Could the expression of CD86 and FcγRIIB on B cells be functionally related and involved in driving rheumatoid arthritis?

Abstract

Aberrant immune responses play a pivotal role in the processes that cause inflammation and joint damage in patients with rheumatoid arthritis (RA). Polyclonal B cell activation and the production of autoantibodies are immunological hallmarks of the disease. However, controversy surrounds the pathogenicity of autoantibodies, mainly because not all patients are seropositive (10% of RA patients are seronegative), suggesting that they could be markers rather than makers of disease. Catal-n and collaborators report that patients with RA display reduced expression of -RIIB on memory B cells and plasma cells, which inversely correlates with autoantibody levels. Considering that -RIIB stimulation down-regulates antibody production, this work strengthens the link between autoantibodies and pathogenicity. © 2010 BioMed Central Ltd.