Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9377
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dc.contributor.authorLuft, Thomasen
dc.contributor.authorJefford, Michaelen
dc.contributor.authorLuetjens, Petraen
dc.contributor.authorHochrein, Hubertusen
dc.contributor.authorMasterman, Kelly-Anneen
dc.contributor.authorMaliszewski, Charlieen
dc.contributor.authorShortman, Kenen
dc.contributor.authorCebon, Jonathan Sen
dc.contributor.authorMaraskovsky, Eugeneen
dc.date.accessioned2015-05-15T22:27:05Z
dc.date.available2015-05-15T22:27:05Z
dc.date.issued2002-01-15en
dc.identifier.citationJournal of Immunology (baltimore, Md. : 1950); 168(2): 713-22en
dc.identifier.govdoc11777965en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9377en
dc.description.abstractCD40 ligand (CD40L) is a membrane-bound molecule expressed by activated T cells. CD40L potently induces dendritic cell (DC) maturation and IL-12p70 secretion and plays a critical role during T cell priming in the lymph nodes. IFN-gamma and IL-4 are required for CD40L-mediated cytokine secretion, suggesting that T cells are required for optimal CD40L activity. Because CD40L is rapidly up-regulated by non-T cells during inflammation, CD40 stimulation may also be important at the primary infection site. However, a role for T cells at the earliest stages of infection is unclear. The present study demonstrates that the innate immune cell-derived cytokine, IL-1beta, can increase CD40L-induced cytokine secretion by monocyte-derived DC, CD34(+)-derived DC, and peripheral blood DC independently of T cell-derived cytokines. Furthermore, IL-1beta is constitutively produced by monocyte-derived DC and monocytes, and is increased in response to intact Escherichia coli or CD40L, whereas neither CD34(+)-derived DC nor peripheral blood DC produce IL-1beta. Finally, DC activated with CD40L and IL-1beta induce higher levels of IFN-gamma secretion by T cells compared with DC activated with CD40L alone. Therefore, IL-1beta is the first non-T cell-derived cytokine identified that enhances CD40L-mediated activation of DC. The synergy between CD40L and IL-1beta highlights a potent, T cell-independent mechanism for DC activation during the earliest stages of inflammatory responses.en
dc.language.isoenen
dc.subject.otherAdjuvants, Immunologic.physiologyen
dc.subject.otherAntigens, CD34.biosynthesisen
dc.subject.otherCD40 Ligand.pharmacology.physiologyen
dc.subject.otherCell Differentiation.immunologyen
dc.subject.otherCells, Cultureden
dc.subject.otherChemotaxis, Leukocyte.immunologyen
dc.subject.otherCulture Media, Conditioned.pharmacologyen
dc.subject.otherCytokines.secretionen
dc.subject.otherDendritic Cells.cytology.immunology.secretionen
dc.subject.otherHumansen
dc.subject.otherInterferon-gamma.secretionen
dc.subject.otherInterleukin-1.blood.pharmacology.physiology.secretionen
dc.subject.otherInterleukin-4.pharmacologyen
dc.subject.otherInterleukin-6.metabolism.pharmacologyen
dc.subject.otherLymphocyte Activationen
dc.subject.otherLymphocyte Culture Test, Mixeden
dc.subject.otherMonocytes.immunology.metabolism.secretionen
dc.subject.otherReceptors, Interleukin-6.physiologyen
dc.subject.otherT-Lymphocytes.immunology.secretionen
dc.subject.otherTumor Necrosis Factor-alpha.pharmacologyen
dc.titleIL-1 beta enhances CD40 ligand-mediated cytokine secretion by human dendritic cells (DC): a mechanism for T cell-independent DC activation.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of Immunology (Baltimore, Md. : 1950)en
dc.identifier.affiliationMelbourne Tumor Biology Branch, Ludwig Institute for Cancer Research, Austin and Repatriation Medical Center, Heidelberg, Victoria, Australiaen
dc.description.pages713-22en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/11777965en
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-
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