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[Cancer Research 50, 4111-4120, July 1, 1990]
© 1990 American Association for Cancer Research

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B-Cell Growth Factor-induced and {alpha}-Interferon-inhibited Proliferation of Hairy Cells Coincides with Modulation of Cell Surface Antigens1

Haim Gamliel2, Bernard H. Brownstein, Dorit Gurfel, Shi-Hua Wu, Michael C. Rosner and Harvey M. Golomb

Joint Hematology/Oncology Section, Department of Medicine, University of Chicago Medical Center and Michael Reese Medical Center, Chicago, Illinois 60637 [H. G., D. G., M. C. R., H. M. G.]; Center for Genetics in Medicine, Washington University School of Medicine, St. Louis, Missouri 63110 [B. H. B.]; and Hematology Section, Department of Medicine, Second Teaching Hospital, Xi'an Medical University, Xi'an, Shaanxi, The People's Republic of China [S.-H. W.]

{alpha}-Interferon (IFN-{alpha}) induced unique ultrastructural alterations in peripheral blood and splenic hairy cell leukemia (HCL) cells (14 of 20 cases) treated in vitro. To further investigate the effects of B-cell growth factor (BCGF) and IFN-{alpha} on target hairy cells (HCs), we utilized immunogold labeling in conjunction with scanning electron microscopy. This methodology, in contrast to other immunological methods, facilitated direct view of the expression, density, and rearrangement of selected antigens/receptors on individual cells before and after BCGF or IFN-{alpha} treatment. In addition to inducing proliferation of HCL cells, BCGF enhanced the expression of interleukin 2 receptors (CD25; T-activated cell antigen) with no change in the expression of class I and class II human leukocyte antigen. On the other hand, IFN-{alpha} did not exert a noticeable proliferative effect on HCL cells but rather inhibited the proliferation of BCGF-treated cells. In addition, IFN-{alpha} treatment revealed an enhanced expression of class I (4 of 9) and class II (12 of 15) human leukocyte antigen on target HCs. Two-day exposure of HCs to IFN-{alpha} resulted in enhanced expression of CD25 (11 of 14), whereas a decrease in CD25 expression was recorded in 4 of 5 cases treated with IFN-{alpha} for 3 days. Also, no significant change in the expression of two other HCL-related surface antigens, CD22 (S-HCL-1; Leu-14) and CD11c (S-HCL-3; Leu-M5), was recorded following up to 3 days of IFN-{alpha} or BCGF treatment. However, a 5-day exposure to IFN-{alpha} resulted in a significant decrease in expression of CD11c on treated HCs. Finally, the IFN-{alpha}-induced immunoultrastructural changes in target HCs were primarily encountered in cells from HCL cases classified as responders to in vivo IFN-{alpha} therapy. Our data add support to the concept that the effect of IFN-{alpha} in HCL is mediated by impairment of the response to B-cell growth factors and induction of further differentiation of the target cells.

1 This investigation was supported in part by The Hematologic Research Foundation and by the Hairy Cell Leukemia Research Foundation.

2 To whom requests for reprints should be addressed, at Joint Hematology/Oncology Section, Department of Medicine, University of Chicago Medical Center, 5841 S. Maryland Ave., Box 420, Chicago, IL 60637.

Received 4/20/89. Revised 1/25/90.


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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
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Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
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Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1990 by the American Association for Cancer Research.