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13 results on '"Galluso, Justine"'

1. High-Dimensional Single-Cell Analysis Identifies Organ-Specific Signatures and Conserved NK Cell Subsets in Humans and Mice

Author

Crinier, Adeline, Milpied, Pierre, Escalière, Bertrand, Piperoglou, Christelle, Galluso, Justine, Balsamo, Anaïs, Spinelli, Lionel, Cervera-Marzal, Inaki, Ebbo, Mikaël, Girard-Madoux, Mathilde, Jaeger, Sébastien, Bollon, Emilie, Hamed, Sami, Hardwigsen, Jean, Ugolini, Sophie, Vély, Frédéric, Narni-Mancinelli, Emilie, and Vivier, Eric

Published
2018
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3. Antitumor immunity induced by antibody-based natural killer cell engager therapeutics armed with not-alpha IL-2 variant

Author

Demaria, Olivier, primary, Gauthier, Laurent, additional, Vetizou, Marie, additional, Blanchard Alvarez, Audrey, additional, Vagne, Constance, additional, Habif, Guillaume, additional, Batista, Luciana, additional, Baron, William, additional, Belaïd, Nourhène, additional, Girard-Madoux, Mathilde, additional, Cesari, Cedric, additional, Caratini, Melody, additional, Bosco, Frédéric, additional, Benac, Olivier, additional, Lopez, Julie, additional, Fenis, Aurore, additional, Galluso, Justine, additional, Trichard, Sylvia, additional, Carrette, Barbara, additional, Carrette, Florent, additional, Maguer, Aurélie, additional, Jaubert, Solène, additional, Sansaloni, Audrey, additional, Letay-Drouet, Robin, additional, Kosthowa, Camille, additional, Lovera, Naouel, additional, Dujardin, Arnaud, additional, Chanuc, Fabien, additional, Le Van, Mélanie, additional, Bokobza, Sivan, additional, Jarmuzynski, Nicolas, additional, Fos, Camille, additional, Gourdin, Nicolas, additional, Remark, Romain, additional, Lechevallier, Eric, additional, Fakhry, Nicolas, additional, Salas, Sébastien, additional, Deville, Jean-Laurent, additional, Le Grand, Roger, additional, Bonnafous, Cécile, additional, Vollmy, Lukas, additional, Represa, Agnès, additional, Carpentier, Sabrina, additional, Rossi, Benjamin, additional, Morel, Ariane, additional, Cornen, Stéphanie, additional, Perrot, Ivan, additional, Morel, Yannis, additional, and Vivier, Eric, additional

Published
2022
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4. Association of COVID-19 inflammation with activation of the C5a–C5aR1 axis

Author

Carvelli, Julien, Demaria, Olivier, Vély, Frédéric, Batista, Luciana, Chouaki Benmansour, Nassima, Fares, Joanna, Carpentier, Sabrina, Thibult, Marie-Laure, Morel, Ariane, Remark, Romain, André, Pascale, Represa, Agnès, Piperoglou, Christelle, Assante Miranda, Laura, Baron, William, Belaid, Nourhène, Caillet, Clarisse, Caraguel, Flavien, Carrette, Barbara, Carrette, Florent, Chanuc, Fabien, Courtois, Rachel, Fenis, Aurore, Giordano, Marilyn, Girard-Madoux, Mathilde, Giraudon-Paoli, Marc, Gourdin, Nicolas, Grondin, Gwendoline, Guillot, Franceline, Habif, Guillaume, Jaubert, Solène, Lopez, Julie, Le Van, Mélanie, Lovera, Naouel, Mansuy, Marine, Bonnet, Elodie, Sansaloni, Audrey, Reboul, Annick, Mitry, Emmanuel, Nekkar-Constant, Camille, Péri, Valentine, Ricaut, Paul, Simon, Léa, Vallier, Jean-Baptiste, Vétizou, Marie, Zerbib, Robert, Ugolini, Sophie, Etiennot, Marion, Galluso, Justine, Lyonnet, Luc, Forel, Jean-Marie, Papazian, Laurent, Velly, Lionel, André, Baptiste, Briantais, Antoine, Faucher, Benoit, Jean, Estelle, Seguier, Julie, Veit, Veronique, Harlé, Jean-Robert, Pastorino, Boris, Delteil, Clémence, Daniel, Laurent, Boudsocq, Jean-Paul, Clerc, Axelle, Delmond, Emmanuel, Vidal, Pierre-Olivier, Savini, Hélène, Coutard, Bruno, Cordier, Pierre Yves, Le Dault, Erwan, Guervilly, Christophe, Simeone, Pierre, Gainnier, Marc, Morel, Yannis, Ebbo, Mikael, Schleinitz, Nicolas, and Vivier, Eric

