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 c ells for 18 hr with medium, anti-CD3 monoclonal antibody (mAb), recomb inant (r) IL-4, or phorbol mirystate acetate (PMA). After T cell deple tion by resetting, mCD23 was assessed by indirect immunofluorescence. RA PB B cells expressed mCD23 in a percentage significantly higher tha n controls unstimulated (16.7% vs. 6.6%) and after culture with anti-C D3-stimulated T cells (53% vs. 37.2%) or IL-4 (47% vs. 30%), but not a fter PMA (37.5% vs. 31%). We did not see differences in the percentage s of resting B cells between RA and controls. Our results show an intr insic RA PB B cell hyperesponsiveness to different T cell signals that might be mediated by in vivo priming through surface immunoglobulin. (C) 1994 Academic Press, Inc.