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Prepublished online as a Blood First Edition Paper on September 5, 2002; DOI 10.1182/blood-2002-05-1327. This Article Full Text (PDF) All Versions of this Article: 2002-05-1327v1 101/3/961    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 Tsujimura, H. Articles by Ozato, K. Search for Related Content PubMed PubMed Citation Articles by Tsujimura, H. Articles by Ozato, K. Social Bookmarking                   What's this? Submitted May 6, 2002 Accepted August 26, 2002 ICSBP/IRF-8 retrovirus transduction rescues dendritic cell development in vitro Hideki Tsujimura, Tomohiko Tamura, Celine Gongora, Julio Aliberti, Caetano Reis e Sousa, Alan Sher, and Keiko Ozato* Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA Laboratory of Parasite Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA Immunobiology Laboratory, Cancer Research UK, London Research Institute, London, United Kingdom * Corresponding author; email: ozatok{at}nih.gov. Dendritic cells (DCs) develop from bone marrow (BM) progenitor cells and mature in response to external signals to elicit functions important for innate and adaptive immunity. ICSBP/IRF-8 is a hematopoietic cell-specific transcription factor expressed in BM progenitor cells that contributes to myeloid cell development. In light of our earlier observation that ICSBP-/- mice lack CD8+ DCs, we investigated the role of ICSBP in DC development in vitro in the presence of Flt3 ligand. Immature ICSBP-/- DCs developed from BM progenitor cells showed assorted were defects, and did not mature in response to activation signals, and failed to express CD8 and IL-12 p40, a feature consistent with ICSBP-/- DCs in vivo. We show that retroviral introduction of ICSBP restores the development of immature DC that can fully mature upon activation signals. All the defects seen with -/- DCs were corrected after ICSBP transduction, including the expression of CD8 and IL-12 p40 as well as MHC class II and other costimulatory molecules. ICSBP is known to regulate gene expression by interacting with partner proteins PU.1 and IRFs, thereby binding to target elements ISRE and EICE. Analysis of a series of ICSBP mutants showed that the intact DNA binding activity as well as the ability to interact with partner proteins are required for the restoration of DC development/maturation, pointing to ICSBP's transcriptional function as a basis of restoration. Taken together, this study identifies ICSBP as a factor critical for both early differentiation and final maturation of DCs. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. K. Middleton, A. M. Zukas, T. Rubinstein, M. Kinder, E. H. Wilson, P. Zhu, I. A. Blair, C. A. Hunter, and E. Pure 12/15-Lipoxygenase-Dependent Myeloid Production of Interleukin-12 Is Essential for Resistance to Chronic Toxoplasmosis Infect. Immun., December 1, 2009; 77(12): 5690 - 5700. [Abstract] [Full Text] [PDF] U. Martin, J. Scholler, J. Gurgel, B. Renshaw, J. E. Sims, and C. A. 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