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3. Autoimmunity affecting the biliary tract fuels the immunosurveillance of cholangiocarcinoma

Author

Paillet, Juliette, Plantureux, Céleste, Lévesque, Sarah, Le Naour, Julie, Stoll, Gautier, Sauvat, Allan, Caudana, Pamela, Boari, Jimena Tosello, Bloy, Norma, Lachkar, Sylvie, Martins, Isabelle, Opolon, Paule, Checcoli, Andrea, Delaune, Agathe, Robil, Noémie, de la Grange, Pierre, Hamroune, Juliette, Letourneur, Franck, Autret, Gwennhael, Leung, Patrick SC, Gershwin, M Eric, Zhu, Jie S, Kurth, Mark J, Lekbaby, Bouchra, Augustin, Jérémy, Kim, Youra, Gujar, Shashi, Coulouarn, Cédric, Fouassier, Laura, Zitvogel, Laurence, Piaggio, Eliane, Housset, Chantal, Soussan, Patrick, Maiuri, Maria Chiara, Kroemer, Guido, and Pol, Jonathan G

Subjects
Rare Diseases, Autoimmune Disease, Liver Disease, Chronic Liver Disease and Cirrhosis, Digestive Diseases, Biotechnology, Cancer, Digestive Diseases - (Gallbladder), Liver Cancer, Aetiology, 2.1 Biological and endogenous factors, Animals, Autoimmunity, Bile Duct Neoplasms, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Cell Line, Tumor, Cholangiocarcinoma, Cholangitis, Cytokines, Female, Forkhead Transcription Factors, Liver, Mice, Inbred C57BL, Monitoring, Immunologic, Neoplasms, Experimental, Medical and Health Sciences, Immunology
Abstract

Cholangiocarcinoma (CCA) results from the malignant transformation of cholangiocytes. Primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) are chronic diseases in which cholangiocytes are primarily damaged. Although PSC is an inflammatory condition predisposing to CCA, CCA is almost never found in the autoimmune context of PBC. Here, we hypothesized that PBC might favor CCA immunosurveillance. In preclinical murine models of cholangitis challenged with syngeneic CCA, PBC (but not PSC) reduced the frequency of CCA development and delayed tumor growth kinetics. This PBC-related effect appeared specific to CCA as it was not observed against other cancers, including hepatocellular carcinoma. The protective effect of PBC was relying on type 1 and type 2 T cell responses and, to a lesser extent, on B cells. Single-cell TCR/RNA sequencing revealed the existence of TCR clonotypes shared between the liver and CCA tumor of a PBC host. Altogether, these results evidence a mechanistic overlapping between autoimmunity and cancer immunosurveillance in the biliary tract.

Published
2021

4. Chemotherapy-induced ileal crypt apoptosis and the ileal microbiome shape immunosurveillance and prognosis of proximal colon cancer

Author

Roberti, Maria Paula, Yonekura, Satoru, Duong, Connie P. M., Picard, Marion, Ferrere, Gladys, Tidjani Alou, Maryam, Rauber, Conrad, Iebba, Valerio, Lehmann, Christian H. K., Amon, Lukas, Dudziak, Diana, Derosa, Lisa, Routy, Bertrand, Flament, Caroline, Richard, Corentin, Daillère, Romain, Fluckiger, Aurélie, Van Seuningen, Isabelle, Chamaillard, Mathias, Vincent, Audrey, Kourula, Stephanie, Opolon, Paule, Ly, Pierre, Pizzato, Eugénie, Becharef, Sonia, Paillet, Juliette, Klein, Christophe, Marliot, Florence, Pietrantonio, Filippo, Benoist, Stéphane, Scoazec, Jean-Yves, Dartigues, Peggy, Hollebecque, Antoine, Malka, David, Pagès, Franck, Galon, Jérôme, Gomperts Boneca, Ivo, Lepage, Patricia, Ryffel, Bernard, Raoult, Didier, Eggermont, Alexander, Vanden Berghe, Tom, Ghiringhelli, François, Vandenabeele, Peter, Kroemer, Guido, and Zitvogel, Laurence

Published
2020
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5. P1403: SI101-01 PHASE I/II STUDY EVALUATING SAFETY AND EFFICACY OF ALLOGENEIC SMART101 T-LYMPHOID PROGENITOR INJECTION TO ACCELERATE IMMUNE RECONSTITUTION AFTER T-CELL DEPLETED ALLOGENEIC HSCT

