PMID- 20410489
OWN - NLM
STAT- MEDLINE
DCOM- 20100719
LR  - 20161125
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Linking)
VI  - 184
IP  - 10
DP  - 2010 May 15
TI  - Activation of liver X receptor sensitizes human dendritic cells to inflammatory 
      stimuli.
PG  - 5456-65
LID - 10.4049/jimmunol.0902399 [doi]
AB  - Dendritic cells (DCs) respond to changes in their lipid environment by altering 
      gene expression and immunophenotype. Some of these alterations are mediated via 
      the nuclear receptor superfamily. However, little is known about the contribution 
      of liver X receptor (LXR) to DC biology. In this study, we present a systematic 
      analysis of LXR, activated by synthetic ligands or naturally occurring oxysterols 
      in developing human monocyte-derived DCs. We found that LXRs are present and can 
      be activated throughout DC differentiation in monocyte- and blood-derived DCs. 
      Administration of LXR-specific natural or synthetic activators induced target 
      gene expression accompanied by increased expression of DC maturation markers, 
      such as CD80 and CD86. In mature DCs, LXR activation augmented the production of 
      inflammatory cytokines IL-12, TNF-alpha, IL-6, and IL-8 and resulted in an 
      increased capacity to activate CD4+ T cell proliferation upon ligation with TLR4 
      or TLR3 ligands. These effects appear to be underpinned by prolonged NF-kappaB 
      signaling. Supporting such an inflammatory role, we found that LXR positive DCs 
      are present in reactive lymph nodes in vivo. We propose that activation of LXR 
      represents a novel lipid-signaling paradigm that alters the inflammatory response 
      of human DCs.
FAU - Torocsik, Daniel
AU  - Torocsik D
AD  - Department of Biochemistry and Molecular Biology, University of Debrecen, Medical 
      and Health Science Center, Hungary.
FAU - Barath, Monika
AU  - Barath M
FAU - Benko, Szilvia
AU  - Benko S
FAU - Szeles, Lajos
AU  - Szeles L
FAU - Dezso, Balazs
AU  - Dezso B
FAU - Poliska, Szilard
AU  - Poliska S
FAU - Hegyi, Zoltan
AU  - Hegyi Z
FAU - Homolya, Laszlo
AU  - Homolya L
FAU - Szatmari, Istvan
AU  - Szatmari I
FAU - Lanyi, Arpad
AU  - Lanyi A
FAU - Nagy, Laszlo
AU  - Nagy L
LA  - eng
SI  - GEO/GSE8658
GR  - Howard Hughes Medical Institute/United States
GR  - Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100421
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Liver X Receptors)
RN  - 0 (NF-kappa B)
RN  - 0 (Orphan Nuclear Receptors)
RN  - 0 (Protein Isoforms)
SB  - IM
MH  - CD4-Positive T-Lymphocytes/immunology/pathology
MH  - Cell Differentiation/*immunology
MH  - Cell Proliferation
MH  - Cells, Cultured
MH  - Cytokines/biosynthesis
MH  - Dendritic Cells/*immunology/*metabolism/pathology
MH  - Humans
MH  - Inflammation Mediators/metabolism/*physiology
MH  - Lipid Metabolism/immunology
MH  - Liver X Receptors
MH  - Lymph Nodes/cytology/immunology/metabolism/pathology
MH  - Monocytes/cytology/immunology/metabolism
MH  - NF-kappa B/physiology
MH  - Orphan Nuclear Receptors/*metabolism/physiology
MH  - Protein Isoforms/metabolism/physiology
MH  - Signal Transduction/immunology
MH  - Up-Regulation/immunology
EDAT- 2010/04/23 06:00
MHDA- 2010/07/20 06:00
CRDT- 2010/04/23 06:00
PHST- 2010/04/23 06:00 [entrez]
PHST- 2010/04/23 06:00 [pubmed]
PHST- 2010/07/20 06:00 [medline]
AID - jimmunol.0902399 [pii]
AID - 10.4049/jimmunol.0902399 [doi]
PST - ppublish
SO  - J Immunol. 2010 May 15;184(10):5456-65. doi: 10.4049/jimmunol.0902399. Epub 2010 
      Apr 21.