Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: B cells from rheumatoid arthritis patients show important alterations in the expression of CD86 and FcgRIIb, which are modulated by anti-tumor necrosis factor therapy. | Catalan et al. Arthritis Research Therapy 2010 12 R68 http content 12 2 R68 RESEARCH ARTICLE Open Access B cells from rheumatoid arthritis patients show important alterations in the expression of CD86 and FcgRIlb which are modulated by anti-tumor necrosis factor therapy 1 1 2 2 2 3 Diego Catalan Octavio Aravena Francisca Sabugo Pamela Wurmann Lilian Soto Alexis M Kalergis Miguel Cuchacovich2 Juan C Aguillón1 Millenium Nucleus on Immunology and Immunotherapy P-07-088-F Abstract Introduction Several molecules help preserve peripheral B cell tolerance but when altered they may predispose to autoimmunity. This work studied the expression of the costimulatory molecule CD86 and the inhibitory receptor for IgG immune complexes FcgRIIb CD32b on B cells from rheumatoid arthritis RA patients and the influence of anti-tumor necrosis factor TNF therapy. Methods 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. Results RA patients exhibited a high percentage of naive and memory B cells expressing CD86. In contrast expression of FcgRIlb 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 naive to memory cells. These alterations on FcgRIlb 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 FcyRIIb mainly on naive B cells. Conclusions Our findings show that peripheral B cells from RA patients have an altered expression of key molecules such as CD86 and FcgRIIb. Because this latter receptor is required for feedback inhibition a deficient expression might contribute to humoral autoimmune responses. Furthermore these molecules .
