R. Rezonzew et Mm. Newkirk, IMPAIRED RELEASE OF SCD23 BY ACTIVATED B-CELLS FROM RA PATIENTS, Clinical immunology and immunopathology, 71(2), 1994, pp. 156-163
To determine the basis of a differential response among B-cells derive
d from rheumatoid arthritis (RA) patients and their normal counterpart
to anti-CD3-activated T-cells (HUT-78 CD4(+)), B-cell responsiveness
was measured in vitro with a focus on IgG and IgM secretion, the abili
ty to differentiate into plasma cells, and the release of soluble CD23
(sCD23) into the culture media. In the patients with RA, plasma sCD23
levels were measured and studied to see if it related to the rheumato
id factor (RF) titer, age, sera immunoglobulin, therapy, and disease a
ctivity. Patients with RA were found to have a significantly increased
level of sCD23 in the plasma when compared to control individuals, ye
t their peripheral blood B-cells were unable to secrete normal levels
of sCD23 following in vitro stimulation by T-cells. The plasma level o
f sCD23 found in the RA patients correlated (P < 0.0001) with the RF t
iter. B-cells from the RA patients secreted significantly increased am
ounts of IgG and IgM after in vitro stimulation by T-cells. It appears
that peripheral blood B-cells of RA patients are more activated initi
ally and it is likely that at the time of coculture with T-cells they
had already passed through the narrow window in cell maturation when s
CD23 is released. (C) 1994 Academic Press, Inc.