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Blood, 15 February 2006, Vol. 107, No. 4, pp. 1445-1453. Prepublished online as a Blood First Edition Paper on October 13, 2005; DOI 10.1182/blood-2005-04-1721. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-04-1721v1 107/4/1445    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 Heinz, L. X. Articles by Strobl, H. Search for Related Content PubMed PubMed Citation Articles by Heinz, L. X. Articles by Strobl, H. Related Collections Hematopoiesis and Stem Cells Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Differential involvement of PU.1 and Id2 downstream of TGF-1 during Langerhans-cell commitment Leonhard X. Heinz, Barbara Platzer, Peter M. Reisner, Almut Jörgl, Sabine Taschner, Florian Göbel, and Herbert Strobl From the Institute of Immunology, Medical University Vienna, Austria. Langerhans cells (LCs) are highly abundant dendritic cells (DCs) in epidermal and mucosal tissues. The transcription factors PU.1 and Id2 have been implicated as positive regulators of LC development from hematopoietic progenitor cells. LC differentiation from progenitors is absolutely dependent on transforming growth factor beta 1 (TGF-1) in vitro as well as in vivo; however, downstream mechanisms are poorly defined. We found that both PU.1 and Id2 are induced by TGF-1 in human CD34+ monocyte/LC (M/LC) progenitor cells, and that neither ectopic PU.1 or Id2 alone, nor both together, could replace TGF-1 in its instructive function on LC commitment. However, both factors critically contributed to LC differentiation by acting at 2 distinct intersection points. Ectopic PU.1 strongly enhanced TGF-1-dependent LC development. Additionally, Notch-induced generation of interstitial-type DCs was associated with PU.1 up-regulation. Thus, PU.1 is generally increased during myeloid DC development. Ectopic Id2 inhibits the acquisition of early monocytic characteristics by cells generated in the absence of TGF-1 and also inhibits monocyte induction by alternative stimuli. Since TGF-1 represses a default monocyte pathway of common progenitor cells, PU.1 and Id2 seem to modulate lineage options of M/LC precursors, downstream of TGF-1. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: F. Gobel, S. Taschner, J. Jurkin, S. Konradi, C. Vaculik, S. Richter, D. Kneidinger, C. Muhlbacher, C. Bieglmayer, A. Elbe-Burger, et al. Reciprocal role of GATA-1 and vitamin D receptor in human myeloid dendritic cell differentiation Blood, October 29, 2009; 114(18): 3813 - 3821. [Abstract] [Full Text] [PDF] B. Platzer, S. Richter, D. Kneidinger, D. Waltenberger, M. Woisetschlager, and H. Strobl Aryl Hydrocarbon Receptor Activation Inhibits In Vitro Differentiation of Human Monocytes and Langerhans Dendritic Cells J. Immunol., July 1, 2009; 183(1): 66 - 74. [Abstract] [Full Text] [PDF] G. Li, S. Abediankenari, Y.-J. Kim, T. B. Campbell, S. Ito, B. Graham-Evans, S. Cooper, and H. E. Broxmeyer TGF-{beta} combined with M-CSF and IL-4 induces generation of immune inhibitory cord blood dendritic cells capable of enhancing cytokine-induced ex vivo expansion of myeloid progenitors Blood, October 15, 2007; 110(8): 2872 - 2879. [Abstract] [Full Text] [PDF] S. Taschner, C. Koesters, B. Platzer, A. Jorgl, W. Ellmeier, T. Benesch, and H. Strobl Down-regulation of RXR{alpha} expression is essential for neutrophil development from granulocyte/monocyte progenitors Blood, February 1, 2007; 109(3): 971 - 979. [Abstract] [Full Text] [PDF]

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