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Your search keyword '"Audrey Esclatine"' showing total 7 results
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7 results on '"Audrey Esclatine"'

1. Essential role of hyperacetylated microtubules in innate immunity escape orchestrated by the EBV-encoded BHRF1 protein.

Author

Damien Glon, Géraldine Vilmen, Daniel Perdiz, Eva Hernandez, Guillaume Beauclair, Frédérique Quignon, Clarisse Berlioz-Torrent, Vincent Maréchal, Christian Poüs, Marion Lussignol, and Audrey Esclatine

Subjects
Immunologic diseases. Allergy, RC581-607, Biology (General), QH301-705.5
Abstract

Innate immunity constitutes the first line of defense against viruses, in which mitochondria play an important role in the induction of the interferon (IFN) response. BHRF1, a multifunctional viral protein expressed during Epstein-Barr virus reactivation, modulates mitochondrial dynamics and disrupts the IFN signaling pathway. Mitochondria are mobile organelles that move through the cytoplasm thanks to the cytoskeleton and in particular the microtubule (MT) network. MTs undergo various post-translational modifications, among them tubulin acetylation. In this study, we demonstrated that BHRF1 induces MT hyperacetylation to escape innate immunity. Indeed, the expression of BHRF1 induces the clustering of shortened mitochondria next to the nucleus. This "mito-aggresome" is organized around the centrosome and its formation is MT-dependent. We also observed that the α-tubulin acetyltransferase ATAT1 interacts with BHRF1. Using ATAT1 knockdown or a non-acetylatable α-tubulin mutant, we demonstrated that this hyperacetylation is necessary for the mito-aggresome formation. Similar results were observed during EBV reactivation. We investigated the mechanism leading to the clustering of mitochondria, and we identified dyneins as motors that are required for mitochondrial clustering. Finally, we demonstrated that BHRF1 needs MT hyperacetylation to block the induction of the IFN response. Moreover, the loss of MT hyperacetylation blocks the localization of autophagosomes close to the mito-aggresome, impeding BHRF1 to initiate mitophagy, which is essential to inhibiting the signaling pathway. Therefore, our results reveal the role of the MT network, and its acetylation level, in the induction of a pro-viral mitophagy.

Published
2022
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2. Autophagic Degradation Is Involved in Cell Protection against Ricin Toxin

Author

Yu Wu, Clémence Taisne, Nassim Mahtal, Alison Forrester, Marion Lussignol, Jean-Christophe Cintrat, Audrey Esclatine, Daniel Gillet, and Julien Barbier

Subjects
ricin toxin, autophagy, degradation, ATG5, SMER28, Medicine
Abstract

Autophagy is a complex and highly regulated degradative process, which acts as a survival pathway in response to cellular stress, starvation and pathogen infection. Ricin toxin is a plant toxin produced by the castor bean and classified as a category B biothreat agent. Ricin toxin inhibits cellular protein synthesis by catalytically inactivating ribosomes, leading to cell death. Currently, there is no licensed treatment for patients exposed to ricin. Ricin-induced apoptosis has been extensively studied; however, whether its intoxication via protein synthesis inhibition affects autophagy is not yet resolved. In this work, we demonstrated that ricin intoxication is accompanied by its own autophagic degradation in mammalian cells. Autophagy deficiency, by knocking down ATG5, attenuates ricin degradation, thus aggravating ricin-induced cytotoxicity. Additionally, the autophagy inducer SMER28 (Small Molecule Enhancer 28) partially protects cells against ricin cytotoxicity, an effect not observed in autophagy-deficient cells. These results demonstrate that autophagic degradation acts as a survival response of cells against ricin intoxication. This suggests that stimulation of autophagic degradation may be a strategy to counteract ricin intoxication.

