Document Detail


High-density lipoprotein phospholipids interfere with dendritic cell Th1 functional maturation.
MedLine Citation:
PMID:  21856032     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Lipoproteins are both lipid carriers in the blood and regulators of essential biological processes. Several studies demonstrated that lipoproteins modified during pathological conditions could alter dendritic cell (DC) maturation. Here the immune function of non-pathological lipoproteins is addressed by analysing their impact on human DC maturation triggered by TLR ligands. Upon TLR4 stimulation, low- and high-density lipoproteins (LDL and HDL) strongly inhibited the ability of DC to induce a Th1 response of T cells, characterized by high levels of IFNγ secretion, whereas the effect of very low-density lipoprotein was subject to variations. HDL also inhibited the Th1 function of DC stimulated by TLR1/2 and TLR2/6 ligands. The phospholipid fraction from HDL retained the inhibitory activity of the lipoprotein. We identified the 1-palmitoyl-2-linoleyl-phosphatidylcholine (PLPC) as one active phospholipid that inhibited the Th1 function of mature DCs whereas the dipalmitoyl-phosphatidylcholine had no significant effect. The treatment of DC by PLPC, 24h before TLR4 stimulation, resulted in reduced activation of NF-κB. This study shows that some HDL phospholipids have a direct immunoregulatory function, by modulating DC ability to activate a Th1 response of T cells.
Authors:
Laure Perrin-Cocon; Olivier Diaz; Martine Carreras; Sandra Dollet; Aurélie Guironnet-Paquet; Patrice André; Vincent Lotteau
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-8-3
Journal Detail:
Title:  Immunobiology     Volume:  -     ISSN:  1878-3279     ISO Abbreviation:  -     Publication Date:  2011 Aug 
Date Detail:
Created Date:  2011-8-22     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8002742     Medline TA:  Immunobiology     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2011. Published by Elsevier GmbH.
Affiliation:
Université de Lyon, France; INSERM, U851, 21 Avenue Tony Garnier, Lyon F-69365, France.
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