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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Miyamoto, T. Articles by Suda, T. Search for Related Content PubMed PubMed Citation Articles by Miyamoto, T. Articles by Suda, T. Related Collections Hematopoiesis and Stem Cells Phagocytes Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 October 2001, Vol. 98, No. 8, pp. 2544-2554 PHAGOCYTES Bifurcation of osteoclasts and dendritic cells from common progenitors Takeshi Miyamoto, Osamu Ohneda, Fumio Arai, Katsuya Iwamoto, Seiji Okada, Katsumasa Takagi, Dirk M. Anderson, and Toshio Suda From the Department of Cell Differentiation, Institute of Molecular Embryology and Genetics, and Department of Orthopedic Surgery, Kumamoto University School of Medicine, Honjo, Japan; Department of Developmental Genetics, Chiba University Graduate School of Medicine, Japan; and Department of Molecular Biology, Immunex Corporation, Seattle, WA. Osteoclasts and dendritic cells are derived from monocyte/macrophage precursor cells; however, how their lineage commitment is regulated is unknown. This study investigated the differentiation pathways of osteoclasts and dendritic cells from common precursor cells at the single-cell level. Osteoclastogenesis induced by macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-B ligand (RANKL) or tumor necrosis factor- (TNF-) is completely inhibited by addition of granulocyte-macrophage colony-stimulating factor (GM-CSF) or interleukin-3 at early stages of differentiation. GM-CSF-treated cells express both c-Fms and RANK and also low levels of CD11c and DEC205, which are detected on dendritic cells. Addition of GM-CSF also reduces expression of both c-Fos and Fra-1, which is an important event for inhibition of osteoclastogenesis. Overexpression of c-Fos by retroviral infection or induction in transgenic mice can rescue a failure in osteoclast differentiation even in the presence of GM-CSF. By contrast, differentiation into dendritic cells is inhibited by M-CSF, indicating that M-CSF and GM-CSF reciprocally regulate the differentiation of both lineages. Dendritic cell maturation is also inhibited when c-Fos is expressed at an early stage of differentiation. Taken together, these findings suggest that c-Fos is a key mediator of the lineage commitment between osteoclasts and dendritic cells. The lineage determination of osteoclast progenitors seen following GM-CSF treatment functions through the regulation of c-Fos expression. © 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: M. Hiasa, M. Abe, A. Nakano, A. Oda, H. Amou, S. Kido, K. Takeuchi, K. Kagawa, K. Yata, T. Hashimoto, et al. GM-CSF and IL-4 induce dendritic cell differentiation and disrupt osteoclastogenesis through M-CSF receptor shedding by up-regulation of TNF-{alpha} converting enzyme (TACE) Blood, November 12, 2009; 114(20): 4517 - 4526. [Abstract] [Full Text] [PDF] S. Apostolakis, G. Y.H. Lip, and E. Shantsila Monocytes in heart failure: relationship to a deteriorating immune overreaction or a desperate attempt for tissue repair? Cardiovasc Res, October 28, 2009; (2009) cvp327v2. [Abstract] [Full Text] [PDF] M. S. Lee, H. S. Kim, J.-T. Yeon, S.-W. Choi, C. H. Chun, H. B. 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