Rheumatoid arthritis is a chronic systemic inflammatory autoimmune disease that affects approximately 1% of the population. Recent studies demonstrate a significant improvement in clinical symptoms in patients treated with Rituximab, an anti-CD20 monoclonal antibody that depletes pro-B cells and mature B cells but not plasma cells. These findings indicate that B cells are an important contributor to the pathogenesis of RA. In this review we will examine the role of B cells in several different murine models of RA. There are a number of antibody-dependent mechanisms by which B cells support inflammatory processes in the joint. However, there are also antibody-independent mechanisms that involve B cell/T cell collaboration where B cells may modulate autoreactive T cell responses. In addition, B cells may be an important source of cytokines that either stimulate or inhibit autoimmune responses. Understanding the role of B cells in RA will provide new and directed therapeutic approaches to the treatment of disease.