Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12535
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dc.contributor.authorCoquet, Jonathan Men
dc.contributor.authorSkak, Krestenen
dc.contributor.authorDavis, Ian Den
dc.contributor.authorSmyth, Mark Jen
dc.contributor.authorGodfrey, Dale Ien
dc.date.accessioned2015-05-16T02:14:41Z
dc.date.available2015-05-16T02:14:41Z
dc.date.issued2013-10-18en
dc.identifier.citationClinical & Translational Immunology 2013; 2(10): e6en
dc.identifier.govdoc25505948en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/12535en
dc.description.abstractInterleukin-21 (IL-21) is a common γ-chain cytokine produced by T helper and natural killer T (NKT) cells. It has been shown to regulate the response of various lymphocyte subsets including NK, NKT, T and B cells. Owing to its potent anti-tumor function in preclinical studies and its ability to induce cytotoxicity and interferon-γ (IFN-γ) production in NK and CD8 T cells, recombinant IL-21 (rIL-21) was fast-tracked into early-phase clinical trials of patients with various malignancies. In a phase 2a trial of patients with metastatic melanoma, we analyzed the frequency and function of NKT cells in patients receiving rIL-21. NKT cells were present at a low frequency, but their levels were relatively stable in patients administered rIL-21. Unlike our observations in NK and CD8 T cells, rIL-21 appeared to reduce IFN-γ and TNF production by NKT cells, whereas it enhanced IL-4 production. It also modulated the expression of cell surface markers, specifically on CD4(-) NKT cells. In addition, an increase in CD3(+)CD56(+) NKT-like cells was observed over the course of rIL-21 administration. These results highlight that IL-21 is a potent regulator of NKT cell function in vivo.en
dc.language.isoenen
dc.subject.otherCanceren
dc.subject.otherIL-21en
dc.subject.otherNKTen
dc.subject.otherT helperen
dc.titleIL-21 Modulates Activation of NKT Cells in Patients with Stage IV Malignant Melanoma.en
dc.typeJournal Articleen
dc.identifier.journaltitleClinical & translational immunologyen
dc.identifier.affiliationLudwig Institute for Cancer Research, Austin Health , Melbourne, Victoria, Australiaen
dc.identifier.affiliationCancer Immunology Program, Peter MacCallum Cancer Centre , East Melbourne, Victoria, Australia ; Immunology in Cancer and Infection Laboratory, Queensland Institute of Medical Research , Herston, Queensland, Australia ; School of Medicine, University of Queensland , Herston, Queensland, Australiaen
dc.identifier.affiliationDepartment of Microbiology and Immunology, University of Melbourne , Parkville, Victoria, Australiaen
dc.identifier.affiliationDepartment of Histology and Cancer Pharmacology, Novo Nordisk A/S , Maalov, Denmark.en
dc.identifier.doi10.1038/cti.2013.7en
dc.description.pagese6en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/25505948en
dc.type.austinJournal Articleen
item.cerifentitytypePublications-
item.languageiso639-1en-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
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