Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-1-3
pubmed:abstractText
Dendritic cells produce IL-12 both in response to microbial stimuli and to T cells, and can thus skew T cell reactivity toward a Th1 pattern. We investigated the capacity of dendritic cells to elaborate IL-12 with special regard to their state of maturation, different maturation stimuli, and its regulation by Th1/Th2-influencing cytokines. Monocyte-derived dendritic cells were generated with GM-CSF and IL-4 for 7 days, followed by another 3 days +/- monocyte-conditioned media, yielding mature (CD83(+)/dendritic cell-lysosome-associated membrane glycoprotein(+)) and immature (CD83(-)/dendritic cell-lysosome-associated membrane glycoprotein(-)) dendritic cells. These dendritic cells were stimulated for another 48 h, and IL-12 p70 was measured by ELISA. We found the following: 1) Immature dendritic cells stimulated with CD154/CD40 ligand or bacteria (both of which concurrently also induced maturation) secreted always more IL-12 than already mature dendritic cells. Mature CD154-stimulated dendritic cells still made significant levels (up to 4 ng/ml). 2) Terminally mature skin-derived dendritic cells did not make any IL-12 in response to these stimuli. 3) Appropriate maturation stimuli are required for IL-12 production: CD40 ligation and bacteria are sufficient; monocyte-conditioned media are not. 4) Unexpectedly, IL-4 markedly increased the amount of IL-12 produced by both immature and mature dendritic cells, when present during stimulation. 5) IL-10 inhibited the production of IL-12. Our results, employing a cell culture system that is now being widely used in immunotherapy, extend prior data that IL-12 is produced most abundantly by dendritic cells that are beginning to respond to maturation stimuli. Surprisingly, IL-12 is only elicited by select maturation stimuli, but can be markedly enhanced by the addition of the Th2 cytokine, IL-4.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
166
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
633-41
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11123347-Adjuvants, Immunologic, pubmed-meshheading:11123347-Animals, pubmed-meshheading:11123347-Antigens, CD40, pubmed-meshheading:11123347-CD40 Ligand, pubmed-meshheading:11123347-Cell Differentiation, pubmed-meshheading:11123347-Cells, Cultured, pubmed-meshheading:11123347-Culture Media, Conditioned, pubmed-meshheading:11123347-Dendritic Cells, pubmed-meshheading:11123347-Flow Cytometry, pubmed-meshheading:11123347-Growth Inhibitors, pubmed-meshheading:11123347-Humans, pubmed-meshheading:11123347-Interferon-gamma, pubmed-meshheading:11123347-Interleukin-10, pubmed-meshheading:11123347-Interleukin-12, pubmed-meshheading:11123347-Interleukin-4, pubmed-meshheading:11123347-Intracellular Fluid, pubmed-meshheading:11123347-Mice, pubmed-meshheading:11123347-Monocytes, pubmed-meshheading:11123347-Skin, pubmed-meshheading:11123347-Staphylococcus aureus, pubmed-meshheading:11123347-Transcription, Genetic
pubmed:year
2001
pubmed:articleTitle
Production of IL-12 by human monocyte-derived dendritic cells is optimal when the stimulus is given at the onset of maturation, and is further enhanced by IL-4.
pubmed:affiliation
Department of Dermatology, University of Innsbruck, Innsbruck, Austria.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't