Rheumatoid arthritis is an autoimmune disorder in which the immune system attacks the lining of the joints.
The immune attack causes an inflammatory response characterized by painful swelling of the joints, and eventually there is bone erosion and joint destruction with deformity. The disease can also cause whole body symptoms such as fever and fatigue. As for most autoimmune diseases, rheumatoid arthritis is more common in women, and there appears to be a genetic component to disease susceptibility. The event that triggers the initial immune attack is unknown, but is likely to be an environmental factor, such as an infection. There is no cure for rheumatoid arthritis, but the symptoms can be improved by several groups of drugs. These include non-steroidal anti-inflammatory drugs (e.g. ibuprofen), corticosteroids (prednisone), disease-modifying antirheumatic drugs (DMARDS; methotrexate), and TNF-alpha inhibitors (etanercept, infliximab, and adalimumab). More recently developed drugs include antibodies that inhibit the immune cells directly, such as rituximab. Despite the wide range of therapeutic options, drugs that dampen the immune system commonly increase the frequency of infections, sometimes with fatal consequences. For these reasons, there remains a continuing need to find safer and effective drugs for rheumatoid arthritis.