Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9395
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dc.contributor.authorLuft, Thomasen
dc.contributor.authorLuetjens, Petraen
dc.contributor.authorHochrein, Hubertusen
dc.contributor.authorToy, Traceyen
dc.contributor.authorMasterman, Kelly-Anneen
dc.contributor.authorRizkalla, Marken
dc.contributor.authorMaliszewski, Charlieen
dc.contributor.authorShortman, Kenen
dc.contributor.authorCebon, Jonathan Sen
dc.contributor.authorMaraskovsky, Eugeneen
dc.date.accessioned2015-05-15T22:28:31Z
dc.date.available2015-05-15T22:28:31Z
dc.date.issued2002-04-01en
dc.identifier.citationInternational Immunology; 14(4): 367-80en
dc.identifier.govdoc11934873en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9395en
dc.description.abstractType I IFN are immune modulatory cytokines that are secreted during early stages of infection. Type I IFN bridge the innate and the adaptive immune system in humans and mice. We compared the capacity of type I and II IFN to induce the functional maturation of monocyte-derived dendritic cells (MoDC). Extending our earlier observation that type I IFN promote DC maturation, we report that these cytokines also enhance DC differentiation by augmenting CD40 ligand (CD40L)-induced cytokine secretion by MoDC. Type I IFN alone were poor inducers of MoDC maturation as compared with other stimuli. They up-regulated the expression of HLA-DR, CD80, CD86, partially CCR7 but not CD83, partially reduced antigen-uptake function, increased the levels of IL-12p35 mRNA, and prolonged surface expression of peptide-MHC class I complexes for presentation to cytotoxic T lymphocytes, but did not induce migration towards CCL21 chemokine. However, type I IFN were potent co-factors for CD40L-mediated function. Here, they enhanced CD40L-mediated IL-6, IL-10 and IL-12p70 secretion. Furthermore, when combined with IL-1beta and/or IL-4, IFN-alpha2a type I IFN increased CD40L-mediated IL-12p70 production by 2- to 3-fold, and biased the IL-12 p40/p70 ratio towards the IFN-gamma inducing p70 heterodimer, this correlating with higher levels of IFN-gamma secretion by allogeneic T cell subsets and NK cells. Our results suggest that the rapid expression of CD40L, IFN and IL-1beta at sites of infection and inflammation can act in concert on immature DC, thereby linking innate and adaptive immune responses. In this way, type I IFN play a dual role as DC maturation factors and enhancers of CD40L-mediated DC activation.en
dc.language.isoenen
dc.subject.otherAdjuvants, Immunologic.genetics.metabolismen
dc.subject.otherAntigen Presentationen
dc.subject.otherAntigens, Neoplasmen
dc.subject.otherCD40 Ligand.metabolismen
dc.subject.otherCell Differentiationen
dc.subject.otherCell Movementen
dc.subject.otherCells, Cultureden
dc.subject.otherCorynebacteriumen
dc.subject.otherDendritic Cells.drug effects.metabolismen
dc.subject.otherGranulocyte-Macrophage Colony-Stimulating Factor.metabolismen
dc.subject.otherHumansen
dc.subject.otherInterferon-alpha.metabolism.pharmacologyen
dc.subject.otherInterferon-gamma.analysisen
dc.subject.otherInterleukin-12.genetics.metabolism.secretionen
dc.subject.otherInterleukin-12 Subunit p35en
dc.subject.otherInterleukins.metabolismen
dc.subject.otherKiller Cells, Natural.secretionen
dc.subject.otherMART-1 Antigenen
dc.subject.otherMonocytes.classification.immunology.metabolismen
dc.subject.otherNeoplasm Proteins.metabolismen
dc.subject.otherProtein Conformationen
dc.subject.otherProtein Subunitsen
dc.subject.otherT-Lymphocytes.secretionen
dc.titleIFN-alpha enhances CD40 ligand-mediated activation of immature monocyte-derived dendritic cells.en
dc.typeJournal Articleen
dc.identifier.journaltitleInternational immunologyen
dc.identifier.affiliationMelbourne Tumour Biology Branch, Ludwig Institute for Cancer Research, Austin and Repatriation Medical Centre, Heidelberg, Victoria 3084, Australiaen
dc.description.pages367-80en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/11934873en
dc.type.austinJournal Articleen
local.name.researcherCebon, Jonathan S
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptOlivia Newton-John Cancer Research Institute-
Appears in Collections:Journal articles
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