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3 results on '"Immunité et cancer ( U932 )"'

1. BTG1 inactivation drives lymphomagenesis and promotes lymphoma dissemination through activation of BCAR1

Author

Lorric Delage, Mireille Lambert, Émilie Bardel, Cindy Kundlacz, Dimitri Chartoire, Axel Conchon, Anne-Laure Peugnet, Lucas Gorka, Patrick Auberger, Arnaud Jacquel, Carole Soussain, Olivier Destaing, Henri-Jacques Delecluse, Susanne Delecluse, Samir Merabet, Alexandra Traverse-Glehen, Gilles Salles, Emmanuel Bachy, Marc Billaud, Hervé Ghesquières, Laurent Genestier, Jean-Pierre Rouault, Pierre Sujobert, Institut Cochin (IC UM3 (UMR 8104 / U1016)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon, Hospices Civils de Lyon (HCL), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Virologie UMR1161 (VIRO), École nationale vétérinaire - Alfort (ENVA)-Laboratoire de santé animale, sites de Maisons-Alfort et de Dozulé, Agence nationale de sécurité sanitaire de l'alimentation, de l'environnement et du travail (ANSES)-Agence nationale de sécurité sanitaire de l'alimentation, de l'environnement et du travail (ANSES)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Institut de Génomique Fonctionnelle de Lyon (IGFL), École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), C3M U1065, Institut National de la Santé et de la Recherche Médicale (INSERM), Centre méditerranéen de médecine moléculaire (C3M), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA), Immunité et cancer (U932), Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Curie [Paris], Institute for Advanced Biosciences / Institut pour l'Avancée des Biosciences (Grenoble) (IAB), Centre Hospitalier Universitaire [Grenoble] (CHU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang - Auvergne-Rhône-Alpes (EFS)-Centre National de la Recherche Scientifique (CNRS)-Université Grenoble Alpes (UGA), Unit F100 [Heidelberg, Allemagne], German Cancer Research Center - Deutsches Krebsforschungszentrum [Heidelberg] (DKFZ), Faculty of Biosciences [Heidelberg, Allemagne], Heidelberg University, Microbiology and infectious diseases, German Cancer Research Center - Deutsches Krebsforschungszentrum [Heidelberg] (DKFZ)-Institut National de la Santé et de la Recherche Médicale (INSERM), German Center for Infection Research - partner site Hannover-Braunschweig (DZIF), CNRS, UMR5242, Inst Genom Fonctionnelle Lyon,Ecole Normale Super, Weill Medical College of Cornell University [New York], Franche-Comté Électronique Mécanique, Thermique et Optique - Sciences et Technologies (UMR 6174) (FEMTO-ST), Université de Technologie de Belfort-Montbeliard (UTBM)-Ecole Nationale Supérieure de Mécanique et des Microtechniques (ENSMM)-Centre National de la Recherche Scientifique (CNRS)-Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Génétique moléculaire, signalisation et cancer (GMSC), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), and Centre Hospitalier Lyon Sud [CHU - HCL] (CHLS)

Subjects
[SDV]Life Sciences [q-bio], Immunology, Cell Biology, Hematology, Biochemistry
Abstract

Understanding the functional role of mutated genes in cancer is required to translate the findings of cancer genomics into therapeutic improvement. BTG1 is recurrently mutated in the MCD/C5 subtype of diffuse large B-cell lymphoma (DLBCL), which is associated with extranodal dissemination. Here, we provide evidence that Btg1 knock out accelerates the development of a lethal lymphoproliferative disease driven by Bcl2 overexpression. Furthermore, we show that the scaffolding protein BCAR1 is a BTG1 partner. Moreover, after BTG1 deletion or expression of BTG1 mutations observed in patients with DLBCL, the overactivation of the BCAR1-RAC1 pathway confers increased migration ability in vitro and in vivo. These modifications are targetable with the SRC inhibitor dasatinib, which opens novel therapeutic opportunities in BTG1 mutated DLBCL.

