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Epstein-Barr virus infection transforms CD25(+) B cells into antibody-secreting cells in rheumatoid arthritis patients

Artikel i vetenskaplig tidskrift
Författare Mikael Brisslert
Maria Rehnberg
Maria Bokarewa
Publicerad i Immunology
Volym 140
Nummer/häfte 4
Sidor 421-429
ISSN 0019-2805
Publiceringsår 2013
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Sidor 421-429
Språk en
Länkar dx.doi.org/10.1111/imm.12151
Ämnesord anti-CD20 treatment, bone marrow, CD25(+) B cells, Epstein-Barr virus, rheumatoid arthritis, RITUXIMAB PLUS METHOTREXATE, PERIPHERAL-BLOOD, JOINT DAMAGE, FUNCTIONAL-CHARACTERIZATION, INADEQUATE RESPONSE, PREDICTS RESPONSE, CONTROLLED-TRIAL
Ämneskategorier Immunologi inom det medicinska området

Sammanfattning

Epstein-Barr virus (EBV) infection may initiate production of autoantibodies and development of cancer and autoimmune diseases. Here we outline phenotypic and functional changes in B cells of patients with rheumatoid arthritis (RA) related to EBV infection. The B-cell phenotype was analysed in blood and bone marrow (BM) of RA patients who had EBV transcripts in BM (EBV+, n=13) and in EBV- (n=22) patients with RA. The functional effect of EBV was studied in the sorted CD25(+) and CD25(-) peripheral B cells of RA patients (n=18) and healthy controls (n=9). Rituximab treatment results in enrichment of CD25(+) B cells in peripheral blood (PB) of EBV+ RA patients. The CD25(+) B-cell subset displayed a more mature phenotype accumulating IgG-expressing cells. It was also enriched with CD27(+) and CD95(+) cells in PB and BM. EBV stimulation of the sorted CD25(+) B cells in vitro induced a polyclonal IgG and IgM secretion in RA patients, while CD25(+) B cells of healthy subjects did not respond to EBV stimulation. CD25(+) B cells were enriched in PB and synovial fluid of RA patients. EBV infection affects the B-cell phenotype in RA patients by increasing the CD25(+) subset and by inducing their immunoglobulin production. These findings clearly link CD25(+) B cells to the EBV-dependent sequence of reactions in the pathogenesis of RA.

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