Antitumor efficacy of radiation plus immunotherapy depends upon dendritic cell activation of effector CD8+ T cellsCitation formats

  • External authors:
  • Simon Dovedi
  • Stephen Beers
  • Lijun Mu
  • Martin J. Glennie

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Antitumor efficacy of radiation plus immunotherapy depends upon dendritic cell activation of effector CD8+ T cells. / Dovedi, Simon; Lipowska-Bhalla, Grazyna; Beers, Stephen; Cheadle, Eleanor; Mu, Lijun; Glennie, Martin J.; Illidge, Timothy; Honeychurch, Jamie.

In: Cancer Immunology Research , Vol. 4, No. 7, 01.07.2016.

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@article{200307ec689e44f79f8f163ecc6a0c06,
title = "Antitumor efficacy of radiation plus immunotherapy depends upon dendritic cell activation of effector CD8+ T cells",
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); 621–30. {\textcopyright}2016 AACR.",
author = "Simon Dovedi and Grazyna Lipowska-Bhalla and Stephen Beers and Eleanor Cheadle and Lijun Mu and Glennie, {Martin J.} and Timothy Illidge and Jamie Honeychurch",
year = "2016",
month = jul,
day = "1",
doi = "10.1158/2326-6066.CIR-15-0253",
language = "English",
volume = "4",
journal = "Cancer Immunology Research ",
issn = "2326-6074",
publisher = "American Association for Cancer Research",
number = "7",

}

RIS

TY - JOUR

T1 - Antitumor efficacy of radiation plus immunotherapy depends upon dendritic cell activation of effector CD8+ T cells

AU - Dovedi, Simon

AU - Lipowska-Bhalla, Grazyna

AU - Beers, Stephen

AU - Cheadle, Eleanor

AU - Mu, Lijun

AU - Glennie, Martin J.

AU - Illidge, Timothy

AU - Honeychurch, Jamie

PY - 2016/7/1

Y1 - 2016/7/1

N2 - 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); 621–30. ©2016 AACR.

AB - 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); 621–30. ©2016 AACR.

U2 - 10.1158/2326-6066.CIR-15-0253

DO - 10.1158/2326-6066.CIR-15-0253

M3 - Article

VL - 4

JO - Cancer Immunology Research

JF - Cancer Immunology Research

SN - 2326-6074

IS - 7

ER -