Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.
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.