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
Author
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Catalán Martina, Diego
Author
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Aravena, Octavio
Author
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Sabugo, Francisca
Author
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Wurmann, Pamela
Author
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Soto, Lilian
Author
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Kalergis, Alexis M.
Author
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Cuchacovich Turteltaub, Miguel
Author
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Aguillón Gutiérrez, Juan Carlos
Admission date
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2019-03-11T12:59:19Z
Available date
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2019-03-11T12:59:19Z
Publication date
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2010
Cita de ítem
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Arthritis Research and Therapy, Volumen 12, Issue 2, 2018,
Identifier
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14786354
Identifier
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14786362
Identifier
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10.1186/ar2985
Identifier
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https://repositorio.uchile.cl/handle/2250/164974
Abstract
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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
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