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Fc gamma receptor II (CD32) on malignant B cells influences modulation
induced by anti-CD19 monoclonal antibody
SF Vervoordeldonk, PA Merle, EF van Leeuwen, CE van der Schoot, AE von dem Borne and IC Slaper-Cortenbach
Central Laboratory of the Red Cross Blood Transfusion Service, Amsterdam,
The Netherlands.
Antigenic modulation is one of many factors determining the effectiveness
of monoclonal antibody (MoAb)-mediated therapy. To select the isotype of a
CD19 MoAb most suitable for radioimmunotherapy of patients with B-cell
malignancies, we studied the influence of MoAb isotype on modulation, after
binding of the MoAb to different cell-line cells. The CD19-IgG1 MoAb was
found to induce modulation of CD19 antigens on Daudi cell line cells more
rapidly than did its IgG2a switch variant. We provide evidence that this
difference in modulation rate is caused by the expression of Fc gamma
receptor II (Fc gamma RII) on these cells. Experiments aimed at elucidating
the mechanism of Fc gamma RII involvement in modulation induction by
CD19-IgG1 showed that Fc gamma RII did not comodulate with CD19 MoAbs.
However, cocrosslinking of CD19 and Fc gamma RII with CD19-IgG1 MoAb
resulted in enhanced calcium mobilization in Daudi cells. This increased
signal induction accompanies the enhanced capping and subsequent modulation
of CD19 antigens. Because Fc gamma RII is expressed in varying densities on
malignant B cells in all differentiation stages, our results have
implications for the MoAb isotype most suitable for use in MoAb-based
therapy of patients with B-cell malignancies.
Volume 83,
Issue 6,
pp. 1632-1639,
03/15/1994
Copyright © 1994 by The American Society of Hematology
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