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Related Collections Hematopoiesis and Stem Cells Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 September 2001, Vol. 98, No. 5, pp. 1402-1407 HEMATOPOIESIS The Notch ligand, Delta-1, inhibits the differentiation of monocytes into macrophages but permits their differentiation into dendritic cells Kohshi Ohishi, Barbara Varnum-Finney, Rita E. Serda, Claudio Anasetti, and Irwin D. Bernstein From the Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA. Notch-mediated cellular interactions are known to regulate cell fate decisions in various developmental systems. A previous report indicated that monocytes express relatively high amounts of Notch-1 and Notch-2 and that the immobilized extracellular domain of the Notch ligand, Delta-1 (Deltaext-myc), induces apoptosis in peripheral blood monocytes cultured with macrophage colony-stimulating factor (M-CSF), but not granulocyte-macrophage CSF (GM-CSF). The present study determined the effect of Notch signaling on monocyte differentiation into macrophages and dendritic cells. Results showed that immobilized Deltaext-myc inhibited differentiation of monocytes into mature macrophages (CD1a+/CD14+/ CD64+) with GM-CSF. However, Deltaext-myc permitted differentiation into immature dendritic cells (CD1a+CD14CD64) with GM-CSF and interleukin 4 (IL-4), and further differentiation into mature dendritic cells (CD1a+CD83+) with GM-CSF, IL-4, and tumor necrosis factor- (TNF-). Notch signaling affected the differentiation of CD1aCD14+ macrophage/dendritic cell precursors derived in vitro from CD34+ cells. With GM-CSF and TNF-, exposure to Deltaext-myc increased the proportion of precursors that differentiated into CD1a+CD14 dendritic cells (51% in the presence of Deltaext-myc versus 10% in control cultures), whereas a decreased proportion differentiated into CD1aCD14+ macrophages (6% versus 65%). These data indicate a role for Notch signaling in regulating cell fate decisions by bipotent macrophage/dendritic precursors. © 2001 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: Y.-C. Wang, X.-B. Hu, F. He, F. Feng, L. Wang, W. Li, P. Zhang, D. Li, Z.-S. Jia, Y.-M. Liang, et al. Lipopolysaccharide-induced Maturation of Bone Marrow-derived Dendritic Cells Is Regulated by Notch Signaling through the Up-regulation of CXCR4 J. Biol. Chem., June 5, 2009; 284(23): 15993 - 16003. [Abstract] [Full Text] [PDF] B. Zhang, R. Liu, D. Shi, X. Liu, Y. Chen, X. Dou, X. Zhu, C. 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Hatton, T. L. Russell, R. G. Ellenbogen, I. D. Bernstein, P. A. Beachy, et al. The SmoA1 Mouse Model Reveals That Notch Signaling Is Critical for the Growth and Survival of Sonic Hedgehog-Induced Medulloblastomas Cancer Res., November 1, 2004; 64(21): 7794 - 7800. [Abstract] [Full Text] [PDF] Z. Duan, F.-Q. Li, J. Wechsler, K. Meade-White, K. Williams, K. F. Benson, and M. Horwitz A Novel Notch Protein, N2N, Targeted by Neutrophil Elastase and Implicated in Hereditary Neutropenia Mol. Cell. Biol., January 1, 2004; 24(1): 58 - 70. [Abstract] [Full Text] [PDF] G. F. Hoyne Notch signaling in the immune system J. Leukoc. Biol., December 1, 2003; 74(6): 971 - 981. [Abstract] [Full Text] P. Cheng, Y. Nefedova, L. Miele, B. A. Osborne, and D. Gabrilovich Notch signaling is necessary but not sufficient for differentiation of dendritic cells Blood, December 1, 2003; 102(12): 3980 - 3988. [Abstract] [Full Text] [PDF] T. Yamada, H. Yamazaki, T. Yamane, M. Yoshino, H. Okuyama, M. Tsuneto, T. 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	Copyright © 2001 by American Society of Hematology         Online ISSN: 1528-0020