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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Elbaz, O. Articles by Lowenberg, B. Search for Related Content PubMed PubMed Citation Articles by Elbaz, O. Articles by Lowenberg, B. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Tumor necrosis factor regulates the expression of granulocyte- macrophage colony-stimulating factor and interleukin-3 receptors on human acute myeloid leukemia cells O Elbaz, LM Budel, H Hoogerbrugge, IP Touw, R Delwel, LA Mahmoud and B Lowenberg Dr Daniel den Hoed Cancer Center, Rotterdam, The Netherlands. Tumor necrosis factor (TNF) acts as a potent enhancer of granulocyte- macrophage colony-stimulating factor (GM-CSF)- and interleukin-3 (IL-3)- induced human acute myeloid leukemia (AML) growth in vitro. We have analyzed the effects of TNF alpha on the expression of GM-CSF and IL-3 receptors on AML cells. Incubation of blasts from seven patients with AML in serum-free medium with TNF (10(3) U/mL) and subsequent binding studies using 125I-GM-CSF and 125I-IL-3 show that TNF increases the specific binding of GM-CSF (30% to 280%) and IL-3 (40% to 600%) in all cases. From Scatchard plot analysis it appears that TNF upregulates (1) low-affinity GM-CSF binding sites, (2) common high-affinity IL-3/GM-CSF binding sites, and (3) unique (non-GM-CSF binding) IL-3 binding sites. The effect of TNF is dose dependent and is half maximal at a concentration of 100 U/mL, and becomes evident at 18 hours of incubation with TNF at 37 degrees C, but not at 0 degree C. The GM-CSF dose-response curve of AML-colony-forming units plateaus at a higher level in the presence of TNF, which indicates that additional numbers of cells become responsive to GM-CSF. Incubation of AML blasts with the phorbol ester 12-0-tetradecanoylphorbol-13-acetate or formyl-Met-Leu- Phe (protein kinase C activators) does not influence GM-CSF receptor expression, suggesting that receptor upregulation by TNF is not mediated through activation of protein kinase C. On the other hand, the protein synthesis inhibitor cycloheximide abrogates receptor upregulation induced by TNF. In contrast to these findings in AML, TNF does not upregulate GM-CSF receptor numbers on blood granulocytes or monocytes. We conclude that TNF exerts positive effects on growth factor receptor expression of hematopoietic cells. Volume 77, Issue 5, pp. 989-995, 03/01/1991 Copyright © 1991 by The American Society of Hematology CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. A. Evans, A. Pierce, S. A. Winter, E. Spooncer, C. M. Heyworth, and A. D. Whetton Activation of Granulocyte-Macrophage Colony-Stimulating Factor and Interleukin-3 Receptor Subunits in a Multipotential Hematopoietic Progenitor Cell Line Leads to Differential Effects on Development Blood, September 1, 1999; 94(5): 1504 - 1514. [Abstract] [Full Text] [PDF] K. Tarte, Z. Y. Lu, G. Fiol, E. Legouffe, J.-F. Rossi, and B. Klein Generation of Virtually Pure and Potentially Proliferating Dendritic Cells From Non-CD34 Apheresis Cells From Patients With Multiple Myeloma Blood, November 1, 1997; 90(9): 3482 - 3495. [Abstract] [Full Text] [PDF] B. Lowenberg, W. van Putten, I. P. Touw, R. Delwel, and V. Santini Autonomous Proliferation of Leukemic Cells in Vitro as a Determinant of Prognosis in Adult Acute Myeloid Leukemia N. Engl. J. Med., March 4, 1993; 328(9): 614 - 619. [Abstract] [Full Text]

	Copyright © 1991 by American Society of Hematology         Online ISSN: 1528-0020