Published
2023
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3. Membrane protective role of autophagic machinery during infection of epithelial cells by Candida albicans

Author

Pierre Lapaquette, Amandine Ducreux, Louise Basmaciyan, Tracy Paradis, Fabienne Bon, Amandine Bataille, Pascale Winckler, Bernhard Hube, Christophe d’Enfert, Audrey Esclatine, Elisabeth Dubus, Marie-Agnès Bringer, Etienne Morel, and Frédéric Dalle

Subjects
candida albicans, autophagy, epithelial cells, plasma membrane damage, lysosomal exocytosis, Diseases of the digestive system. Gastroenterology, RC799-869
Abstract

Candida albicans (C. albicans) is an opportunistic pathogen causing infections ranging from superficial to life-threatening disseminated infections. In a susceptible host, C. albicans is able to translocate through the gut barrier, promoting its dissemination into deeper organs. C. albicans hyphae can invade human epithelial cells by two well-documented mechanisms: epithelial-driven endocytosis and C. albicans-driven active penetration. One mechanism by which host cells protect themselves against intracellular C. albicans is termed autophagy. The protective role of autophagy during C. albicans infection has been investigated in myeloid cells; however, far less is known regarding the role of this process during the infection of epithelial cells. In the present study, we investigated the role of autophagy-related proteins during the infection of epithelial cells, including intestinal epithelial cells and gut explants, by C. albicans. Using cell imaging, we show that key molecular players of the autophagy machinery (LC3-II, PI3P, ATG16L1, and WIPI2) were recruited at Candida invasion sites. We deepened these observations by electron microscopy analyses that reveal the presence of autophagosomes in the vicinity of invading hyphae. Importantly, these events occur during active penetration of C. albicans into host cells and are associated with plasma membrane damage. In this context, we show that the autophagy-related key proteins ATG5 and ATG16L1 contribute to plasma membrane repair mediated by lysosomal exocytosis and participate in protecting epithelial cells against C. albicans-induced cell death. Our findings provide a novel mechanism by which epithelial cells, forming the first line of defense against C. albicans in the gut, can react to limit C. albicans invasion.

Published
2022
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4. The Autophagy Receptor TAX1BP1 ( T6BP ) improves antigen presentation by MHC‐II molecules

Author

Gabriela Sarango, Clémence Richetta, Mathias Pereira, Anita Kumari, Michael Ghosh, Lisa Bertrand, Cédric Pionneau, Morgane Le Gall, Sylvie Grégoire, Raphaël Jeger‐Madiot, Elina Rosoy, Frédéric Subra, Olivier Delelis, Mathias Faure, Audrey Esclatine, Stéphanie Graff‐Dubois, Stefan Stevanović, Bénédicte Manoury, Bertha Cecilia Ramirez, Arnaud Moris, Institut de Biologie Intégrative de la Cellule (I2BC), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Centre d'Immunologie et des Maladies Infectieuses (CIMI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de biologie et pharmacologie appliquée (LBPA), Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Ecole Normale Supérieure Paris-Saclay (ENS Paris Saclay), University of Tübingen, Plateforme Post-génomique de la Pitié-Salpêtrière (PASS-P3S), Unité Mixte de Service Production et Analyse de données en Sciences de la vie et en Santé (PASS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Plateforme protéomique 3P5 [Institut Cochin] (3P5), 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)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Centre International de Recherche en Infectiologie (CIRI), École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut Necker Enfants-Malades (INEM - UM 111 (UMR 8253 / U1151)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Immunité infection vaccination (I2V), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-IFR128-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de Biologie et de Pharmacologie Appliquée (LBPA), École normale supérieure - Cachan (ENS Cachan)-Centre National de la Recherche Scientifique (CNRS), Autophagie infection et immunité - Autophagy Infection Immunity (APY), Centre International de Recherche en Infectiologie - UMR (CIRI), École normale supérieure - Lyon (ENS 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)-École normale supérieure - Lyon (ENS 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), Hémostase, bio-ingénierie et remodelage cardiovasculaires (LBPC), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Institut Galilée-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Immunité et Infection, Université Pierre et Marie Curie - Paris 6 (UPMC)-IFR113-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Rétrovirus et Transfert Génétique, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), and RAMIREZ, Cecilia

Subjects
Antigen Presentation, immunopeptidome, CD4 + T cell activation, virus Subject Categories Autophagy & Cell Death, [SDV]Life Sciences [q-bio], Immunology, Histocompatibility Antigens Class II, [SDV.CAN]Life Sciences [q-bio]/Cancer, interactome, calnexin, Biochemistry, [SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity, [SDV] Life Sciences [q-bio], [SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], Autophagy, Genetics, Peptides, Molecular Biology, Signal Transduction
Abstract

