CD23 hyperexpression in rheumatoid arthritis: evidence for a B cell hyperresponsiveness to cognate and noncognate T-cell signals.
We have studied the causes of membrane CD23 (mCD23) hyperexpression in rheumatoid arthritis (RA). Modifying a previously developed in vitro system, we cultured RA and control peripheral blood (PB) mononuclear cells for 18 hr with medium, anti-CD3 monoclonal antibody (mAb), recombinant (r) IL-4, or phorbol myristate acetate (PMA). After T cell depletion by rosetting, mCD23 was assessed by indirect immunofluorescence. RA PB B cells expressed mCD23 in a percentage significantly higher than controls unstimulated (16.7% vs. 6.6%) and after culture with anti-CD3-stimulated T cells (53% vs. 37.2%) or IL-4 (47% vs. 30%), but not after PMA (37.5% vs. 31%). We did not see differences in the percentages of resting B cells between RA and controls. Our results show an intrinsic RA PB B cell hyperesponsiveness to different T cell signals that might be mediated by in vivo priming through surface immunoglobulin.
Fernández-Gutiérrez
B
B
Rheumatology Service, Hospital Universitario San Carlos, Madrid, Spain.
Hernández-García
C
C
Bañares
A A
AA
Jover
J A
JA
D001172:Arthritis, Rheumatoid / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology*; D002450:Cell Communication / Q000276:immunology*; D002478:Cells, Cultured; D006801:Humans; D008213:Lymphocyte Activation / Q000276:immunology; D008211:Lymphocyte Cooperation; D011493:Protein Kinase C / Q000502:physiology; D017455:Receptors, IgE / Q000096:biosynthesis*; D015398:Signal Transduction / Q000276:immunology; D013582:Synovial Fluid / Q000166:cytology; D013601:T-Lymphocytes / Q000276:immunology*; D015854:Up-Regulation / Q000276:immunology
D017455:Receptors, IgE; D011493:Protein Kinase C