Cited by 202Immunotherapy and Immune ResponsesCell death mechanisms and regulationEndoplasmic Reticulum Stress and Disease

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Ecto‐calreticulin in immunogenic chemotherapy

Obeid, Michel, Tesniere, Antoine, Panaretakis, Theocharis, Tufi, Roberta, Joza, Nick, Van Endert, Peter, Ghiringhelli, François, Apetoh, Lionel, Chaput, Nathalie, Flament, Caroline, Ullrich, Evelyn, De Botton, Stéphane, Zitvogel, Laurence, Kroemer, Guido·2007·Immunological Reviews

DOI 10.1111/j.1600-065x.2007.00567.x

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Abstract

Summary: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 γ‐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.

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Authors: 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.
Affiliations: Université Paris-Sud (FR)
Corresponding author: Kroemer, Guido
ORCID: Panaretakis, Theocharis
Tufi, Roberta
Ghiringhelli, François
Chaput, Nathalie
Flament, Caroline
Ullrich, Evelyn
Zitvogel, Laurence
Kroemer, Guido
Venue: Immunological Reviews
Publisher: Wiley
Published: 2007-10-30
Volume: 220
Issue: 1
Pages: 22-34
ISSN: 0105-2896 (ISSN-L)
1600-065X
DOI: 10.1111/j.1600-065x.2007.00567.x
OpenAlex: W1984068314
Cited by: 202
References: 72
Citations by year: 2026: 3 · 2025: 3 · 2024: 5 · 2023: 8 · 2022: 6 · 2021: 17 · 2020: 12 · 2019: 14 · 2018: 12 · 2017: 11 · 2016: 15 · 2015: 11 · 2014: 6 · 2013: 13 · 2012: 8
FWCI: 1.20
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Immunological Reviews (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
Keywords: immunogenic cell death, calreticulin, dendritic cells, anthracyclines, gamma irradiation, apoptosis, tumor immunology, cancer immunotherapy, mitomycin C, etoposide
MeSH terms: Animals, Cell Membrane, Humans, Neoplasms, Vaccination, Apoptosis, Anthracyclines, Protein Transport, Calreticulin, Mice

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Ecto‐calreticulin in immunogenic chemotherapy

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