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Prepublished online as a Blood First Edition Paper on August 15, 2002; DOI 10.1182/blood-2002-04-1164. This Article Full Text (PDF) All Versions of this Article: 2002-04-1164v1 101/1/143    most recent 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 Delneste, Y. Articles by Jeannin, P. Search for Related Content PubMed PubMed Citation Articles by Delneste, Y. Articles by Jeannin, P. Social Bookmarking                   What's this? Submitted April 17, 2002 Accepted August 6, 2002 Interferon- switches monocyte differentiation from dendritic cells to macrophages Yves Delneste, Peggy Charbonnier, Nathalie Herbault, Giovanni Magistrelli, Gersende Caron, Jean-Yves Bonnefoy, and Pascale Jeannin* Cellular Biology, Centre d'Immunologie Pierre Fabre, Saint Julien en Genevois, France * Corresponding author; email: pascale.jeannin{at}pierre-fabre.com. Human monocytes differentiate into dendritic cells (DC) or macrophages according to the nature of environmental signals. Monocytes stimulated with granulocyte-macrophage colony-stimulating factor (GM-CSF) plus interleukin-4 (IL-4) yield DCs. We tested here whether interferon-gamma (IFN), a potent activator of macrophages, may modulate monocyte differentiation. Addition of IFN to IL-4 plus GM-CSF-stimulated monocytes switches their differentiation from DC to CD14- CD64+ macrophages. IFNg increases M-CSF and IL-6 production by IL-4 plus GM-CSF-stimulated monocytes by acting at the transcriptional level, and acts together with IL-4 to upregulate M-CSF but not IL-6 production. IFN also increases M-CSF receptor internalization. Results from neutralizing experiments show that both M-CSF and IL-6 are involved in the ability of IFN to skew monocyte differentiation from DC to macrophages. Finally, this effect of IFN is limited to early stages of differentiation. When added to immature DC, IFN upregulates IL-6 but not M-CSF production and does not convert them to macrophages, even in the presence of exogenous M-CSF. In conclusion, IFN shifts monocyte differentiation to macrophages rather than DCs through autocrine M-CSF and IL-6 production. These data show that IFN controls the differentiation of antigen-presenting cells and thereby evidence a new mechanism by which IFN orchestrates the outcome of specific immune responses. 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