Source:http://linkedlifedata.com/resource/pubmed/id/15589055
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1-2
|
| pubmed:dateCreated |
2004-12-13
|
| pubmed:abstractText |
Interferon-beta (IFN-beta), an approved drug for multiple sclerosis (MS), acts on dendritic cells (DC) by suppressing IL-12p40 and increasing IL-10. This results in Th2-biased immune responses. The nature of IFN-beta-modulated DC remains elusive. Previously, we observed that IFN-beta dose dependently induces expression of CD123, i.e., a classical marker for plasmacytoid DC, on human blood monocyte-derived myeloid DC. Such IFN-beta-modulated DCs produce predominantly IL-10 but are IL-12 deficient, with potent Th2 promotion. In the present study, we further characterize IFN-beta-modulated DC by using recently identified blood DC antigens (BDCA), and investigate their ability to produce type I IFN in response to virus stimulation. We show that IFN-beta induces development of CD123+ DC from human blood monocytes, which coexpress BDCA4+ but are negative for BDCA2-, a specific marker for plasmacytoid DC. Such IFN-beta-modulated DC can produce IL-6 and IL-10 but not IL-12p40, and have no enhanced IFN-alpha and IFN-beta production. The findings indicate that IFN-beta-modulated DCs represent a myeloid DC subset with diminished CD11c, BDCA-1 and CD1a expression. They may promote Th2 and B cell differentiation through IL-6 and IL-10 production, and suppression of IL-12p40, but they have no enhanced antiviral capacity.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/IL3RA protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-beta,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-3 Receptor alpha Subunit,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-3
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jan
|
| pubmed:issn |
0165-5728
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
158
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
204-12
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:15589055-Adult,
pubmed-meshheading:15589055-Cell Count,
pubmed-meshheading:15589055-Cells, Cultured,
pubmed-meshheading:15589055-Dendritic Cells,
pubmed-meshheading:15589055-Disability Evaluation,
pubmed-meshheading:15589055-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:15589055-Female,
pubmed-meshheading:15589055-Flow Cytometry,
pubmed-meshheading:15589055-Humans,
pubmed-meshheading:15589055-Interferon-beta,
pubmed-meshheading:15589055-Interleukin-10,
pubmed-meshheading:15589055-Interleukin-3 Receptor alpha Subunit,
pubmed-meshheading:15589055-Interleukin-6,
pubmed-meshheading:15589055-Male,
pubmed-meshheading:15589055-Middle Aged,
pubmed-meshheading:15589055-Multiple Sclerosis,
pubmed-meshheading:15589055-Receptors, Interleukin-3,
pubmed-meshheading:15589055-Sendai virus,
pubmed-meshheading:15589055-Simplexvirus
|
| pubmed:year |
2005
|
| pubmed:articleTitle |
Multiple sclerosis: interferon-beta induces CD123(+)BDCA2- dendritic cells that produce IL-6 and IL-10 and have no enhanced type I interferon production.
|
| pubmed:affiliation |
Division of Neuroimmunology, Karolinska Institute, Alfred Nobels allé 10, 141 83 Stockholm, Sweden. yu-min.huang@neurotec.ki.se
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| pubmed:publicationType |
Journal Article,
Clinical Trial,
Comparative Study,
Research Support, Non-U.S. Gov't
|