Author

Jan Boelens, Jaap, primary, Umair Mushtaq, Muhammad, additional, Mcguirk, Joseph, additional, Bauquet, Aurelie, additional, Simons, Laura, additional, Heimendinger, Pierre, additional, Gaudeaux, Pierre, additional, Andre, Isabelle, additional, Paillet, Juliette, additional, Negre, Olivier, additional, Soheili, Tayebeh-Shabi, additional, Oster, Sebastien, additional, van den Brink, Marcel R.M., additional, Lehmann, Frederic, additional, Cavazzana, Marina, additional, and Perales, Miguel-Angel, additional

Published
2023
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6. P1257: SMART101 DONOR T-LYMPHOID PROGENITORS TO ACCELERATE IMMUNE RECONSTITUTION POST-HAPLOIDENTICAL PERIPHERAL BLOOD STEM CELL TRANSPLANTATION WITH POST-TRANSPLANT CYCLOPHOSPHAMIDE: SI101-02 PHASE I/II

Author

Ciceri, Fabio, primary, Peffault de Latour, Régis, additional, Devillier, Raynier, additional, Chiusolo, Patrizia, additional, Bauquet, Aurelie, additional, Simons, Laura, additional, Heimendinger, Pierre, additional, Gaudeaux, Pierre, additional, Negre, Olivier, additional, Soheili, Tayebeh-Shabi, additional, Paillet, Juliette, additional, Andre, Isabelle, additional, Oster, Sebastien, additional, Cavazzana, Marina, additional, and Lehmann, Frederic, additional

Published
2023
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7. Formyl peptide receptor-1 (FPR1) represses intestinal oncogenesis

Author

Le Naour, Julie, primary, Montégut, Léa, additional, Pan, Yuhong, additional, Scuderi, Sarah Adriana, additional, Cordier, Pierre, additional, Joseph, Adrien, additional, Sauvat, Allan, additional, Iebba, Valerio, additional, Paillet, Juliette, additional, Ferrere, Gladys, additional, Brechard, Ludivine, additional, Mulot, Claire, additional, Dubourg, Grégory, additional, Zitvogel, Laurence, additional, Pol, Jonathan G., additional, Vacchelli, Erika, additional, Puig, Pierre-Laurent, additional, and Kroemer, Guido, additional

Published
2023
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8. New hormone receptor-positive breast cancer mouse cell line mimicking the immune microenvironment of anti-PD-1 resistant mammary carcinoma

Author

Perez-Lanzon, Maria, primary, Carbonnier, Vincent, additional, Cordier, Pierre, additional, De Palma, Fatima Domenica Elisa, additional, Petrazzuolo, Adriana, additional, Klein, Christophe, additional, Arbaretaz, Floriane, additional, Mangane, Khady, additional, Stoll, Gautier, additional, Martins, Isabelle, additional, Fohrer Ting, Helene, additional, Paillet, Juliette, additional, Mouillet-Richard, Sophie, additional, Le Corre, Delphine, additional, Xiao, Wenjjin, additional, Sroussi, Marine, additional, Desdouets, Chantal, additional, Laurent-Puig, Pierre, additional, Pol, Jonathan, additional, Lopez-Otin, Carlos, additional, Maiuri, Maria Chiara, additional, and Kroemer, Guido, additional

Published
2023
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10. Table S4 from A TLR3 Ligand Reestablishes Chemotherapeutic Responses in the Context of FPR1 Deficiency

Author

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

Published
2023
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11. Supplementary Figures and Tables from A TLR3 Ligand Reestablishes Chemotherapeutic Responses in the Context of FPR1 Deficiency

Author

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

Published
2023
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12. Data from A TLR3 Ligand Reestablishes Chemotherapeutic Responses in the Context of FPR1 Deficiency

Author

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

Published
2023
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14. SMART101 Donor T-Lymphoid Progenitors to Accelerate Immune Reconstitution Post-Haploidentical Peripheral Blood Stem Cell Transplantation with Post-Transplant Cyclophosphamide: SI101-02 First-in-Human Phase I/II

Author

Devillier, Raynier, Peffault De Latour, Regis, Chevallier, Patrice, Huynh, Anne, Chiusolo, Patrizia, Bauquet, Aurelie, Simons, Laura, Heimendinger, Pierre, Negre, Olivier, Soheili, Shabi, Paillet, Juliette, Andre, Isabelle, Oster, Sebastien, Cavazzana, Marina, Lehmann, Frédéric François, and Ciceri, Fabio

