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.