Show simple item record

dc.contributor.authorDovedi, S
dc.contributor.authorLipowska-Bhalla, G
dc.contributor.authorBeers, S
dc.contributor.authorCheadle, Eleanor J
dc.contributor.authorMu, L
dc.contributor.authorGlennie, M
dc.contributor.authorIllidge, Timothy M
dc.contributor.authorHoneychurch, Jamie
dc.date.accessioned2016-06-24T11:04:19Z
dc.date.available2016-06-24T11:04:19Z
dc.date.issued2016-05-30
dc.identifier.citationAntitumor efficacy of radiation plus immunotherapy depends upon dendritic cell activation of effector CD8+ T cells. 2016: Cancer Immunol Resen
dc.identifier.issn2326-6074
dc.identifier.pmid27241845
dc.identifier.doi10.1158/2326-6066.CIR-15-0253
dc.identifier.urihttp://hdl.handle.net/10541/614528
dc.description.abstractTumor cells dying after cytotoxic therapy are a potential source of antigen for T-cell priming. Antigen-presenting cells (APC) can cross-present MHC I-restricted peptides after the uptake of dying cells. Depending on the nature of the surrounding environmental signals, APCs then orchestrate a spectrum of responses ranging from immune activation to inhibition. Previously, we had demonstrated that combining radiation with either agonistic monoclonal antibody (mAb) to CD40 or a systemically administered TLR7 agonist could enhance CD8 T-cell-dependent protection against syngeneic murine lymphoma models. However, it remains unknown how individual APC populations affect this antitumor immune response. Using APC depletion models, we now show that dendritic cells (DC), but not macrophages or B cells, were responsible for the generation of long-term immunologic protection following combination therapy with radiotherapy and either agonistic CD40 mAb or systemic TLR7 agonist therapy. Novel immunotherapeutic approaches that augment antigen uptake and presentation by DCs may further enhance the generation of therapeutic antitumor immune responses, leading to improved outcomes after radiotherapy. Cancer Immunol Res; 4(7); 1-10. ©2016 AACR.
dc.languageENGen
dc.language.isoenen
dc.rightsArchived with thanks to Cancer immunology researchen
dc.titleAntitumor efficacy of radiation plus immunotherapy depends upon dendritic cell activation of effector CD8+ T cells.en
dc.typeArticleen
dc.contributor.departmentTargeted Therapy Group, School of Cancer and Enabling Sciences, University of Manchesteren
dc.identifier.journalCancer Immunology Researchen
dc.description.collectionLymphoma Research Teamen
refterms.dateFOA2020-04-03T15:12:09Z
html.description.abstractTumor cells dying after cytotoxic therapy are a potential source of antigen for T-cell priming. Antigen-presenting cells (APC) can cross-present MHC I-restricted peptides after the uptake of dying cells. Depending on the nature of the surrounding environmental signals, APCs then orchestrate a spectrum of responses ranging from immune activation to inhibition. Previously, we had demonstrated that combining radiation with either agonistic monoclonal antibody (mAb) to CD40 or a systemically administered TLR7 agonist could enhance CD8 T-cell-dependent protection against syngeneic murine lymphoma models. However, it remains unknown how individual APC populations affect this antitumor immune response. Using APC depletion models, we now show that dendritic cells (DC), but not macrophages or B cells, were responsible for the generation of long-term immunologic protection following combination therapy with radiotherapy and either agonistic CD40 mAb or systemic TLR7 agonist therapy. Novel immunotherapeutic approaches that augment antigen uptake and presentation by DCs may further enhance the generation of therapeutic antitumor immune responses, leading to improved outcomes after radiotherapy. Cancer Immunol Res; 4(7); 1-10. ©2016 AACR.


Files in this item

Thumbnail
Name:
Antitumor efficacy of radiation ...
Size:
1.122Mb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record