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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 Vellenga, E. Articles by Halie, M. R. Search for Related Content PubMed PubMed Citation Articles by Vellenga, E. Articles by Halie, M. R. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Divergent effects of interleukin-4 (IL-4) on the granulocyte colony- stimulating factor and IL-3-supported myeloid colony formation from normal and leukemic bone marrow cells E Vellenga, JT de Wolf, JA Beentjes, MT Esselink, JW Smit and MR Halie Department of Medicine, University of Groningen, The Netherlands. Human recombinant interleukin-4 (IL-4) was studied for its effects on myeloid progenitor cells from normal and leukemic bone marrow cells in the presence and absence of additional growth factors. IL-4 itself did not support myeloid cluster or colony formation (CFU-GM). However, cultures supplied with IL-4 (300 U/mL) and IL-3 demonstrated a significant decline in myeloid colony numbers (CFU-GM) compared with the effects of IL-3 alone: (48 +/- 27 v 88 +/- 27 CFU-GM/10(5) MNC). In contrast, IL-4 augmented the G-CSF-supported CFU-GM: (80 +/- 31 v 148 +/- 52 CFU-GM/10(5) MNC). The effects of IL-4 were not mediated by accessory cells because similar results were obtained with and without T-cell, B-cell, or adherent depleted cell fractions. Morphologic analysis of clusters (day 7) and the colonies (day 14) demonstrated that IL-4 enhanced myeloid colony formation in the presence of G-CSF, whereas the cultures supplied with IL-3 and IL-4 did not show a lineage- restricted decline of CFU-GM. A heterogeneity in growth response was observed in the leukemic counterpart. With the 3H-thymidine proliferation assay, IL-4 augmented the G-CSF-induced proliferation of acute myeloid leukemic (AML) cells in 4 of the 12 cases, while the IL-3- supported proliferation was antagonized in 3 of the 12 cases. In the blast colony assay, IL-4 suppressed the IL-3-supported AML-CFU in the majority of cases, but enhanced the G-CSF stimulated AML-CFU in 3 of 6 cases. These data demonstrate divergent effects of IL-4 on the normal myeloid progenitor cell in the presence of IL-3 or G-CSF, while a variability in responsiveness is observed in the leukemic counterpart. Volume 75, Issue 3, pp. 633-637, 02/01/1990 Copyright © 1990 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: G. F.J.D. Benus, A. T.J. Wierenga, D. J.J. de Gorter, J. J. Schuringa, A. M. van Bennekum, L. Drenth-Diephuis, E. Vellenga, and B. J.L. Eggen Inhibition of the Transforming Growth Factor {beta} (TGF{beta}) Pathway by Interleukin-1{beta} Is Mediated through TGF{beta}-activated Kinase 1 Phosphorylation of SMAD3 Mol. Biol. Cell, August 1, 2005; 16(8): 3501 - 3510. [Abstract] [Full Text] [PDF] C. P. Schröder, B.-J. Kroesen, L. F. M. H. de Leij, and E. G. E. de Vries Purging of Epithelial Tumor Cells from Peripheral Blood Stem Cells by Means of the Bispecific Antibody BIS-1 Clin. Cancer Res., June 1, 2000; 6(6): 2521 - 2527. [Abstract] [Full Text]

	Copyright © 1990 by American Society of Hematology         Online ISSN: 1528-0020