Subjects
0301 basic medicine, Acute Lung Injury, Complement C5a, Inflammation, Complement factor I, Lung injury, Article, Mice, 03 medical and health sciences, 0302 clinical medicine, Immune system, medicine, Animals, Humans, Myeloid Cells, Lung, Receptor, Anaphylatoxin C5a, Respiratory Distress Syndrome, CD11b Antigen, Multidisciplinary, medicine.diagnostic_test, SARS-CoV-2, business.industry, COVID-19, respiratory system, Pathophysiology, 3. Good health, Complement system, Mice, Inbred C57BL, Disease Models, Animal, 030104 developmental biology, Bronchoalveolar lavage, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Immunology, Female, medicine.symptom, Cytokine Release Syndrome, business, Bronchoalveolar Lavage Fluid
Abstract

Coronavirus disease 2019 (COVID-19) is a disease caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has resulted in a pandemic1. The C5a complement factor and its receptor C5aR1 (also known as CD88) have a key role in the initiation and maintenance of several inflammatory responses by recruiting and activating neutrophils and monocytes1. Here we provide a longitudinal analysis of immune responses, including phenotypic analyses of immune cells and assessments of the soluble factors that are present in the blood and bronchoalveolar lavage fluid of patients at various stages of COVID-19 severity, including those who were paucisymptomatic or had pneumonia or acute respiratory distress syndrome. The levels of soluble C5a were increased in proportion to the severity of COVID-19 and high expression levels of C5aR1 receptors were found in blood and pulmonary myeloid cells, which supports a role for the C5a-C5aR1 axis in the pathophysiology of acute respiratory distress syndrome. Anti-C5aR1 therapeutic monoclonal antibodies prevented the C5a-mediated recruitment and activation of human myeloid cells, and inhibited acute lung injury in human C5aR1 knock-in mice. These results suggest that blockade of the C5a-C5aR1 axis could be used to limit the infiltration of myeloid cells in damaged organs and prevent the excessive lung inflammation and endothelialitis that are associated with acute respiratory distress syndrome in patients with COVID-19.

Published
2020
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7. Somatotroph Tumors and the Epigenetic Status of the GNAS Locus

Author

Romanet, Pauline, primary, Galluso, Justine, additional, Kamenicky, Peter, additional, Hage, Mirella, additional, Theodoropoulou, Marily, additional, Roche, Catherine, additional, Graillon, Thomas, additional, Etchevers, Heather C., additional, De Murat, Daniel, additional, Mougel, Grégory, additional, Figarella-Branger, Dominique, additional, Dufour, Henry, additional, Cuny, Thomas, additional, Assié, Guillaume, additional, and Barlier, Anne, additional

Published
2021
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9. A point mutation in the Ncr1 signal peptide impairs the development of innate lymphoid cell subsets

Author

Almeida, Francisca F., primary, Tognarelli, Sara, additional, Marçais, Antoine, additional, Kueh, Andrew J., additional, Friede, Miriam E., additional, Liao, Yang, additional, Willis, Simon N., additional, Luong, Kylie, additional, Faure, Fabrice, additional, Mercier, Francois E., additional, Galluso, Justine, additional, Firth, Matthew, additional, Narni-Mancinelli, Emilie, additional, Rais, Bushra, additional, Scadden, David T., additional, Spallotta, Francesco, additional, Weil, Sandra, additional, Giannattasio, Ariane, additional, Kalensee, Franziska, additional, Zöller, Tobias, additional, Huntington, Nicholas D., additional, Schleicher, Ulrike, additional, Chiocchetti, Andreas G., additional, Ugolini, Sophie, additional, Herold, Marco J., additional, Shi, Wei, additional, Koch, Joachim, additional, Steinle, Alexander, additional, Vivier, Eric, additional, Walzer, Thierry, additional, Belz, Gabrielle T., additional, and Ullrich, Evelyn, additional

