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Editorial

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

Claudia Mauri* and Elizabeth C Jury

Author Affiliations

Centre for Rheumatology Research, Department of Medicine, University College London, 46 Cleveland Street, London W1T4 JF, UK

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Arthritis Research & Therapy 2010, 12:133  doi:10.1186/ar3092


See related research by Catalán et al., http://arthritis-research.com/content/12/2/R68

Published: 13 August 2010

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. Catalán and collaborators report that patients with RA display reduced expression of FcγRIIB on memory B cells and plasma cells, which inversely correlates with autoantibody levels. Considering that FcγRIIB stimulation down-regulates antibody production, this work strengthens the link between autoantibodies and pathogenicity.