Published
2022

2. Toll-like receptor control of glucocorticoid-induced apoptosis in human plasmacytoid predendritic cells (pDCs)

Author

Françoise Raynaud, Vassili Soumelis, Yong-Jun Liu, Réda Hadj-Slimane, Raphaël Zollinger, Yves Lepelletier, Cristina Ghirelli, Antonio Cappuccio, Olivier Hermine, Immunité et cancer (U932), Université Paris Descartes - Paris 5 (UPD5)-Institut Curie-Institut National de la Santé et de la Recherche Médicale (INSERM), Pharmacochimie Moléculaire et Cellulaire (PMC - UMR_S 648), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Descartes - Paris 5 (UPD5), Cancer et génôme: Bioinformatique, biostatistiques et épidémiologie d'un système complexe, MINES ParisTech - École nationale supérieure des mines de Paris-Institut Curie-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Descartes - Faculté de Médecine (UPD5 Médecine), Université Paris Descartes - Paris 5 (UPD5), The University of Texas M.D. Anderson Cancer Center [Houston], R.Z. was supported by the European Community Sixth Framework Program (grant EXT 014162 to V.S.) and by a fellowship from the Fondation pour la Recherche Médicale (FRM). C.G. was supported by a fellowship from Association pour la Recherche contre le Cancer (ARC). A.C. was supported by a grant from Agence National pour la Recherche (ANR). Y.L. is the recipient of a grant from Association pour la Recherche contre le Cancer., We thank Zofia Maciorowski and Annick Viguier for cell sorting, and Dr J. A. Ribeil (Department of Biotherapy, Hospital Necker-Enfants Malades) for providing us with blood samples., Université Paris Descartes - Paris 5 (UPD5)-Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Cancer et génome: Bioinformatique, biostatistiques et épidémiologie d'un système complexe, Institut Curie [Paris]-MINES ParisTech - École nationale supérieure des mines de Paris, Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM), Cytokines, hématopoïèse et réponse immune (CHRI), Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS), Department of Immunology (FONDATION OSWALDO CRUZ), Fundação Oswaldo Cruz (FIOCRUZ), and Réseau International des Instituts Pasteur (RIIP) - Fundação Oswaldo Cruz (FIOCRUZ) - Réseau International des Instituts Pasteur (RIIP) - Fundação Oswaldo Cruz (FIOCRUZ)

Subjects
Small interfering RNA, [SDV]Life Sciences [q-bio], Immunology, CASP8 and FADD-Like Apoptosis Regulating Protein, Apoptosis, [SDV.CAN]Life Sciences [q-bio]/Cancer, Biology, Caspase 8, Biochemistry, CFLAR, 03 medical and health sciences, 0302 clinical medicine, Immunity, Humans, Autocrine signalling, Glucocorticoids, ComputingMilieux_MISCELLANEOUS, Cells, Cultured, 030304 developmental biology, 0303 health sciences, Toll-like receptor, Innate immune system, Tumor Necrosis Factor-alpha, Toll-Like Receptors, Interferon-alpha, [SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/Hematology, Dendritic Cells, Cell Biology, Hematology, Cell biology, [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology, Proto-Oncogene Proteins c-bcl-2, Toll-Like Receptor 7, Toll-Like Receptor 9, Tumor necrosis factor alpha, 030215 immunology
Abstract

Microbial infection triggers the endogenous production of immunosuppressive glucocorticoid (GC) hormones and simultaneously activates innate immunity through toll-like receptors (TLRs). How innate immune cells integrate these 2 opposing signals in dictating immunity or tolerance to infection is not known. In this study, we show that human plasmacytoid predendritic cells (pDCs) were highly sensitive to GC-induced apoptosis. Strikingly, they were protected by microbial stimulation through TLR-7 and TLR-9, but not by microbial-independent stimuli, such as interleukin-3, granulocyte macrophage colony-stimulating factor, or CD40-ligand. This protection was dependent on TLR-induced autocrine tumor necrosis factor-α and interferon-α, which collectively increased the expression ratio between antiapoptotic genes (Bcl-2, Bcl-xL, BIRC3, CFLAR) versus proapoptotic genes (Caspase-8, BID, BAD, BAX). In particular, virus-induced Bcl-2 up-regulation was dependent on autocrine interferon-α. Using small interfering RNA technology, we demonstrated that Bcl-2 and CFLAR/c-flip were essential for TLR-induced protection of pDCs from GC-induced caspase-8–mediated apoptosis. Our results demonstrate a novel property of the TLR pathway in regulating the interface between GC and innate immunity and reveal a previously undescribed mechanism of GC resistance.