Published
2018
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10. A point mutation in the Ncr1 signal peptide impairs the development of innate lymphoid cell subsets

Author

Almeida, Francisca F., Tognarelli, Sara, Marçais, Antoine, Kueh, Andrew J., Friede, Miriam Elisabeth, Liao, Yang, Willis, Simon N., Luong, Kylie, Faure, Fabrice, Mercier, Francois E., Galluso, Justine, Firth, Matthew, Narni-Mancinelli, Emilie, Rais, Bushra, Scadden, David T., Spallotta, Francesco, Weil, Sandra, Giannattasio, Ariane, Kalensee, Franziska, Zöller, Tobias, Huntington, Nicholas D., Schleicher, Ulrike, Geburtig-Chiocchetti, Andreas, Ugolini, Sophie, Herold, Marco, Shi, Wei, Koch, Joachim, Steinle, Alexander, Vivier, Eric, Walzer, Thierry, Belz, Gabrielle T., Ullrich, Evelyn, Almeida, Francisca F., Tognarelli, Sara, Marçais, Antoine, Kueh, Andrew J., Friede, Miriam Elisabeth, Liao, Yang, Willis, Simon N., Luong, Kylie, Faure, Fabrice, Mercier, Francois E., Galluso, Justine, Firth, Matthew, Narni-Mancinelli, Emilie, Rais, Bushra, Scadden, David T., Spallotta, Francesco, Weil, Sandra, Giannattasio, Ariane, Kalensee, Franziska, Zöller, Tobias, Huntington, Nicholas D., Schleicher, Ulrike, Geburtig-Chiocchetti, Andreas, Ugolini, Sophie, Herold, Marco, Shi, Wei, Koch, Joachim, Steinle, Alexander, Vivier, Eric, Walzer, Thierry, Belz, Gabrielle T., and Ullrich, Evelyn

Abstract

NKp46 (CD335) is a surface receptor shared by both human and mouse natural killer (NK) cells and innate lymphoid cells (ILCs) that transduces activating signals necessary to eliminate virus-infected cells and tumors. Here, we describe a spontaneous point mutation of cysteine to arginine (C14R) in the signal peptide of the NKp46 protein in congenic Ly5.1 mice and the newly generated NCRB6C14R strain. Ly5.1C14R NK cells expressed similar levels of Ncr1 mRNA as C57BL/6, but showed impaired surface NKp46 and reduced ability to control melanoma tumors in vivo. Expression of the mutant NKp46C14R in 293T cells showed that NKp46 protein trafficking to the cell surface was compromised. Although Ly5.1C14R mice had normal number of NK cells, they showed an increased number of early maturation stage NK cells. CD49a+ILC1s were also increased but these cells lacked the expression of TRAIL. ILC3s that expressed NKp46 were not detectable and were not apparent when examined by T-bet expression. Thus, the C14R mutation reveals that NKp46 is important for NK cell and ILC differentiation, maturation and function.

Published
2018

12. A point mutation in the Ncr1signal peptide impairs the development of innate lymphoid cell subsets

Author

Almeida, Francisca F., Tognarelli, Sara, Marçais, Antoine, Kueh, Andrew J., Friede, Miriam E., Liao, Yang, Willis, Simon N., Luong, Kylie, Faure, Fabrice, Mercier, Francois E., Galluso, Justine, Firth, Matthew, Narni-Mancinelli, Emilie, Rais, Bushra, Scadden, David T., Spallotta, Francesco, Weil, Sandra, Giannattasio, Ariane, Kalensee, Franziska, Zöller, Tobias, Huntington, Nicholas D., Schleicher, Ulrike, Chiocchetti, Andreas G., Ugolini, Sophie, Herold, Marco J., Shi, Wei, Koch, Joachim, Steinle, Alexander, Vivier, Eric, Walzer, Thierry, Belz, Gabrielle T., and Ullrich, Evelyn