Published
2023
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16. The Link between Autoimmunity and Cancer Immunosurveillance in the Context of Cholangitis and Cholangiocarcinoma

Author

Paillet, Juliette, Métabolisme, cancer et immunité = Metabolism, Cancer & Immunity [CRC] (Equipe labellisée Ligue contre le cancer), Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité), Université Paris-Saclay, Guido Kroemer, and STAR, ABES

Subjects
Cholangiocarcinoma, Anti-Tumor immunity, Cholangite, [SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunology, [SDV.CAN] Life Sciences [q-bio]/Cancer, Cholangitis, Cholangiocarcinome, Auto-Immunité, [SDV.IMM.IA] Life Sciences [q-bio]/Immunology/Adaptive immunology, Immunosurveillance, Autoimmunity, [SDV.CAN]Life Sciences [q-bio]/Cancer, Immunité anti-Tumorale
Abstract

Bile duct cancer or cholangiocarcinoma (CCA) is the second most common primary liver tumor. The arsenal of treatments for CCA is highly limited due to the resistance to standard chemoradiotherapies and to the low resection efficiency. Chronic inflammation is a well-known risk factor for cancer development, and two chronic inflammatory diseases of the bile ducts are characterized: primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC). Hence, PSC is the 1st etiology established of CCA in Western countries. In contrast, patients with PBC never develop CCA. Based on this observation, we hypothesized that PBC- associated autoimmunity would fuel CCA immunosurveillance and protect the patients from its emergence. In our mouse models, we observed that PBC reduced the frequency of tumor onset and delayed the tumor growth kinetic. Conversely, PSC did not impact the progression of the CCA. We demonstrated that this protection was CCA-specific and did not have any effects on others tumor histotypes. It was also dependent on CD4+ and CD8+ T lymphocytes, B cells, and especially dependent on the IFNγ-mediated response. Altogether, these results evidence a mechanistic overlapping between autoimmunity and cancer immunosurveillance, with autoimmune reactions against organ-specific self-antigens contributing to the elimination of malignant cells originating from the same tissue., Le cancer des voies biliaires ou cholangiocarcinome (CC) est le 2è cancer hépatique primaire le plus fréquent. L'arsenal des traitements contre le CC est extrêmement limité en raison de la résistance aux chimioradiothérapies standardes et la faible efficacité de la résection chirurgicale. L'inflammation chronique est un facteur de risque reconnu pour le développement du cancer et deux maladies inflammatoires chroniques des voies biliaires sont caractérisées : la cholangite sclérosante primitive (CSP) et la cholangite biliaire primitive (CBP). Dans cette ligne, la CSP est la 1è étiologie du CC dans les pays occidentaux. En revanche, les patients atteints de CBP ne développent jamais de CC. De cette observation, nous avons émis l’hypothèse que l’autoimmunité associée à la CBP alimenterait l’immunosurveillance du CC et protégerait les patients de son émergence. Dans nos modèles murins, nous avons pu observer que la CBP réduisait la fréquence de développement de tumeurs et retardait la cinétique de croissance tumorale. A l'inverse, la CSP n’impactait pas la progression du CC. Nous avons également mis en évidence que cette protection était spécifique du CC et sans effet contre d’autres histotype de tumeur ; qu’elle était dépendante des lymphocytes T CD4+ et CD8+, des lymphocytes B, et en particulier dépendante de la réponse médiée par l’IFNγ. Dans l'ensemble, ces résultats appuient la possibilité que des réactions auto-immunes contre un autoantigène spécifique d'un tissu, contribuent à l'immunosurveillance des cellules malignes de ce même tissu.

