Artículos de revistas
B cells from rheumatoid arthritis patients show important alterations in the expression of CD86 and FcγRIIb, which are modulated by anti-tumor necrosis factor therapy
Fecha
2010Registro en:
Arthritis Research and Therapy, Volumen 12, Issue 2, 2018,
14786354
14786362
10.1186/ar2985
Autor
Catalán Martina, Diego
Aravena, Octavio
Sabugo, Francisca
Wurmann, Pamela
Soto, Lilian
Kalergis, Alexis M.
Cuchacovich Turteltaub, Miguel
Aguillón Gutiérrez, Juan Carlos
Institución
Resumen
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 FcγRIIb (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 naïve and memory B cells expressing CD86. In contrast, expression of FcγRIIb 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 naïve to memory cells. These alterations on FcγRIIb were associated with high levels o