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Prepublished online as a Blood First Edition Paper on July 10, 2003; DOI 10.1182/blood-2002-11-3521.
Submitted November 19, 2002
Accepted June 30, 2003
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*
Department of Hematology and Oncology, University of Regensburg, Regensburg, Germany
* Corresponding author; email: marina.kreutz{at}klinik.uni-regensburg.de.
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 (MAC). Here we show for the first time constitutive expression of 25(OH)2D3-1-hydroxylase in monocyte-derived dendritic cells (DC) which was increased after stimulation with LPS. Accordingly, DC 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 was found in blood-DC, but not in CD34+-derived DC. Next we analyzed the functional consequences of these results. Addition of 1,25(OH)2D3 at concentrations comparable to those produced by DC inhibited the allo-stimulatory potential of DC during the early phase of DC differentiation. However, terminal differentiation decreased the responsiveness of DC to 1,25(OH)2D3. In conclusion, DC are able to produce 1,25(OH)2D3 especially following stimulation with LPS. Terminal maturation renders DC unresponsive to the effects of 1,25(OH)2D3 but those cells are capable to suppress the differentiation of their own precursor cells in a paracrine way through the production of 1,25(OH)2D3.
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