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Prepublished online as a Blood First Edition Paper on June 28, 2002; DOI 10.1182/blood-2002-04-1088. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-04-1088v1 101/1/305    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 Aliberti, J. Articles by Sher, A. Search for Related Content PubMed PubMed Citation Articles by Aliberti, J. Articles by Sher, A. Related Collections Immunobiology Phagocytes Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 January 2003, Vol. 101, No. 1, pp. 305-310 PHAGOCYTES Essential role for ICSBP in the in vivo development of murine CD8+ dendritic cells Julio Aliberti, Oliver Schulz, Daniel J. Pennington, Hideki Tsujimura, Caetano Reis e Sousa, Keiko Ozato, and Alan Sher From the Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), and Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Bethesda, MD; and Immunobiology and Lymphocyte Molecular Biology Laboratories, Cancer Research United Kingdom, London Research Institute, London, United Kingdom. Interferon (IFN) consensus sequence-binding protein (ICSBP) is an important transcription factor regulating proinflammatory cytokine production and the development of mononuclear phagocytes in vitro. Here we analyzed the role of ICSBP in the in vivo differentiation of 3 major subsets of murine dendritic cells (DCs). We found that ICSBP is predominantly expressed by the CD8+ subset, and more important, that ICSBP/ mice have a profound and selective deficiency in CD8+ DEC205+ DCs in lymphoid tissues. Studies using wild-type/ICSBP/ chimeras revealed that this defect in CD8+ DC development is intrinsic to bone marrow-derived progenitors and not dependent on ICSBP expression in the nonhemopoietic compartment. Because DC precursor frequencies are unaltered in the bone marrow of ICSBP/ mice, ICSBP appears to function by regulating CD8+ DC differentiation downstream from the generation of common DC progenitors. Although CD8 DCs are present in normal numbers in ICSBP/ animals, up-regulation of CD40, CD80, and major histocompatibility complex (MHC) class II expression was found to be impaired in this subset after in vivo microbial stimulation. Together these results demonstrate that ICSBP is critically required for the in vivo differentiation of CD8+ DCs and may also influence the functional maturation of the CD8 subsets. © 2003 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: T. Marafioti, J. C. Paterson, E. Ballabio, K. K. Reichard, S. Tedoldi, K. Hollowood, M. Dictor, M.-L. Hansmann, S. A. Pileri, M. J. Dyer, et al. Novel markers of normal and neoplastic human plasmacytoid dendritic cells Blood, April 1, 2008; 111(7): 3778 - 3792. [Abstract] [Full Text] [PDF] Q.-G. Steiner, L. A. Otten, M. J. Hicks, G. Kaya, F. Grosjean, E. Saeuberli, C. Lavanchy, F. Beermann, K. L. 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