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Blood, 15 May 2004, Vol. 103, No. 10, pp. 3813-3820. Prepublished online as a Blood First Edition Paper on January 15, 2004; DOI 10.1182/blood-2003-09-3046. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-09-3046v1 103/10/3813    most recent 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 Castellano, G. Articles by van Kooten, C. Search for Related Content PubMed PubMed Citation Articles by Castellano, G. Articles by van Kooten, C. Related Collections Immunobiology Phagocytes Cell Adhesion and Motility Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Maturation of dendritic cells abrogates C1q production in vivo and in vitro Giuseppe Castellano, Andrea M. Woltman, Alma J. Nauta, Anja Roos, Leendert A. Trouw, Marc A. Seelen, Francesco Paolo Schena, Mohamed R. Daha, and Cees van Kooten From the Department of Nephrology, Leiden University Medical Center, Leiden, the Netherlands; and the Division of Nephrology, Department of Emergency and Organ Transplantation, Policlinico, University of Bari, Italy. Dendritic cells (DCs) and complement are essential components of the innate immune system. Immature DCs (immDCs) and mature DCs (mDCs) can migrate to lymphoid areas inducing, respectively, tolerance and immune responses. Primary deficiency of complement component C1q (C1q) leads to autoimmunity, suggesting a role in the maintenance of tolerance. In the present study, we investigated the production of C1q by immDCs, mDCs, and macrophages. We demonstrated that monocyte-derived and CD34+-derived interstitial DCs are a rich source of C1q. C1q produced by immDCs is functionally active in complement activation and binding to apoptotic cells. The production of C1q is completely down-regulated upon DC maturation in vitro. Moreover, we found that DC differentiation in the presence of interferon- (IFN-) accelerated DC maturation and strongly impaired overall C1q production. Finally, we demonstrated the presence, in significant numbers, of DC-SIGN+/C1q+ cells in T-cell areas of tonsils, next to DC-LAMP+ mDCs lacking C1q. We conclude from these results that immDC, a cell with tolerogenic properties, is a rich source of active C1q in vitro and in vivo, which is down-regulated on maturation. Therefore, immDCs may be considered an additional source of C1q in humans. 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Camps, T. W. J. Huizinga, C. van Kooten, M. R. Daha, J. S. Verbeek, F. Ossendorp, et al. A Novel Role of Complement Factor C1q in Augmenting the Presentation of Antigen Captured in Immune Complexes to CD8+ T Lymphocytes J. Immunol., June 15, 2007; 178(12): 7581 - 7586. [Abstract] [Full Text] [PDF] P. Baruah, I. E. Dumitriu, G. Peri, V. Russo, A. Mantovani, A. A. Manfredi, and P. Rovere-Querini The tissue pentraxin PTX3 limits C1q-mediated complement activation and phagocytosis of apoptotic cells by dendritic cells J. Leukoc. Biol., July 1, 2006; 80(1): 87 - 95. [Abstract] [Full Text] [PDF] S. Rutella, G. Bonanno, A. Procoli, A. Mariotti, D. G. de Ritis, A. Curti, S. Danese, G. Pessina, S. Pandolfi, F. Natoni, et al. Hepatocyte growth factor favors monocyte differentiation into regulatory interleukin (IL)-10++IL-12low/neg accessory cells with dendritic-cell features Blood, July 1, 2006; 108(1): 218 - 227. [Abstract] [Full Text] [PDF]

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