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Epstein- Barr virus infection transforms CD25+ B cells into antibody-secreting cells in rheumatoid arthritis patients.
- Source :
- Immunology; Dec2013, Vol. 140 Issue 4, p421-429, 9p
- Publication Year :
- 2013
-
Abstract
- 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<superscript>+</superscript>, n = 13) and in EBV<superscript>−</superscript> ( n = 22) patients with RA. The functional effect of EBV was studied in the sorted CD25<superscript>+</superscript> and CD25<superscript>−</superscript> peripheral B cells of RA patients ( n = 18) and healthy controls ( n = 9). Rituximab treatment results in enrichment of CD25<superscript>+</superscript> B cells in peripheral blood ( PB) of EBV<superscript>+</superscript> RA patients. The CD25<superscript>+</superscript> B-cell subset displayed a more mature phenotype accumulating IgG-expressing cells. It was also enriched with CD27<superscript>+</superscript> and CD95<superscript>+</superscript> cells in PB and BM. EBV stimulation of the sorted CD25<superscript>+</superscript> B cells in vitro induced a polyclonal IgG and IgM secretion in RA patients, while CD25<superscript>+</superscript> B cells of healthy subjects did not respond to EBV stimulation. CD25<superscript>+</superscript> 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<superscript>+</superscript> subset and by inducing their immunoglobulin production. These findings clearly link CD25<superscript>+</superscript> B cells to the EBV-dependent sequence of reactions in the pathogenesis of RA. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00192805
- Volume :
- 140
- Issue :
- 4
- Database :
- Complementary Index
- Journal :
- Immunology
- Publication Type :
- Academic Journal
- Accession number :
- 91666094
- Full Text :
- https://doi.org/10.1111/imm.12151