In patients with rheumatoid arthritis, chronic inflammation in affected joints may lead to the development of tertiary lymphoid tissue. A micro-environment is generated in the synovial membrane which supports the activation and differentiation of B cells into plasma cells. Through a process of affinity maturation, plasma cells may be generated locally which secrete antibodies of high affinity. Rheumatoid arthritis is characterised by autoantibodies specific for self immunoglobulin. These rheumatoid factors form large antigen/antibody complexes which may enhance the process of joint destruction. The poor prognosis of rheumatoid factor-positive patients is indicitive of the critical role of immunoglobulin complexes in the continuous stimulation of the immune system and thus of the inflammatory processes. In general, treatment of patients with rheumatoid arthritis aims at suppressing inflammation. The currently most successful reagents are those which interfere with the network of cytokines, such as tumour necrosis factor or interleukin-1 receptor antagonists. Only recently have immunosuppressive therapies targeted directly at the B cell response been developed. These first studies suggest that therapies which directly affect the humoral immune response are of great therapeutic potential in the treatment of patients with rheumatoid arthritis.