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Blood, 1 November 2003, Vol. 102, No. 9, pp. 3314-3316. Prepublished online as a Blood First Edition Paper on July 10, 2003; DOI 10.1182/blood-2002-11-3521. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-11-3521v1 102/9/3314    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 Fritsche, J. Articles by Kreutz, M. Search for Related Content PubMed PubMed Citation Articles by Fritsche, J. Articles by Kreutz, M. Related Collections Immunobiology Phagocytes Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Brief report Regulation of 25-hydroxyvitamin D3-1-hydroxylase and production of 1,25-dihydroxyvitamin D3 by human dendritic cells Jana Fritsche, Krishna Mondal, Achim Ehrnsperger, Reinhard Andreesen, and Marina Kreutz From the Department of Hematology and Oncology, University of Regensburg, Germany. 25-Hydroxyvitamin D3-1-hydroxylase (25(OH)D3-1-hydroxylase), the key enzyme of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) production, is expressed in monocyte-derived macrophages (MACs). Here we show for the first time constitutive expression of 25(OH)D3-1-hydroxylase in monocyte-derived dendritic cells (DCs), which was increased after stimulation with lipopolysaccharide (LPS). Accordingly, DCs showed low constitutive production of 1,25(OH)2D3, but activation by LPS increased 1,25(OH)2D3 synthesis. In addition, 25(OH)D3-1-hydroxylase expression was found in blood DCs but not in CD34+-derived DCs. Next we analyzed the functional consequences of these results. Addition of 1,25(OH)2D3 at concentrations comparable with those produced by DCs inhibited the allostimulatory potential of DCs during the early phase of DC differentiation. However, terminal differentiation decreased the responsiveness of DCs to 1,25(OH)2D3. In conclusion, DCs are able to produce 1,25(OH)2D3 especially following stimulation with LPS. Terminal maturation renders DCs unresponsive to the effects of 1,25(OH)2D3, but those cells are able to suppress the differentiation of their own precursor cells in a paracrine way through the production of 1,25(OH)2D3. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. S. Adams, S. Ren, P. T. Liu, R. F. Chun, V. Lagishetty, A. F. Gombart, N. Borregaard, R. L. Modlin, and M. 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