A TLR3 ligand reestablishes chemotherapeutic responses in the context of FPR1 deficiency

Julie Le Naour; Peng Liu; Liwei Zhao; Sandy Adjemian; Zsofia Sztupinszki; Julien Taieb; Claire Mulot; Aymeric Silvin; Charles Antoine Dutertre; Florent Ginhoux; Allan Sauvat; Giulia Cerrato; Francesca Castoldi; Isabelle Martins; Gautier Stoll; Juliette Paillet; Khady Mangane; Cornelia Richter; Oliver Kepp; Maria Chiara Maiuri; Federico Pietrocola; Peter Vandenabeele; Fabrice André; Suzette Delaloge; Zoltan Szallasi; Pierre Laurent-Puig; Jessica Zucman-Rossi; Laurence Zitvogel; Jonathan G. Pol; Erika Vacchelli; Guido Kroemer

doi:10.1158/2159-8290.CD-20-0465

A TLR3 ligand reestablishes chemotherapeutic responses in the context of FPR1 deficiency

Julie Le Naour, Peng Liu, Liwei Zhao, Sandy Adjemian, Zsofia Sztupinszki, Julien Taieb, Claire Mulot, Aymeric Silvin, Charles Antoine Dutertre, Florent Ginhoux, Allan Sauvat, Giulia Cerrato, Francesca Castoldi, Isabelle Martins, Gautier Stoll, Juliette Paillet, Khady Mangane, Cornelia Richter, Oliver Kepp, Maria Chiara MaiuriFederico Pietrocola, Peter Vandenabeele, Fabrice André, Suzette Delaloge, Zoltan Szallasi, Pierre Laurent-Puig, Jessica Zucman-Rossi, Laurence Zitvogel, Jonathan G. Pol, Erika Vacchelli, Guido Kroemer

Résultats de recherche: Contribution à un journal › Article › Revue par des pairs

32 Citations (Scopus)

Résumé

For anthracycline-based chemotherapy to be immunogenic, dying cancer cells must release annexin A1 (ANXA1) that subsequently interacts with the pattern recognition receptor, formyl peptide receptor 1 (FPR1), on the surface of dendritic cells (DC). Approximately 30% of individuals bear loss-of-function alleles of FPR1, calling for strategies to ameliorate their anticancer immune response. Here, we show that immunotherapy with a ligand of Toll-like receptor-3, polyinosinic:polycytidylic acid (pIC), restores the defi cient response to chemotherapy of tumors lacking ANXA1 developing in immunocompetent mice or those of normal cancers growing in FPR1-defi cient mice. This effect was accompanied by improved DC- and T-lymphocyte-mediated anticancer immunity. Of note, carcinogen-induced breast cancers precociously developed in FPR1-defi cient mice as compared with wild-type controls. A similar tendency for earlier cancer development was found in patients carrying the loss-of-function allele of FPR1. These fi ndings have potential implications for the clinical management of FPR1-defi cient patients.

langue originale	Anglais
Pages (de - à)	408-423
Nombre de pages	16
journal	Cancer Discovery
Volume	11
Numéro de publication	2
Les DOIs	https://doi.org/10.1158/2159-8290.CD-20-0465
état	Publié - 1 févr. 2021

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10.1158/2159-8290.CD-20-0465

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Le Naour, J., Liu, P., Zhao, L., Adjemian, S., Sztupinszki, Z., Taieb, J., Mulot, C., Silvin, A., Dutertre, C. A., Ginhoux, F., Sauvat, A., Cerrato, G., Castoldi, F., Martins, I., Stoll, G., Paillet, J., Mangane, K., Richter, C., Kepp, O., ... Kroemer, G. (2021). A TLR3 ligand reestablishes chemotherapeutic responses in the context of FPR1 deficiency. Cancer Discovery, 11(2), 408-423. https://doi.org/10.1158/2159-8290.CD-20-0465

@article{4f2b3b7c1faa4657931db663e9ee14f7,

title = "A TLR3 ligand reestablishes chemotherapeutic responses in the context of FPR1 deficiency",

abstract = "For anthracycline-based chemotherapy to be immunogenic, dying cancer cells must release annexin A1 (ANXA1) that subsequently interacts with the pattern recognition receptor, formyl peptide receptor 1 (FPR1), on the surface of dendritic cells (DC). Approximately 30% of individuals bear loss-of-function alleles of FPR1, calling for strategies to ameliorate their anticancer immune response. Here, we show that immunotherapy with a ligand of Toll-like receptor-3, polyinosinic:polycytidylic acid (pIC), restores the defi cient response to chemotherapy of tumors lacking ANXA1 developing in immunocompetent mice or those of normal cancers growing in FPR1-defi cient mice. This effect was accompanied by improved DC- and T-lymphocyte-mediated anticancer immunity. Of note, carcinogen-induced breast cancers precociously developed in FPR1-defi cient mice as compared with wild-type controls. A similar tendency for earlier cancer development was found in patients carrying the loss-of-function allele of FPR1. These fi ndings have potential implications for the clinical management of FPR1-defi cient patients.",