Published
2020

17. Le lien entre auto-immunité et immunosurveillance des cancers dans le cas des cholangites et du cholangiocarcinome

Author

Paillet, Juliette, Métabolisme, cancer et immunité = Metabolism, Cancer & Immunity [CRC] (Equipe labellisée Ligue contre le cancer), Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université de Paris (UP)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université de Paris (UP), Université Paris-Saclay, and Guido Kroemer

Subjects
Cholangiocarcinoma, Anti-Tumor immunity, Cholangite, [SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunology, Cholangitis, Cholangiocarcinome, Auto-Immunité, Immunosurveillance, Autoimmunity, [SDV.CAN]Life Sciences [q-bio]/Cancer, Immunité anti-Tumorale
Abstract

Bile duct cancer or cholangiocarcinoma (CCA) is the second most common primary liver tumor. The arsenal of treatments for CCA is highly limited due to the resistance to standard chemoradiotherapies and to the low resection efficiency. Chronic inflammation is a well-known risk factor for cancer development, and two chronic inflammatory diseases of the bile ducts are characterized: primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC). Hence, PSC is the 1st etiology established of CCA in Western countries. In contrast, patients with PBC never develop CCA. Based on this observation, we hypothesized that PBC- associated autoimmunity would fuel CCA immunosurveillance and protect the patients from its emergence. In our mouse models, we observed that PBC reduced the frequency of tumor onset and delayed the tumor growth kinetic. Conversely, PSC did not impact the progression of the CCA. We demonstrated that this protection was CCA-specific and did not have any effects on others tumor histotypes. It was also dependent on CD4+ and CD8+ T lymphocytes, B cells, and especially dependent on the IFNγ-mediated response. Altogether, these results evidence a mechanistic overlapping between autoimmunity and cancer immunosurveillance, with autoimmune reactions against organ-specific self-antigens contributing to the elimination of malignant cells originating from the same tissue.; Le cancer des voies biliaires ou cholangiocarcinome (CC) est le 2è cancer hépatique primaire le plus fréquent. L'arsenal des traitements contre le CC est extrêmement limité en raison de la résistance aux chimioradiothérapies standardes et la faible efficacité de la résection chirurgicale. L'inflammation chronique est un facteur de risque reconnu pour le développement du cancer et deux maladies inflammatoires chroniques des voies biliaires sont caractérisées : la cholangite sclérosante primitive (CSP) et la cholangite biliaire primitive (CBP). Dans cette ligne, la CSP est la 1è étiologie du CC dans les pays occidentaux. En revanche, les patients atteints de CBP ne développent jamais de CC. De cette observation, nous avons émis l’hypothèse que l’autoimmunité associée à la CBP alimenterait l’immunosurveillance du CC et protégerait les patients de son émergence. Dans nos modèles murins, nous avons pu observer que la CBP réduisait la fréquence de développement de tumeurs et retardait la cinétique de croissance tumorale. A l'inverse, la CSP n’impactait pas la progression du CC. Nous avons également mis en évidence que cette protection était spécifique du CC et sans effet contre d’autres histotype de tumeur ; qu’elle était dépendante des lymphocytes T CD4+ et CD8+, des lymphocytes B, et en particulier dépendante de la réponse médiée par l’IFNγ. Dans l'ensemble, ces résultats appuient la possibilité que des réactions auto-immunes contre un autoantigène spécifique d'un tissu, contribuent à l'immunosurveillance des cellules malignes de ce même tissu.

Published
2020

18. A TLR3 Ligand Reestablishes Chemotherapeutic Responses in the Context of FPR1 Deficiency

Author

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

Published
2021
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20. Inhibition of transcription by dactinomycin reveals a new characteristic of immunogenic cell stress

Author

Humeau, Juliette, primary, Sauvat, Allan, additional, Cerrato, Giulia, additional, Xie, Wei, additional, Loos, Friedemann, additional, Iannantuoni, Francesca, additional, Bezu, Lucillia, additional, Lévesque, Sarah, additional, Paillet, Juliette, additional, Pol, Jonathan, additional, Leduc, Marion, additional, Zitvogel, Laurence, additional, de Thé, Hugues, additional, Kepp, Oliver, additional, and Kroemer, Guido, additional

Published
2020
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21. A synergistic triad of chemotherapy, immune checkpoint inhibitors, and caloric restriction mimetics eradicates tumors in mice

Author

Lévesque, Sarah, Le Naour, Julie, Pietrocola, Federico, Paillet, Juliette, Kremer, Margerie, Castoldi, Francesca, Baracco, Elisa E., Wang, Yan, Vacchelli, Erika, Stoll, Gautier, Jolly, Ariane, De La Grange, Pierre, Zitvogel, Laurence, Kroemer, Guido, Pol, Jonathan G., Institut Gustave Roussy (IGR), Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Université de Paris (UP), AP-HP Hôpital Bicêtre (Le Kremlin-Bicêtre), Immunologie des tumeurs et immunothérapie (UMR 1015), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d’Investigation Clinique en Biothérapies [CHU Pitié-Salpêtrière] (CIC-BT), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Service de biologie [CHU HEGP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Karolinska University Hospital [Stockholm], Université Paris Cité (UPCité), Centre d'investigation clinique Biothérapie [CHU Pitié-Salpêtrière] (CIC-BTi), Centre d'investigation clinique pluridisciplinaire [CHU Pitié Salpêtrière] (CIC-P 1421), Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), and Gestionnaire, Hal Sorbonne Université

