Exploiting the stress response to radiation to sensitize poorly immunogenic tumors to anti-CTLA-4 treatment

Radiotherapy sensitizes unresponsive tumors to the antineoplastic activity of antibodies that target the inhibitory receptor CTLA-4 on T cells. One molecular mechanism accounting for this therapeutic synergy is the induction of NKG2D ligands on irradiated tumor cells. The fact that NKG2D receptors m...

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Detalles Bibliográficos
Autores principales: Demaria, Sandra, Pilones, Karsten A., Formenti, Silvia C., Dustin, Michael L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2013
Materias:
Author's View
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3661148/
https://www.ncbi.nlm.nih.gov/pubmed/23802063
http://dx.doi.org/10.4161/onci.23127
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author Demaria, Sandra
Pilones, Karsten A.
Formenti, Silvia C.
Dustin, Michael L.
author_facet Demaria, Sandra
Pilones, Karsten A.
Formenti, Silvia C.
Dustin, Michael L.
author_sort Demaria, Sandra
collection PubMed
description Radiotherapy sensitizes unresponsive tumors to the antineoplastic activity of antibodies that target the inhibitory receptor CTLA-4 on T cells. One molecular mechanism accounting for this therapeutic synergy is the induction of NKG2D ligands on irradiated tumor cells. The fact that NKG2D receptors must be engaged for the elicitation of CD8(+) T-cell antitumor responses has important clinical implications.
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spelling pubmed-36611482013-06-25 Exploiting the stress response to radiation to sensitize poorly immunogenic tumors to anti-CTLA-4 treatment Demaria, Sandra Pilones, Karsten A. Formenti, Silvia C. Dustin, Michael L. Oncoimmunology Author's View Radiotherapy sensitizes unresponsive tumors to the antineoplastic activity of antibodies that target the inhibitory receptor CTLA-4 on T cells. One molecular mechanism accounting for this therapeutic synergy is the induction of NKG2D ligands on irradiated tumor cells. The fact that NKG2D receptors must be engaged for the elicitation of CD8(+) T-cell antitumor responses has important clinical implications. Landes Bioscience 2013-03-01 2013-03-01 /pmc/articles/PMC3661148/ /pubmed/23802063 http://dx.doi.org/10.4161/onci.23127 Text en Copyright © 2013 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Author's View
Demaria, Sandra
Pilones, Karsten A.
Formenti, Silvia C.
Dustin, Michael L.
Exploiting the stress response to radiation to sensitize poorly immunogenic tumors to anti-CTLA-4 treatment
title Exploiting the stress response to radiation to sensitize poorly immunogenic tumors to anti-CTLA-4 treatment
title_full Exploiting the stress response to radiation to sensitize poorly immunogenic tumors to anti-CTLA-4 treatment
title_fullStr Exploiting the stress response to radiation to sensitize poorly immunogenic tumors to anti-CTLA-4 treatment
title_full_unstemmed Exploiting the stress response to radiation to sensitize poorly immunogenic tumors to anti-CTLA-4 treatment
title_short Exploiting the stress response to radiation to sensitize poorly immunogenic tumors to anti-CTLA-4 treatment
title_sort exploiting the stress response to radiation to sensitize poorly immunogenic tumors to anti-ctla-4 treatment
topic Author's View
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3661148/
https://www.ncbi.nlm.nih.gov/pubmed/23802063
http://dx.doi.org/10.4161/onci.23127
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