Abstract

ABSTRACTNKp46 (CD335) is a surface receptor shared by both human and mouse natural killer (NK) cells and innate lymphoid cells (ILCs) that transduces activating signals necessary to eliminate virus-infected cells and tumors. Here, we describe a spontaneous point mutation of cysteine to arginine (C14R) in the signal peptide of the NKp46 protein in congenic Ly5.1 mice and the newly generated NCRB6C14Rstrain. Ly5.1C14RNK cells expressed similar levels of Ncr1mRNA as C57BL/6, but showed impaired surface NKp46 and reduced ability to control melanoma tumors in vivo. Expression of the mutant NKp46C14Rin 293T cells showed that NKp46 protein trafficking to the cell surface was compromised. Although Ly5.1C14Rmice had normal number of NK cells, they showed an increased number of early maturation stage NK cells. CD49a+ILC1s were also increased but these cells lacked the expression of TRAIL. ILC3s that expressed NKp46 were not detectable and were not apparent when examined by T-bet expression. Thus, the C14R mutation reveals that NKp46 is important for NK cell and ILC differentiation, maturation and function.SignificanceInnate lymphoid cells (ILCs) play important roles in immune protection. Various subsets of ILCs express the activating receptor NKp46 which is capable of recognizing pathogen derived and tumor ligands and is necessary for immune protection. Here, we describe a spontaneous point mutation in the signal peptide of the NKp46 protein in congenic Ly5.1 mice which are widely used for tracking cells in vivo. This Ncr1C14R mutation impairs NKp46 surface expression resulting in destabilization of Ncr1and accumulation of NKp46 in the endoplasmic reticulum. Loss of stable NKp46 expression impaired the maturation of NKp46+ILCs and altered the expression of TRAIL and T-bet in ILC1 and ILC3, respectively.

Published
2018
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13. A tetraspecific engager armed with a non-alpha IL-2 variant harnesses natural killer cells against B cell non-Hodgkin lymphoma.

Author

Demaria O, Habif G, Vetizou M, Gauthier L, Remark R, Chiossone L, Vagne C, Rebuffet L, Courtois R, Denis C, Le Floch F, Muller M, Girard-Madoux M, Augier S, Lopez J, Carrette B, Maguer A, Vallier JB, Grondin G, Baron W, Galluso J, Yessaad N, Giordano M, Simon L, Chanuc F, Alvarez AB, Perrot I, Bonnafous C, Represa A, Rossi B, Morel A, Morel Y, Paturel C, and Vivier E

Subjects
Animals, Humans, Mice, Lymphoma, B-Cell immunology, Lymphoma, B-Cell genetics, Lymphoma, B-Cell therapy, Cell Line, Tumor, Female, Xenograft Model Antitumor Assays, Lymphoma, Non-Hodgkin immunology, Mice, SCID, Mice, Inbred NOD, Killer Cells, Natural immunology, Interleukin-2 immunology, Interleukin-2 genetics
Abstract

NK cells offer a promising alternative to T cell therapies in cancer. We evaluated IPH6501, a clinical-stage, tetraspecific NK cell engager (NKCE) armed with a non-alpha IL-2 variant (IL-2v), which targets CD20 and was developed for treating B cell non-Hodgkin lymphoma (B-NHL). CD20-NKCE-IL2v boosts NK cell proliferation and cytotoxicity, showing activity against a range of B-NHL cell lines, including those with low CD20 density. Whereas it presented reduced toxicities compared with those commonly associated with T cell therapies, CD20-NKCE-IL2v showed greater killing efficacy over a T cell engager targeting CD20 in in vitro preclinical models. CD20-NKCE-IL2v also increased the cell surface expression of NK cell-activating receptors, leading to activity against CD20-negative tumor cells. In vivo studies in nonhuman primates and tumor mouse models further validated its efficacy and revealed that CD20-NKCE-IL2v induces peripheral NK cell homing at the tumor site. CD20-NKCE-IL2v emerges as a potential alternative in the treatment landscape of B-NHL.

Published
2024
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