%0 Journal Article
%T Could the expression of CD86 and Fc¦ÃRIIB on B cells be functionally related and involved in driving rheumatoid arthritis?
%A Claudia Mauri
%A Elizabeth C Jury
%J Arthritis Research & Therapy
%D 2010
%I BioMed Central
%R 10.1186/ar3092
%X In a recent article Catal¨¢n and colleagues [1] examined the expression of Fc¦ÃRIIB in na£¿ve, memory and plasmablast B cell subsets from peripheral blood of patients with rheumatoid arthritis (RA) and the results were correlated with levels of autoantibodies to cyclic citrullinated proteins (anti-CCP) detected in matching serum. Firstly, they observed reduced Fc¦ÃRIIB expression in memory and plasmablast B cells from patients compared to the levels expressed on B cells from healthy controls. Secondly, the expression levels of Fc¦ÃRIIB inversely correlated with the titre of anti-CCP antibodies in patients' serum. Indeed, RA patients with low autoantibody titres expressed higher levels of this receptor. Th irdly, they also report an increased frequency of CD86, usually up-regulated upon activation, on memory and na£¿ve B cells [2]. Intriguingly, RA patients responding to adalimumab treatment display 'normalized' levels of CD86 only on memory B cells, but not on na£¿ve B cells, and reduced expression of Fc¦ÃRIIB only on na£¿ve B cells, but not on memory B cells, and this was accompanied by unchanged levels of anti-CCP antibodies. Although these results are based on a relatively small group of patients, they could, if confirmed, advocate the use of Fc¦ÃRIIB expression coupled to anti-CCP responses as a predictive biomarker to monitor the early stage of disease and progression.Human Fc receptors for IgG (Fc¦ÃRI, Fc¦ÃRIIA, Fc¦ÃRIIC, Fc¦ÃRIIIA, Fc¦ÃRIIIB, Fc¦ÃRIIB) exert different functions and have diverse affinities for the Fc fragment of IgG, and these receptors are differentially expressed by a variety of cells [3]. B cells, however, exclusively express Fc¦ÃRIIB, an inhibitory receptor that binds IgG immune complexes and negatively regulates B cell receptor activation. Fc¦ÃRIIB is able to suppress or block B cell receptor activation by transmitting inhibitory signals via its cytoplasmic immunoreceptor tyrosine-based inhibitory (ITIM) motif upon simultaneous engagement with the B cell r
%U http://arthritis-research.com/content/12/4/133