%0 Journal Article
%T B cells from rheumatoid arthritis patients show important alterations in the expression of CD86 and Fc¦ÃRIIb, which are modulated by anti-tumor necrosis factor therapy
%A Diego Catal¨¢n
%A Octavio Aravena
%A Francisca Sabugo
%A Pamela Wurmann
%A Lilian Soto
%A Alexis M Kalergis
%A Miguel Cuchacovich
%A Juan C Aguill¨®n
%A Millenium Nucleus on Immunology and Immunotherapy P-07-088-F
%J Arthritis Research & Therapy
%D 2010
%I BioMed Central
%R 10.1186/ar2985
%X Peripheral B cells from 18 RA patients and 13 healthy donors were characterized using flow cytometry. Eleven patients who underwent a six-month adalimumab therapy were further assessed for phenotypic changes on their B cells.RA patients exhibited a high percentage of na£¿ve and memory B cells expressing CD86. In contrast, expression of Fc¦ÃRIIb was significantly reduced on RA memory B cells and plasmablasts as compared to healthy donors, probably due to downregulation of this receptor when differentiating from na£¿ve to memory cells. These alterations on Fc¦ÃRIIb were associated with high levels of anti-citrullinated vimentin autoantibodies. In addition, treatment with adalimumab normalized the expression of CD86 on memory B cells and reduced the expression of Fc¦ÃRIIb, mainly on na£¿ve B cells.Our findings show that peripheral B cells from RA patients have an altered expression of key molecules, such as CD86 and Fc¦ÃRIIb. Because this latter receptor is required for feedback inhibition, a deficient expression might contribute to humoral autoimmune responses. Furthermore, these molecules are likely to be influenced by inflammatory factors, since they were modulated by TNF inhibition.Rheumatoid arthritis (RA) is a chronic, inflammatory, and autoimmune disease that affects mainly synovial joints, leading to progressive destruction, pain, and disability. It is well known from mouse models that B cells play a pivotal role in the development of the autoimmune process as a precursor of antibody-secreting cells but also as antigen-presenting cells (APCs) [1,2].Immune cells express an array of receptors that bind the Fc portion of IgG-containing immune complexes (Fc¦ÃRs). Particularly, it has been stated that B cells and plasma cells express only the low-affinity receptor Fc¦ÃRIIb, which, in contrast to Fc¦ÃRIIa, has an immunoreceptor tyrosine-based inhibitory motif on the cytoplasmic domain. This characteristic confers an inhibitory function to the receptor which is essential in sev
%U http://arthritis-research.com/content/12/2/R68