheumatoid arthritis (RA) is one of the most common forms of autoimmune disease, a term used to describe a large number of conditions that all arise in the same or similar way. A central role is played by the human immune system, which normally protects us against external factors such as viruses, bacteria and other foreign bodies. In autoimmune disease, faulty programming turns the body against its own tissue. Instead of fighting potentially harmful micro-organisms or antigens, the immune system identifies parts of its own body as 'foreign' and attacks them. The process may be triggered by viruses or bacteria.

In RA, immune cells known as B lymphocytes, or simply B cells, attack the healthy joint lining (synovium). They migrate from the blood into the synovium, where they damage the cartilage. Immune cell mediators, known as cytokines, ensure that more immune cells are available to fight the invaders. Research results suggest that an imbalance between the cytokines that promote inflammation and those responsible for healthy immune function plays an important role in the genesis of RA.

In RA, cytokines stimulate the cells to produce proinflammatory molecules or mediators. Interleukin-6 (IL-6) is one of several cytokines that act as biochemical messengers between cells that play a role in the maintenance of good health. IL-6 and its receptor IL-6R are overproduced in people with RA. This results in pain and inflammation. The inflamed cells release cartilage-destroying enzymes, leading to loss of bone substance and eventual joint destruction.