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Blood, 15 May 2007, Vol. 109, No. 10, pp. 4288-4295. Prepublished online as a Blood First Edition Paper on January 25, 2007; DOI 10.1182/blood-2006-08-043422. This Article Full Text Full Text (PDF) Supplemental Figure All Versions of this Article: blood-2006-08-043422v1 109/10/4288    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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Geyeregger, R. Articles by Stulnig, T. M. Search for Related Content PubMed PubMed Citation Articles by Geyeregger, R. Articles by Stulnig, T. M. Related Collections Immunobiology Cytoskeleton Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Liver X receptors regulate dendritic cell phenotype and function through blocked induction of the actin-bundling protein fascin René Geyeregger1, Maximilian Zeyda1, Wolfgang Bauer2,3, Ernst Kriehuber2,3, Marcus D. Säemann4, Gerhard J. Zlabinger5, Dieter Maurer2,3, and Thomas M. Stulnig1 1 Department of Internal Medicine III, Clinical Division of Endocrinology and Metabolism, Medical University of Vienna, Austria; 2 Division of Immunology, Allergy and Infectious Diseases, Department of Dermatology, Medical University of Vienna, Austria; 3 Center of Molecular Medicine (CeMM) of the Austrian Academy of Sciences, Vienna, Austria; 4 Department of Internal Medicine III, Nephrology and Dialysis, Medical University of Vienna, Austria; 5 Institute of Immunology, Medical University of Vienna, Austria Liver X receptors (LXRs) are nuclear receptors regulating lipid and cholesterol metabolism. Recent data revealed a cross talk between LXR and Toll-like receptor signaling in macrophages, indicating a role in immunity. Here, we show that LXR is expressed in human myeloid dendritic cells (DCs) and induced during differentiation of monocyte-derived DCs, whereas LXRß is expressed constitutively at a very low level. LXR activation by 2 different LXR agonists strongly interfered with lipopolysaccharide (LPS)–induced but not with CD40L-induced DC maturation by altering DC morphology and suppressing interleukin-12—but enhancing interleukin-10—secretion. LXR activation in DCs largely blocked their T-cell stimulatory ability despite essentially unaltered expression of various antigen-presenting and costimulatory molecules. Immunologic synapse formation was significantly inhibited by LXR activation along with a complete block in LPS- but not CD40L-induced expression of the actin-bundling protein fascin. Notably, overexpression of fascin in LXR agonist–treated DCs restored immunologic synapse formation and restored their ability to activate T cells. In conclusion, our data reveal LXR as a potent modulator of DC maturation and function mediated in part by blocking the expression of fascin. Due to the central position of DCs in immunity, LXR could be a potential novel target for immunomodulation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: "Stimulate the phagocytes!" Fascin-ating! Are DCs actin' up? Philip L. McCarthy Blood 2007 109: 4112-4113. [Full Text] [PDF]

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