Ecto-calreticulin in immunogenic chemotherapy.

Détails

ID Serval
serval:BIB_73A26D3A014F
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Ecto-calreticulin in immunogenic chemotherapy.
Périodique
Immunological reviews
Auteur(s)
Obeid M., Tesniere A., Panaretakis T., Tufi R., Joza N., van Endert P., Ghiringhelli F., Apetoh L., Chaput N., Flament C., Ullrich E., de Botton S., Zitvogel L., Kroemer G.
ISSN
0105-2896 (Print)
ISSN-L
0105-2896
Statut éditorial
Publié
Date de publication
12/2007
Peer-reviewed
Oui
Volume
220
Pages
22-34
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review
Publication Status: ppublish
Résumé
The conventional treatment of cancer relies upon radiotherapy and chemotherapy. Such treatments supposedly mediate their effects via the direct elimination of tumor cells. Nonetheless, there are circumstances in which conventional anti-cancer therapy can induce a modality of cellular demise that elicits innate and cognate immune responses, which in turn mediate part of the anti-tumor effect. Although different chemotherapeutic agents may kill tumor cells through an apparently homogeneous apoptotic pathway, they differ in their capacity to stimulate immunogenic cell death. We discovered that the pre-apoptotic translocation of intracellular calreticulin (endo-CRT) to the plasma membrane surface (ecto-CRT) is critical for the recognition and engulfment of dying tumor cells by dendritic cells. Thus, anthracyclines and gamma-irradiation that induce ecto-CRT cause immunogenic cell death, while other pro-apoptotic agents (such as mitomycin C and etoposide) induce neither ecto-CRT nor immunogenic cell death. Depletion of CRT abolishes the immunogenicity of cell death elicited by anthracyclines, while exogenous supply of CRT or enforcement of CRT exposure by pharmacological agents that favor CRT translocation can enhance the immunogenicity of cell death. For optimal anti-tumor vaccination and immunogenic chemotherapy, the same cells have to expose ecto-CRT and to succumb to apoptosis; if these events affect different cells, no anti-tumor immune response is elicited. These results may have far reaching implications for tumor immunology because (i) ecto-CRT exposure by tumor cells allows for the prediction of therapeutic outcome and because (ii) the re-establishment of ecto-CRT may ameliorate the efficacy of chemotherapy.

Mots-clé
Animals, Anthracyclines/therapeutic use, Apoptosis/immunology, Calreticulin/antagonists & inhibitors, Calreticulin/metabolism, Calreticulin/therapeutic use, Cell Membrane/chemistry, Cell Membrane/metabolism, Humans, Mice, Neoplasms/drug therapy, Neoplasms/immunology, Protein Transport, Vaccination
Pubmed
Web of science
Création de la notice
13/09/2017 17:32
Dernière modification de la notice
20/08/2019 14:31
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