Subjects
lcsh:Immunologic diseases. Allergy, [SDV.CAN]Life Sciences [q-bio]/Cancer, [SDV.IMM.IMM]Life Sciences [q-bio]/Immunology/Immunotherapy, chemotherapy, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, lcsh:RC254-282, immune checkpoint blockers, [SDV.CAN] Life Sciences [q-bio]/Cancer, tumor immune infiltrate, [SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology, [SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology, [SDV.IMM.IMM] Life Sciences [q-bio]/Immunology/Immunotherapy, combination therapies, lcsh:RC581-607, caloric restriction mimetics, Original Research
Abstract

International audience; We have recently shown that chemotherapy with immunogenic cell death (ICD)-inducing agents can be advantageously combined with fasting regimens or caloric restriction mimetics (CRMs) to achieve superior tumor growth control via a T cell-dependent mechanism. Here, we show that the blockade of the CD11b-dependent extravasation of myeloid cells blocks such a combination effect as well. Based on the characterization of the myeloid and lymphoid immune infiltrates, including the expression pattern of immune checkpoint proteins (and noting a chemotherapy-induced overexpression of programmed death-ligand 1, PD-L1, on both cancer cells and leukocytes, as well as a reduced frequency of exhausted CD8+ T cells positive for programmed cell death 1 protein, PD-1), we then evaluated the possibility to combine ICD inducers, CRMs and targeting of the PD-1/PD-L1 interaction. While fasting or CRMs failed to improve tumor growth control by PD-1 blockade, ICD inducers alone achieved a partial sensitization to treatment with a PD-1-specific antibody. However, definitive cure of most of the tumor-bearing mice was only achieved by a tritherapy combining (i) ICD inducers exemplified by mitoxantrone and oxaliplatin, (ii) CRMs exemplified by hydroxycitrate and spermidine and substitutable for by fasting, and (iii) immune checkpoint inhibitors (ICIs) targeting the PD-1/PD-L1 interaction. Altogether, these results point to the possibility of synergistic interactions among distinct classes of anticancer agents.

Published
2019

24. Effects of interleukin-2 in immunostimulation and immunosuppression

Author

Pol, Jonathan G., Caudana, Pamela, Paillet, Juliette, Piaggio, Eliane, and Kroemer, Guido

Abstract

Historically, interleukin-2 (IL-2) was first described as an immunostimulatory factor that supports the expansion of activated effector T cells. A layer of sophistication arose when regulatory CD4+ T lymphocytes (Tregs) were shown to require IL-2 for their development, homeostasis, and immunosuppressive functions. Fundamental distinctions in the nature and spatiotemporal expression patterns of IL-2 receptor subunits on naive/memory/effector T cells versus Tregs are now being exploited to manipulate the immunomodulatory effects of IL-2 for therapeutic purposes. Although high-dose IL-2 administration has yielded discrete clinical responses, low-dose IL-2 as well as innovative strategies based on IL-2 derivatives, including “muteins,” immunocomplexes, and immunocytokines, are being explored to therapeutically enhance or inhibit the immune response.

Published
2020
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25. A TLR3 Ligand Reestablishes Chemotherapeutic Responses in the Context of FPR1 Deficiency

