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Monoclonal antibody to the interferon-inducible protein Leu-13 triggers
aggregation and inhibits proliferation of leukemic B cells
SS Evans, DB Lee, T Han, TB Tomasi and RL Evans
Department of Molecular Medicine and Immunology, Roswell Park Cancer
Institute, Buffalo, NY 14263.
Interferon (IFN)-alpha inhibits DNA synthesis stimulated by low molecular
weight B-cell growth factor (BCGF) in hairy cells in vitro, suggesting that
the therapeutic efficacy of IFN-alpha in hairy cell leukemia (HCL) involves
growth inhibition of malignant B cells. Evidence that the 16-Kd cell
surface protein Leu-13 mediates an antiproliferative signal in T
lymphocytes and is IFN-inducible in endothelial cells prompted us to
examine the expression and functional role of this molecule in leukemic B
cells. Leu-13 density, determined by flow cytometry, was upregulated in
vitro and in vivo by IFN-alpha on malignant B cells from patients with HCL,
chronic lymphocytic leukemia, and prolymphocytic leukemia. Monoclonal
anti-Leu-13 triggered homotypic aggregation of leukemic B cells via an
adhesion pathway that was not inhibited by antibodies to leukocyte function
associated antigen-1 (LFA- 1) or intercellular adhesion molecule-1
(ICAM-1). Moreover, anti-Leu-13 potentiated the inhibitory effects of
IFN-alpha on BCGF-stimulated DNA synthesis, assessed by [3H]-thymidine and
[3H]-deoxyadenosine incorporation into DNA. These results indicate that
Leu-13 is part of a novel IFN-inducible signaling pathway which may modify
the growth and adhesive properties of leukemic B cells under physiologic or
therapeutic conditions.
Volume 76,
Issue 12,
pp. 2583-2593,
12/15/1990
Copyright © 1990 by The American Society of Hematology
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