author = "{Le Naour}, Julie and Peng Liu and Liwei Zhao and Sandy Adjemian and Zsofia Sztupinszki and Julien Taieb and Claire Mulot and Aymeric Silvin and Dutertre, {Charles Antoine} and Florent Ginhoux and Allan Sauvat and Giulia Cerrato and Francesca Castoldi and Isabelle Martins and Gautier Stoll and Juliette Paillet and Khady Mangane and Cornelia Richter and Oliver Kepp and Maiuri, {Maria Chiara} and Federico Pietrocola and Peter Vandenabeele and Fabrice Andr{\'e} and Suzette Delaloge and Zoltan Szallasi and Pierre Laurent-Puig and Jessica Zucman-Rossi and Laurence Zitvogel and Pol, {Jonathan G.} and Erika Vacchelli and Guido Kroemer",

note = "Publisher Copyright: {\textcopyright} 2020 American Association for Cancer Research.",

year = "2021",

month = feb,

day = "1",

doi = "10.1158/2159-8290.CD-20-0465",

language = "English",

volume = "11",

pages = "408--423",

journal = "Cancer Discovery",

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Le Naour, J, Liu, P, Zhao, L, Adjemian, S, Sztupinszki, Z, Taieb, J, Mulot, C, Silvin, A, Dutertre, CA, Ginhoux, F, Sauvat, A, Cerrato, G, Castoldi, F, Martins, I, Stoll, G, Paillet, J, Mangane, K, Richter, C, Kepp, O, Maiuri, MC, Pietrocola, F, Vandenabeele, P, André, F, Delaloge, S, Szallasi, Z, Laurent-Puig, P, Zucman-Rossi, J, Zitvogel, L, Pol, JG, Vacchelli, E & Kroemer, G 2021, 'A TLR3 ligand reestablishes chemotherapeutic responses in the context of FPR1 deficiency', Cancer Discovery, VOL. 11, Numéro 2, p. 408-423. https://doi.org/10.1158/2159-8290.CD-20-0465

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T1 - A TLR3 ligand reestablishes chemotherapeutic responses in the context of FPR1 deficiency

AU - Le Naour, Julie

AU - Liu, Peng

AU - Zhao, Liwei

AU - Adjemian, Sandy

AU - Sztupinszki, Zsofia

AU - Taieb, Julien

AU - Mulot, Claire

AU - Silvin, Aymeric

AU - Dutertre, Charles Antoine

AU - Ginhoux, Florent

AU - Sauvat, Allan

AU - Cerrato, Giulia

AU - Castoldi, Francesca

AU - Martins, Isabelle

AU - Stoll, Gautier

AU - Paillet, Juliette

AU - Mangane, Khady

AU - Richter, Cornelia

AU - Kepp, Oliver

AU - Maiuri, Maria Chiara

AU - Pietrocola, Federico

AU - Vandenabeele, Peter

AU - André, Fabrice

AU - Delaloge, Suzette

AU - Szallasi, Zoltan

AU - Laurent-Puig, Pierre

AU - Zucman-Rossi, Jessica

AU - Zitvogel, Laurence

AU - Pol, Jonathan G.

AU - Vacchelli, Erika

AU - Kroemer, Guido

PY - 2021/2/1

Y1 - 2021/2/1

N2 - For anthracycline-based chemotherapy to be immunogenic, dying cancer cells must release annexin A1 (ANXA1) that subsequently interacts with the pattern recognition receptor, formyl peptide receptor 1 (FPR1), on the surface of dendritic cells (DC). Approximately 30% of individuals bear loss-of-function alleles of FPR1, calling for strategies to ameliorate their anticancer immune response. Here, we show that immunotherapy with a ligand of Toll-like receptor-3, polyinosinic:polycytidylic acid (pIC), restores the defi cient response to chemotherapy of tumors lacking ANXA1 developing in immunocompetent mice or those of normal cancers growing in FPR1-defi cient mice. This effect was accompanied by improved DC- and T-lymphocyte-mediated anticancer immunity. Of note, carcinogen-induced breast cancers precociously developed in FPR1-defi cient mice as compared with wild-type controls. A similar tendency for earlier cancer development was found in patients carrying the loss-of-function allele of FPR1. These fi ndings have potential implications for the clinical management of FPR1-defi cient patients.

AB - For anthracycline-based chemotherapy to be immunogenic, dying cancer cells must release annexin A1 (ANXA1) that subsequently interacts with the pattern recognition receptor, formyl peptide receptor 1 (FPR1), on the surface of dendritic cells (DC). Approximately 30% of individuals bear loss-of-function alleles of FPR1, calling for strategies to ameliorate their anticancer immune response. Here, we show that immunotherapy with a ligand of Toll-like receptor-3, polyinosinic:polycytidylic acid (pIC), restores the defi cient response to chemotherapy of tumors lacking ANXA1 developing in immunocompetent mice or those of normal cancers growing in FPR1-defi cient mice. This effect was accompanied by improved DC- and T-lymphocyte-mediated anticancer immunity. Of note, carcinogen-induced breast cancers precociously developed in FPR1-defi cient mice as compared with wild-type controls. A similar tendency for earlier cancer development was found in patients carrying the loss-of-function allele of FPR1. These fi ndings have potential implications for the clinical management of FPR1-defi cient patients.

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U2 - 10.1158/2159-8290.CD-20-0465

DO - 10.1158/2159-8290.CD-20-0465

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