Published
2010

3. Free HTLV-1 induces TLR7-dependent innate immune response and TRAIL relocalization in killer plasmacytoid dendritic cells

Author

Françoise Raynaud, Yves Lepelletier, Olivier Hermine, Réda Hadj-Slimane, Christophe Gras, Claudine Pique, Jean-Philippe Herbeuval, Lucie Barblu, Renaud Colisson, Cytokines, hématopoïèse et réponse immune (CHRI), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Immunité et cancer (U932), Université Paris Descartes - Paris 5 (UPD5)-Institut Curie-Institut National de la Santé et de la Recherche Médicale (INSERM), Pharmacochimie Moléculaire et Cellulaire (PMC - UMR_S 648), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Descartes - Paris 5 (UPD5), Institut Cochin (UMR_S567 / UMR 8104), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5), We also thank the Agence Nationale de la Recherche sur le SIDA (ANRS) for its financial support., We thank Gene Shearer (Experimental Immunology Branch, National Cancer Institute, National Institutes of Health) for comments and manuscript critiques. We greatly acknowledge the Nikon Imaging Center@curie.fr (Institut Curie-CNRS, http://nimce.curie.fr) and the PICT-IBiSA Imaging Facility (http://pict-ibisa.curie.fr)., Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS), Department of Immunology (FONDATION OSWALDO CRUZ), Fundação Oswaldo Cruz (FIOCRUZ), Réseau International des Instituts Pasteur (RIIP) - Fundação Oswaldo Cruz (FIOCRUZ) - Réseau International des Instituts Pasteur (RIIP) - Fundação Oswaldo Cruz (FIOCRUZ), and Université Paris Descartes - Paris 5 (UPD5)-Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Cytotoxicity, Immunologic, [SDV]Life Sciences [q-bio], viruses, Plasmacytoid dendritic cell, MESH: Dendritic Cells/virology, Biochemistry, immune response, TNF-Related Apoptosis-Inducing Ligand, chloroquine, 0302 clinical medicine, MESH: Cell-Free System, MESH: Cytotoxicity, Immunologic, ComputingMilieux_MISCELLANEOUS, Microscopy, 0303 health sciences, virus diseases, hemic and immune systems, Hematology, MESH: Immunity, Innate/immunology, 3. Good health, Cell biology, Protein Transport, Phenotype, Tumor necrosis factor alpha, MESH: Protein Transport, MESH: Microscopy, Immunology, Biology, MESH: Phenotype, Virus, MESH: TNF-Related Apoptosis-Inducing Ligand/metabolism, Interferon-gamma, 03 medical and health sciences, Immune system, Humans, human t-lymphotropic virus 1, dendritic cells, Antigen-presenting cell, 030304 developmental biology, MESH: Humans, Innate immune system, Cell-Free System, Virion, Cell Biology, Dendritic cell, TLR7, MESH: Virion/immunology, Immunity, Innate, Toll-Like Receptor 7, MESH: Interferon-gamma/biosynthesis, MESH: Toll-Like Receptor 7/immunology, MESH: Human T-lymphotropic virus 1/immunology, MESH: Dendritic Cells/immunology, 030215 immunology
Abstract

A recent report demonstrated that free human T-cell leukemia virus 1 (HTLV-1) could infect plasmacytoid dendritic cells (pDCs). The major role of pDCs is to secrete massive levels of interferon-α (IFN-α) upon virus exposure; however, the induction of IFN-α by HTLV-1 remains unknown. We demonstrate here that cell-free HTLV-1 generated a pDC innate immune response by producing massive levels of IFN-α that were inhibited by anti–HTLV-1 antibodies. HTLV-1 induced costimulatory molecules and rapid expression of the apoptotic ligand tumor necrosis factor–related apoptosis-inducing ligand (TRAIL). Furthermore, HTLV-1 stimulated pDC-induced apoptosis of CD4+ T cells expressing DR5, transforming pDCs into IFN-producing killer pDCs. We also observed that an endosomal acidification inhibitor and a Toll-like receptor-7 (TLR7)–specific blocker drastically inhibited pDC response to HTLV-1. Three-dimensional microscopy analysis revealed that unstimulated pDCs were “dormant” IFN-producing killer pDCs with high levels of intracellular TRAIL that could be rapidly mobilized to the surface in response to TLR7 activation. Inhibition of viral degradation in endosomes by chloroquine maintained viral integrity, allowing virus detection by 3-dimensional microscopy. We demonstrate that pDCs respond to cell-free HTLV-1 by producing high levels of IFN-α and by mobilizing TRAIL on cell surface after TLR7 triggering. This is the first demonstration of an innate immune response induced by free HTLV-1.

Published
2010

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