B lymphocytes, or B cells, a subclass of white blood cells which originate in the bone marrow, play a key role in RA as they have a very important role in the immune system. The precise contribution of B cells to the immunopathogenesis of RA is not completely characterized. However, there are several possible mechanisms by which B cells may participate in the disease process. B cells’ main task is to mature into plasma B cells, which then produce antibodies in vast quantities. Antibodies are Y-shaped proteins that can recognise specific proteins and, if possible, bind every non-self (foreign) structure before releasing it to be attacked by phagocytes and other inflammatory cells. In RA, such antibodies – termed rheumatoid factor- are released in excess and are ultimately directed against the body and the joints. B cells may promote their own function as well as that of other cells by producing cytokines. TNF-alpha, IL-1, IL-6 and IL_10 are amongst some of the cytokines that B cells may produce in the synovium of RA patients.

Research results suggest that an imbalance between the cytokines that promote inflammation and those responsible for healthy immune system function plays an important role in the genesis of RA. In particular, IL-6 has been identified as a key player in the development of RA. Studies have confirmed that excessive amounts of IL-6 are produced in the joints of people with RA, particularly the synovium. The high levels of IL-6 and IL-6R contribute to inflammation, swelling, joint damage and destruction associated with RA. Increased IL-6 concentrations also correlate with systemic complications that range from fatigue and fever to increased cardiovascular disease and bone degeneration.

TNF-alpha is another inflammatory cytokine with an extensive variety of effects. In addition to having growth-stimulating and growth-inhibiting properties, it is also self-regulating. There is well-documented evidence of the role of TNF-alpha in RA.