Source:http://linkedlifedata.com/resource/pubmed/id/15212715
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
|
pubmed:dateCreated |
2004-6-23
|
pubmed:abstractText |
In this study, we compared dendritic cells (DCs) differentiated from positively selected monocytes (CD14-DCs) to DCs differentiated from adherence-selected monocytes (adh-DCs) with emphasis on lentiviral transduction. Using a second-generation, triple-helix containing, self-inactivating lentiviral vector at a multiplicity of infection (MOI) of 15, we observed enhanced transduction of CD14-DCs (72.8 +/- 5.3%, mean fluorescence intensity [MFI] = 166 +/- 76) compared to adh-DCs (32.3 +/- 13.1%, MFI = 119 +/- 76, n = 5). More importantly, the efficiency to transduce adh-DCs was significantly increased when monocytes were incubated with antiCD14 antibody coupled beads, anti-CD14 antibodies, or lipopolysaccharide (LPS), reaching transduction efficiencies up to 86.6%, 53.3%, and 80.9%, respectively. We showed that this enhanced transduction was correlated to an activation of the monocytes, characterized by the up regulation of the cytokines interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha and the de novo synthesis of IL-6 and IL-10. However, the enhanced transduction of immature CD14-DCs was not correlated with a progression in the cell cycle from G(0) to G(1). We further showed that CD14-DCs were phenotypically comparable to adh-DCs. Functional analysis revealed that there were no differences in allostimulatory capacity, production of IL-12 p70 on CD40 ligation or expression of IL-1beta, IL-6, IL-8, IL-10, IL-12, and TNF-alpha as evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR). Finally, we showed that lentivirally transduced CD14-DCs were equally capable as adh-DCs in stimulating MAGE-A3 antigen-specific CD4(+) and CD8(+) T cells in vitro.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD14,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/MAGEA3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Neoplasm Proteins
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jun
|
pubmed:issn |
1043-0342
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
15
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
562-73
|
pubmed:dateRevised |
2006-11-15
|
pubmed:meshHeading |
pubmed-meshheading:15212715-Antibodies, Monoclonal,
pubmed-meshheading:15212715-Antigens, CD14,
pubmed-meshheading:15212715-Antigens, Neoplasm,
pubmed-meshheading:15212715-CD4-Positive T-Lymphocytes,
pubmed-meshheading:15212715-CD8-Positive T-Lymphocytes,
pubmed-meshheading:15212715-Cell Cycle,
pubmed-meshheading:15212715-Cell Differentiation,
pubmed-meshheading:15212715-Cytokines,
pubmed-meshheading:15212715-Dendritic Cells,
pubmed-meshheading:15212715-Gene Transfer Techniques,
pubmed-meshheading:15212715-Genetic Vectors,
pubmed-meshheading:15212715-Humans,
pubmed-meshheading:15212715-Immunophenotyping,
pubmed-meshheading:15212715-Lentivirus,
pubmed-meshheading:15212715-Leukocytes, Mononuclear,
pubmed-meshheading:15212715-Lipopolysaccharides,
pubmed-meshheading:15212715-Lymphocyte Activation,
pubmed-meshheading:15212715-Monocytes,
pubmed-meshheading:15212715-Neoplasm Proteins,
pubmed-meshheading:15212715-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:15212715-Transduction, Genetic
|
pubmed:year |
2004
|
pubmed:articleTitle |
Activation of monocytes via the CD14 receptor leads to the enhanced lentiviral transduction of immature dendritic cells.
|
pubmed:affiliation |
Laboratory of Molecular and Cellular Therapy, Department of Physiology and Immunology, Medical School of the Vrije Universiteit Brussel (V.U.B.), Laarbeeklaan 103/E, 1090 Brussels, Belgium.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|