International audience; CD4 + T lymphocytes play a major role in the establishment and maintenance of immunity. They are activated by antigenic peptides derived from extracellular or newly synthesized (endogenous) proteins presented by the MHC-II molecules. The pathways leading to endogenous MHC-II presentation remain poorly characterized. We demonstrate here that the autophagy receptor, T6BP, influences both autophagy-dependent and-independent endogenous presentation of HIV-and HCMV-derived peptides. By studying the immunopeptidome of MHC-II molecules, we show that T6BP affects both the quantity and quality of peptides presented. T6BP silencing induces the mislocalization of the MHC-II-loading compartments and rapid degradation of the invariant chain (CD74) without altering the expression and internalization kinetics of MHC-II molecules. Defining the interactome of T6BP, we identify calnexin as a T6BP partner. We show that the calnexin cytosolic tail is required for this interaction. Remarkably, calnexin silencing replicates the functional consequences of T6BP silencing: decreased CD4 + T cell activation and exacerbated CD74 degradation. Altogether, we unravel T6BP as a key player of the MHC-II-restricted endogenous presentation pathway, and we propose one potential mechanism of action.

Published
2022
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6. Liste des auteurs

Author

Julio, Aires, Véronique, Apaire-Marchais, Corinne, Arpin, Frédéric, Barbut, Francis, Barin, Olivier, Barraud, Isabelle, Bertrand, Nadège, Bourgeois-Nicolaos, Denys, Brand, Étienne, Brochot, Anais, Brosse, Nathalie, Caroff, Camille, Chagneau, Sabine, Chapuy-Regaud, Marius, Colin, Philippe, Colson, Héloise, Coullon, Jeanne, Couturier, Lise, Cremet, Sandrine, Dahyot, Ghislaine, Descours, Caroline, Deshayes, Anne, Dhalluin, Anne, Doleans-Jordheim, Pierre-Yves, Donnio, Florence, Doucet-Populaire, Véronique, Dubois, Gilles, Duverlie, Sophie, Edouard, Audrey, Esclatine, Matthieu, Eveillard, Virginie, Ferre, Vincent, Foulongne, Émilie, Frobert, Sophie, Gangloff, Agnès, Gautheret-Dejean, Raphaële, Germi, Anne, Goffard, François, Helle, Claire, Hennequin, Berthe-Marie, Imbert, Claire, Janoir, Anne, Jolivet-Gougeon, Frédéric, Jorand, Jérôme, Josse, Philippe, Lanotte, Floriane, Laumay, Alban, Le Monnier, Patricia, Licznar-Fajardo, Marion, Lussignol, Hélène, Marchandin, Julien, Marlet, Océane, Martin, Florence, Morfin, Christophe, Pasquier, Séverine, Pechine, Martine, Pestel-Caron, Ludovic, Pilloux, Fany, Reffuveille, Sylvie, Rogez, Jean-Marc, Rolain, Sarah, Romano-Bertrand, and Aurélie, Truffot

Published
2024
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7. Liste des auteurs

Author

Julio, Aires, Véronique, Apaire-Marchais, Corinne, Arpin, Frédéric, Barbut, Francis, Barin, Isabelle, Bertrand, Nadège, Bourgeois-Nicolaos, Denys, Brand, Etienne, Brochot, Nathalie, Caroff, Sabine, Chapuy-Regaud, Philippe, Colson, Jeanne, Couturier, Lise, Cremet, Sandrine, Dahyot, Ghislaine, Descours, Caroline, Deshayes, Anne, Dhalluin, Anne, Doleans-Jordheim, Pierre-Yves, Donnio, Florence, Doucet-Populaire, Véronique, Dubois, Gilles, Duverlie, Sophie, Edouard, Audrey, Esclatine, Matthieu, Eveillard, Virginie, Ferre, Vincent, Foulongne, Émilie, Frobert, Sophie, Gangloff, Agnès, Gautheret-Dejean, Raphaële, Germi, Anne, Goffard, François, Helle, Claire, Hennequin, Berthe-Marie, Imbert, Claire, Janoir, Anne, Jolivet-Gougeon, Frédéric, Jorand, Philippe, Lanotte, Alban, Le Monnier, Patricia, Licznar-Fajardo, Marion, Lussignol, Hélène, Marchandin, Julien, Marlet, Océane, Martin, Florence, Morfin, Christophe, Pasquier, Séverine, Pechine, Martine, Pestel-Caron, Fany, Reffuveille, Sylvie, Rogez, Jean-Marc, Rolain, and Sarah, Romano-Bertrand

Published
2022
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