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* Institute of Experimental Dermatology and Department of Dermatology, University of Münster, Münster, Germany;
Department of Dermatology and Allergology, University of Ulm, Ulm, Germany;
Department of Immunology, Erasmus MC, Rotterdam, The Netherlands;
Section of Infectious Diseases, Oklahoma University Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City, OK 73014; and
¶
Department of Molecular Cell Biology, Free University Medical Center, Amsterdam, The Netherlands
Blood monocytes are well-characterized precursors for macrophages and dendritic cells. Subsets of human monocytes with differential representation in various disease states are well known. In contrast, mouse monocyte subsets have been characterized minimally. In this study we identify three subpopulations of mouse monocytes that can be distinguished by differential expression of Ly-6C, CD43, CD11c, MBR, and CD62L. The subsets share the characteristics of extensive phagocytosis, similar expression of M-CSF receptor (CD115), and development into macrophages upon M-CSF stimulation. By eliminating blood monocytes with dichloromethylene-bisphosphonate-loaded liposomes and monitoring their repopulation, we showed a developmental relationship between the subsets. Monocytes were maximally depleted 18 h after liposome application and subsequently reappeared in the circulation. These cells were exclusively of the Ly-6Chigh subset, resembling bone marrow monocytes. Serial flow cytometric analyses of newly released Ly-6Chigh monocytes showed that Ly-6C expression on these cells was down-regulated while in circulation. Under inflammatory conditions elicited either by acute infection with Listeria monocytogenes or chronic infection with Leishmania major, there was a significant increase in immature Ly-6Chigh monocytes, resembling the inflammatory left shift of granulocytes. In addition, acute peritoneal inflammation recruited preferentially Ly-6Cmed-high monocytes. Taken together, these data identify distinct subpopulations of mouse blood monocytes that differ in maturation stage and capacity to become recruited to inflammatory sites.
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M. G. Frid, J. A. Brunetti, D. L. Burke, T. C. Carpenter, N. J. Davie, J. T. Reeves, M. T. Roedersheimer, N. van Rooijen, and K. R. Stenmark Hypoxia-Induced Pulmonary Vascular Remodeling Requires Recruitment of Circulating Mesenchymal Precursors of a Monocyte/Macrophage Lineage Am. J. Pathol., February 1, 2006; 168(2): 659 - 669. [Abstract] [Full Text] [PDF] |
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D. K. Fogg, C. Sibon, C. Miled, S. Jung, P. Aucouturier, D. R. Littman, A. Cumano, and F. Geissmann A Clonogenic Bone Marrow Progenitor Specific for Macrophages and Dendritic Cells Science, January 6, 2006; 311(5757): 83 - 87. [Abstract] [Full Text] [PDF] |
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H. Xu, A. Manivannan, R. Dawson, I. J. Crane, M. Mack, P. Sharp, and J. Liversidge Differentiation to the CCR2+ Inflammatory Phenotype In Vivo Is a Constitutive, Time-Limited Property of Blood Monocytes and Is Independent of Local Inflammatory Mediators J. Immunol., November 15, 2005; 175(10): 6915 - 6923. [Abstract] [Full Text] [PDF] |
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S. B. Geutskens, T. Otonkoski, M-A. Pulkkinen, H. A. Drexhage, and P. J. M. Leenen Macrophages in the murine pancreas and their involvement in fetal endocrine development in vitro J. Leukoc. Biol., October 1, 2005; 78(4): 845 - 852. [Abstract] [Full Text] [PDF] |
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T. Nikolic, G. Bouma, H. A. Drexhage, and P. J. M. Leenen Diabetes-prone NOD mice show an expanded subpopulation of mature circulating monocytes, which preferentially develop into macrophage-like cells in vitro J. Leukoc. Biol., July 1, 2005; 78(1): 70 - 79. [Abstract] [Full Text] [PDF] |
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C. Qu, E. W. Edwards, F. Tacke, V. Angeli, J. Llodra, G. Sanchez-Schmitz, A. Garin, N. S. Haque, W. Peters, N. van Rooijen, et al. Role of CCR8 and Other Chemokine Pathways in the Migration of Monocyte-derived Dendritic Cells to Lymph Nodes J. Exp. Med., November 15, 2004; 200(10): 1231 - 1241. [Abstract] [Full Text] [PDF] |
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