Author

Francesca Castoldi, Maria Chiara Maiuri, Julie Le Naour, Julien Taieb, Allan Sauvat, Suzette Delaloge, Charles-Antoine Dutertre, Jessica Zucman-Rossi, Juliette Paillet, Erika Vacchelli, Liwei Zhao, Giulia Cerrato, Guido Kroemer, Claire Mulot, Isabelle Martins, Oliver Kepp, Federico Pietrocola, Pierre Laurent-Puig, Aymeric Silvin, Florent Ginhoux, Fabrice Andre, Peng Liu, Laurence Zitvogel, Sandy Adjemian, Cornelia Richter, Zoltan Szallasi, Peter Vandenabeele, Zsofia Sztupinszki, Jonathan Pol, Gautier Stoll, Khady Mangane, Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité), Institut Gustave Roussy (IGR), Institut Universitaire de France (IUF), Ministère de l'Education nationale, de l’Enseignement supérieur et de la Recherche (M.E.N.E.S.R.), Universidade de São Paulo = University of São Paulo (USP), Boston Children's Hospital, Harvard Medical School [Boston] (HMS), Cancer Research and Personalized Medicine - CARPEM [Paris], Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Immunologie des tumeurs et immunothérapie (UMR 1015), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Agency for science, technology and research [Singapore] (A*STAR), Singapore Immunology Network (SIgN), Biomedical Sciences Institute (BMSI), School of Medicine [Shanghai Jiaotong University], Shanghai Jiaotong University, Métabolisme, Cancer et Immunité (CRC - UMR_S 1138), Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité)-Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité)-École Pratique des Hautes Études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), University of Oslo (UiO), Direction de la recherche [Gustave Roussy], Département de médecine oncologique [Gustave Roussy], Pathologie mammaire, Institut Gustave Roussy (IGR)-Institut Gustave Roussy (IGR), Immunologie anti-tumorale et immunothérapie des cancers (ITIC), Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, ANR-16-RHUS-0008,LUMIERE,LUMIERE(2016), European Project: 825410,ONCOBIOME, Le Naour, Julie, Liu, Peng, Zhao, Liwei, Adjemian, Sandy, Sztupinszki, Zsofia, Taieb, Julien, Mulot, Claire, Silvin, Aymeric, Dutertre, Charles-Antoine, Ginhoux, Florent, Sauvat, Allan, Cerrato, Giulia, Castoldi, Francesca, Martins, Isabelle, Stoll, Gautier, Paillet, Juliette, Mangane, Khady, Richter, Cornelia, Kepp, Oliver, Maiuri, Maria Chiara, Pietrocola, Federico, Vandenabeele, Peter, André, Fabrice, Delaloge, Suzette, Szallasi, Zoltan, Laurent-Puig, Pierre, Zucman-Rossi, Jessica, Zitvogel, Laurence, Pol, Jonathan G, Vacchelli, Erika, Kroemer, Guido, École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPC), Universidade de São Paulo (USP), Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPC)-Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPC)-École pratique des hautes études (EPHE), and Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPC)

Subjects
0301 basic medicine, Anthracycline, medicine.medical_treatment, [SDV]Life Sciences [q-bio], Mice, Transgenic, Ligands, 03 medical and health sciences, Mice, 0302 clinical medicine, Immune system, Medicine, Animals, Humans, ComputingMilieux_MISCELLANEOUS, business.industry, Pattern recognition receptor, Wild type, Immunotherapy, Receptors, Formyl Peptide, Toll-Like Receptor 3, Disease Models, Animal, 030104 developmental biology, Cell Transformation, Neoplastic, Poly I-C, Oncology, 030220 oncology & carcinogenesis, Cancer cell, TLR3, Cancer research, business, Colorectal Neoplasms, Annexin A1
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 deficient response to chemotherapy of tumors lacking ANXA1 developing in immunocompetent mice or those of normal cancers growing in FPR1-deficient mice. This effect was accompanied by improved DC- and T-lymphocyte–mediated anticancer immunity. Of note, carcinogen-induced breast cancers precociously developed in FPR1-deficient 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 findings have potential implications for the clinical management of FPR1-deficient patients. Significance: The loss-of-function variant rs867228 in FPR1, harbored by approximately 30% of the world population, is associated with the precocious manifestation of breast, colorectal, esophageal, and head and neck carcinomas. pIC restores deficient chemotherapeutic responses in mice lacking Fpr1, suggesting a personalized strategy for compensating for the FPR1 defect. This article is highlighted in the In This Issue feature, p. 211

Published
2021

26. Oncogene-Driven Induction of Orthotopic Cholangiocarcinoma in Mice.

Author

Plantureux C, Paillet J, Autret G, Pérez-Lanzón M, Kroemer G, Maiuri MC, and Pol J

Subjects
Mice, Animals, Bile Ducts, Intrahepatic, Oncogenes genetics, Liver pathology, Bile Duct Neoplasms genetics, Cholangiocarcinoma genetics
Abstract

