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    Antitumor efficacy of radiation plus immunotherapy depends upon dendritic cell activation of effector CD8+ T cells.

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    Authors
    Dovedi, S
    Lipowska-Bhalla, G
    Beers, S
    Cheadle, Eleanor J
    Mu, L
    Glennie, M
    Illidge, Timothy M
    Honeychurch, Jamie
    Affiliation
    Targeted Therapy Group, School of Cancer and Enabling Sciences, University of Manchester
    Issue Date
    2016-05-30
    
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    Abstract
    Tumor 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.
    Citation
    Antitumor efficacy of radiation plus immunotherapy depends upon dendritic cell activation of effector CD8+ T cells. 2016: Cancer Immunol Res
    Journal
    Cancer Immunology Research
    URI
    http://hdl.handle.net/10541/614528
    DOI
    10.1158/2326-6066.CIR-15-0253
    PubMed ID
    27241845
    Type
    Article
    Language
    en
    ISSN
    2326-6074
    ae974a485f413a2113503eed53cd6c53
    10.1158/2326-6066.CIR-15-0253
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