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Editorial
. 2010;12(4):133.
doi: 10.1186/ar3092. Epub 2010 Aug 13.

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

Claudia Mauri, Elizabeth C Jury
Editorial

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

Claudia Mauri et al. Arthritis Res Ther. 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.

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