Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9492
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dc.contributor.authorJefford, Michaelen
dc.contributor.authorSchnurr, Maxen
dc.contributor.authorToy, Traceyen
dc.contributor.authorMasterman, Kelly-Anneen
dc.contributor.authorShin, Amandaen
dc.contributor.authorBeecroft, Tinaen
dc.contributor.authorTai, Tsin Yeeen
dc.contributor.authorShortman, Kenen
dc.contributor.authorShackleton, Marken
dc.contributor.authorDavis, Ian Den
dc.contributor.authorParente, Philen
dc.contributor.authorLuft, Thomasen
dc.contributor.authorChen, Weisanen
dc.contributor.authorCebon, Jonathan Sen
dc.contributor.authorMaraskovsky, Eugeneen
dc.date.accessioned2015-05-15T22:36:24Z
dc.date.available2015-05-15T22:36:24Z
dc.date.issued2003-05-08en
dc.identifier.citationBlood 2003; 102(5): 1753-63en
dc.identifier.govdoc12738673en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9492en
dc.description.abstractDendritic cells (DCs) are a family of leukocytes that initiate T- and B-cell immunity against pathogens. Migration of antigen-loaded DCs from sites of infection into draining lymphoid tissues is fundamental to the priming of T-cell immune responses. In humans, the major peripheral blood DC (PBDC) types, CD1c+ DCs and interleukin 3 receptor-positive (IL-3R+) plasmacytoid DCs, are significantly expanded in vivo with the use of Flt3 ligand (FL). DC-like cells can also be generated from monocyte precursors (MoDCs). A detailed comparison of the functional potential of these types of DCs (in an autologous setting) has yet to be reported. Here, we compared the functional capacity of FL-expanded CD1c+ PBDCs with autologous MoDCs in response to 3 different classes of stimuli: (1) proinflammatory mediators, (2) soluble CD40 ligand trimer (CD40L), and (3) intact bacteria (Escherichia coli). Significant differences in functional capacities were found with respect to changes in phenotype, migratory capacity, cytokine secretion, and T-cell stimulation. MoDCs required specific stimuli for the expression of functions. They responded vigorously to CD40L or E coli, expressing cytokines known to regulate interferon-gamma (IFN-gamma) in T cells (IL-12p70, IL-18, and IL-23), but required prostaglandin E2 (PGE2) during stimulation to migrate to chemokines. In contrast, PBDCs matured in response to minimal stimulation, rapidly acquired migratory function in the absence of PGE2-containing stimuli, and were low cytokine producers. Interestingly, both types of DCs were equivalent with respect to stimulation of allogeneic T-cell proliferation and presentation of peptides to cytotoxic T lymphocyte (CTL) lines. These distinct differences are of particular importance when considering the choice of DC types for clinical applications.en
dc.language.isoenen
dc.subject.otherAntigens, CD1.metabolismen
dc.subject.otherCD40 Ligand.pharmacologyen
dc.subject.otherCell Differentiation.drug effects.immunologyen
dc.subject.otherCell Division.immunologyen
dc.subject.otherCell Movement.immunologyen
dc.subject.otherCells, Cultureden
dc.subject.otherCytokines.biosynthesisen
dc.subject.otherDendritic Cells.cytology.immunology.metabolismen
dc.subject.otherEscherichia colien
dc.subject.otherGlycoproteins.metabolismen
dc.subject.otherHumansen
dc.subject.otherImmunophenotypingen
dc.subject.otherIn Vitro Techniquesen
dc.subject.otherInflammation Mediators.pharmacologyen
dc.subject.otherLymphocyte Activation.immunologyen
dc.subject.otherMelanoma.immunologyen
dc.subject.otherMembrane Proteins.pharmacologyen
dc.subject.otherMonocytes.cytologyen
dc.subject.otherPeptides.pharmacologyen
dc.subject.otherStimulation, Chemicalen
dc.subject.otherT-Lymphocytes.cytology.immunologyen
dc.titleFunctional comparison of DCs generated in vivo with Flt3 ligand or in vitro from blood monocytes: differential regulation of function by specific classes of physiologic stimuli.en
dc.typeJournal Articleen
dc.identifier.journaltitleBlooden
dc.identifier.affiliationLudwig Institute Oncology Unit, Austin and Repatriation Medical Centre, Studley Rd, Heidelberg, Victoria 3084, Australiaen
dc.identifier.doi10.1182/blood-2002-12-3854en
dc.description.pages1753-63en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/12738673en
dc.type.austinJournal Articleen
local.name.researcherCebon, Jonathan S
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
crisitem.author.deptOlivia Newton-John Cancer Research Institute-
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