Cholangiocarcinoma (CCA) is a malignancy affecting the epithelial cells that line the bile ducts. This cancer shows a poor prognosis and current treatments remain inefficient. Orthotopic CCA mouse models are useful for the development of innovative therapeutic strategies. Here, we describe an orthotopic model of intrahepatic CCA that can be easily induced in mice within 5 weeks at a high incidence. It is achieved by expressing two oncogenes, namely, (i) the intracellular domain of the Notch1 receptor (NICD) and (ii) AKT, in hepatocytes by means of the sleeping beauty transposon system. These plasmid vectors are delivered by hydrodynamic injection into the tail vein. The present chapter also describes how to perform magnetic resonance imaging (MRI) of the livers to visualize intrahepatic CCA nodules., (© 2024. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

Published
2024
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27. Flow Cytometry Assessment of Lymphocyte Populations Infiltrating Liver Tumors.

Author

Pérez-Lanzón M, Plantureux C, Paillet J, Sotty J, Soussan P, Kroemer G, Maiuri MC, and Pol J

Subjects
Humans, Flow Cytometry methods, Lymphocyte Subsets, Bile Ducts, Intrahepatic, Liver Neoplasms, Bile Duct Neoplasms
Abstract

Tissue-resident and recruited immune cells are essential mediators of natural and therapy-induced immunosurveillance of liver neoplasia. This idea has been recently reinforced by the clinical approval of immune checkpoint inhibitors for the immunotherapy of hepatocellular carcinoma and cholangiocarcinoma. Such research progress relies on the in-depth characterization of the immune populations that are present in pre-neoplastic and neoplastic hepatic lesions. A convenient technology for advancing along this path is high-dimensional cytometry.In this chapter, we present a protocol to assess the subtype and differentiation state of hepatic lymphocyte populations by multicolor immunofluorescence staining and flow cytometry. We detail the steps required for viability assessment and immune cell phenotyping of single-cell suspensions of liver cells by means of surface and intracellular staining of more than a dozen markers of interest. This protocol does not require prior removal of debris and dead cells and allows to process multiple samples in parallel. The procedure includes the use of a fixative-resistant viability dye that allows cell fixation and permeabilization after cell surface staining and before intracellular staining and data acquisition on a flow cytometer. Moreover, we provide a panel of fluorochrome-labeled antibodies designed for the characterization of lymphocytic subsets that can be adapted to distinct experimental settings. Finally, we present an overview of the post-staining pipeline, including data acquisition on a flow cytometer and tools for post-acquisition analyses., (© 2024. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

Published
2024
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28. A synergistic triad of chemotherapy, immune checkpoint inhibitors, and caloric restriction mimetics eradicates tumors in mice.

Author

Lévesque S, Le Naour J, Pietrocola F, Paillet J, Kremer M, Castoldi F, Baracco EE, Wang Y, Vacchelli E, Stoll G, Jolly A, De La Grange P, Zitvogel L, Kroemer G, and Pol JG

Abstract

We have recently shown that chemotherapy with immunogenic cell death (ICD)-inducing agents can be advantageously combined with fasting regimens or caloric restriction mimetics (CRMs) to achieve superior tumor growth control via a T cell-dependent mechanism. Here, we show that the blockade of the CD11b-dependent extravasation of myeloid cells blocks such a combination effect as well. Based on the characterization of the myeloid and lymphoid immune infiltrates, including the expression pattern of immune checkpoint proteins (and noting a chemotherapy-induced overexpression of programmed death-ligand 1, PD-L1, on both cancer cells and leukocytes, as well as a reduced frequency of exhausted CD8 + T cells positive for programmed cell death 1 protein, PD-1), we then evaluated the possibility to combine ICD inducers, CRMs and targeting of the PD-1/PD-L1 interaction. While fasting or CRMs failed to improve tumor growth control by PD-1 blockade, ICD inducers alone achieved a partial sensitization to treatment with a PD-1-specific antibody. However, definitive cure of most of the tumor-bearing mice was only achieved by a tritherapy combining (i) ICD inducers exemplified by mitoxantrone and oxaliplatin, (ii) CRMs exemplified by hydroxycitrate and spermidine and substitutable for by fasting, and (iii) immune checkpoint inhibitors (ICIs) targeting the PD-1/PD-L1 interaction. Altogether, these results point to the possibility of synergistic interactions among distinct classes of anticancer agents., (© 2019 The Author(s). Published with license by Taylor & Francis Group, LLC.)

Published
2019
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