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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 Menetrier-Caux, C. Articles by Blay, J.Y. Search for Related Content PubMed PubMed Citation Articles by Menetrier-Caux, C. Articles by Blay, J.Y. Related Collections Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, Vol. 92 No. 12 (December 15), 1998: pp. 4778-4791 Inhibition of the Differentiation of Dendritic Cells From CD34+ Progenitors by Tumor Cells: Role of Interleukin-6 and Macrophage Colony-Stimulating Factor C. Menetrier-Caux, G. Montmain, M.C. Dieu, C. Bain, M.C. Favrot, C. Caux, and J.Y. Blay From Unité Cytokine et Cancer, Unité INSERM 453, Centre Léon Bérard, Lyon, France; and Schering Plough, Dardilly, France. The escape of malignant cells from the immune response against the tumor may result from a defective differentiation or function of professional antigen-presenting cells (APC), ie, dendritic cells (DC). To test this hypothesis, the effect of human renal cell carcinoma cell lines (RCC) on the development of DC from CD34+ progenitors was investigated in vitro. RCC cell lines were found to release soluble factors that inhibit the differentiation of CD34+ cells into DC and trigger their commitment towards monocytic cells (CD14+CD64+CD1aCD86CD80HLA-DRlow) with a potent phagocytic capacity but lacking APC function. RCC CM were found to act on the two distinct subpopulations emerging in the culture at day 6 ([CD14+CD1a] and [CD14CD1a+]) by inhibiting the differentiation into DC of [CD14+CD1a] precursors and blocking the acquisition of APC function of the [CD14CD1a+] derived DC. Interleukin-6 (IL-6) and macrophage colony-stimulating factor (M-CSF) were found to be responsible for this phenomenon: antibodies against IL-6 and M-CSF abrogated the inhibitory effects of RCC CM; and recombinant IL-6 and/or M-CSF inhibited the differentiation of DC similarly to RCC CM. The inhibition of DC differentiation by RCC CM was preceeded by an induction of M-CSF receptor (M-CSFR; CD115) and a loss of granulocyte-macrophage colony-stimulating factor receptor (GM-CSFR; CD116) expression at the surface of CD34+ cells, two phenomenon reversed by anti-IL-6/IL-6R and anti-M-CSF antibodies, respectively. Finally, a panel of tumor cell lines producing IL-6 and M-CSF induced similar effects. Taken together, the results suggest that the inhibition of DC development could represent a frequent mechanism by which tumor cells will escape immune recognition. 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. Shinriki, H. Jono, K. Ota, M. Ueda, M. Kudo, T. Ota, Y. Oike, M. Endo, M. Ibusuki, A. Hiraki, et al. Humanized Anti-Interleukin-6 Receptor Antibody Suppresses Tumor Angiogenesis and In vivo Growth of Human Oral Squamous Cell Carcinoma Clin. Cancer Res., September 1, 2009; 15(17): 5426 - 5434. [Abstract] [Full Text] [PDF] M. Gobert, I. 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