• B cells
• rheumatoid arthritis
• rituximab

• ACR, American College of Rheumatology
• AEs, adverse effects
• DMARDs, disease modifying antirheumatic drugs
• NCI-CTC, National Cancer Institute Common Toxicity Criteria
• NHL, non-Hodgkin’s lymphoma
• NSAIDs, non-steroidal anti-inflammatory drugs
• RA, rheumatoid arthritis
• RF, rheumatoid factor
• TNFα, tumour necrosis factor α
• IV, intravenous

Rheumatoid arthritis (RA) is a complex condition that is well characterised by chronic inflammation in the synovial membrane of affected joints, often with systemic manifestations. Yet the aetiology and precise pathogenesis of RA remain unclear. It has been postulated that there are multiple exogenous and/or endogenous antigenic triggers, which act on a predisposed genetic background to initiate a self perpetuating series of autoimmune responses in the synovial compartment, which are expressed as the signs and symptoms of RA.

The traditional principles of the treatment of RA are empirical. The use of analgesics and non-steroidal anti-inflammatory drugs (NSAIDs) for the control of pain and inflammation is combined with disease modifying antirheumatic drug (DMARD) treatment to slow the processes that result in joint destruction in RA, shown by radiological changes, anatomical deformities, and joint dysfunction. The conventional mainstays of DMARD treatment include antimalarial drugs, sulfasalazine, and methotrexate.

To elucidate the aetiology and pathogenesis of RA much attention has been focused on the putative effects on the continuing inflammatory process of different synovial cell populations, including macrophages, fibroblasts, endothelial cells, T cells, and B cells,¹ and on the influence of numerous cytokines. Studies have led to the development and introduction into clinical practice of treatments directed towards limiting these inflammatory driving effects. Such treatments include anti-tumour necrosis factor α (anti-TNFα) drugs (etanercept, infliximab, and adalimumab) and interleukin based treatments (anakinra). Although these treatments have been shown to be very effective, they do not work in all patients. In recent years there has been growing interest in, and enhanced understanding of, the contribution of B cells to the immunopathogenesis of RA. This article will briefly review the potential role of B cells in RA and the current evidence that B cell therapy is a promising approach in its treatment.