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1. CD45 Isoform Profile Identifies Natural Killer (NK) Subsets with Differential Activity

Author

Amélie Cornillon, Nathalie Fegueux, Yosr Hicheri, Martin Villalba, Jean-François Rossi, Zhao-Yang Lu, Ewelina Krzywinska, Dang-Nghiem Vo, Céline René, Patrick Ceballos, Michal Sobecki, Nerea Allende-Vega, Guillaume Cartron, Christine Pasero, Daniel Olive, Cellules Souches, Plasticité Cellulaire, Médecine Régénératrice et Immunothérapies (IRMB), Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Centre de Recherche en Cancérologie de Marseille (CRCM), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Aix Marseille Université (AMU), Service d'hématologie et oncologie médicale, Université Montpellier 1 (UM1)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Hôpital Lapeyronie-Université de Montpellier (UM), 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), Dynamique des interactions membranaires normales et pathologiques (DIMNP), Université Montpellier 1 (UM1)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), All of the authors’ funders are public or charitable organizations. This work was supported by a scientific program from the 'Communauté de Travail des Pyrénées' (CTPP5/12 to MV), the charities CIEL, L'Un pour l'Autre and Ensangble (09/ 2013) (MV), a grant from the European Community Program SUDOE (CLiNK SOE2/P1/E341 to MV and J-FR), an AOI from the CHU Montpellier (N°221826) (GC and MV), a grant from Fondation de France (0057921) and fellowships from the ARC (DOC20121206007) and La Ligue Contre le Cancer (TDKB13362) to EK, and Ministère de l'Enseignement Supérieur et de la Recherche (MESR) (DNV)., European Project, villalba, martin, CLINK, SUDOE, SOE2/P1/E341 - INCOMING, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Aix Marseille Université (AMU)-Institut Paoli-Calmettes, and Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
0301 basic medicine, Antigens, Differentiation, T-Lymphocyte, lcsh:Medicine, NK cells, CD49b, Plasma Cell Disorders, Hematologic Cancers and Related Disorders, Interleukin 21, 0302 clinical medicine, NK-92, Bone Marrow, immune system diseases, Multiple myeloma, Cellular types, Protein Isoforms, Lymphocytes, lcsh:Science, Staining, Multidisciplinary, Janus kinase 3, Immune cells, Hematopoietic Stem Cell Transplantation, hemic and immune systems, Hematology, Natural killer T cell, Cell staining, Cell biology, Killer Cells, Natural, Oncology, Interleukin 12, White blood cells, Research Article, Blood cells, Cell Physiology, Immunology, T cells, chemical and pharmacologic phenomena, [SDV.CAN]Life Sciences [q-bio]/Cancer, Biology, Research and Analysis Methods, Cell degranulation, 03 medical and health sciences, [SDV.CAN] Life Sciences [q-bio]/Cancer, Antigens, CD, Cell Line, Tumor, Humans, Lectins, C-Type, Antibody-Producing Cells, Medicine and health sciences, B cells, Lymphokine-activated killer cell, Biology and life sciences, lcsh:R, Cancers and Neoplasms, 030104 developmental biology, Animal cells, Specimen Preparation and Treatment, Myeloid-derived Suppressor Cell, Leukocyte Common Antigens, lcsh:Q, K562 Cells, Biomarkers, 030215 immunology
Abstract

International audience; The leucocyte-specific phosphatase CD45 is present in two main isoforms: the large CD45RA and the short CD45RO. We have recently shown that distinctive expression of these isoforms distinguishes natural killer (NK) populations. For example, co-expression of both isoforms identifies in vivo the anti tumor NK cells in hematological cancer patients. Here we show that low CD45 expression associates with less mature, CD56 bright , NK cells. Most NK cells in healthy human donors are CD45RA + CD45RO-. The CD45RA-RO + phenotype , CD45RO cells, is extremely uncommon in B or NK cells, in contrast to T cells. However , healthy donors possess CD45RA dim RO-(CD45RA dim cells), which show immature markers and are largely expanded in hematopoietic stem cell transplant patients. Blood borne cancer patients also have more CD45RA dim cells that carry several features of immature NK cells. However, and in opposition to their association to NK cell progenitors, they do not proliferate and show low expression of the transferrin receptor protein 1/CD71, suggesting low metabolic activity. Moreover, CD45RA dim cells properly respond to in vitro encounter with target cells by degranulating or gaining CD69 expression. In summary, they are quies-cent NK cells, with low metabolic status that can, however, respond after encounter with target cells.

Published
2016
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2. Factors influencing extramedullary relapse after allogeneic transplantation for multiple myeloma

Author

Zhao Yang Lu, Carine Plassot, Bernard Klein, R. Navarro, Guillaume Cartron, Vanessa Szablewski, Catherine Cyteval, Patrice Ceballos, Tarik Kanouni, Philippe Quittet, Jérôme Moreaux, Jean-Côme Meniane, Laure Vincent, Nathalie Fegueux, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Université de Montpellier (UM), Cellules Souches, Plasticité Cellulaire, Médecine Régénératrice et Immunothérapies (IRMB), Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Département d'hématologie biologique[Montpellier], Université Montpellier 1 (UM1)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-CHU Saint-Eloi, Institut de génétique humaine (IGH), and Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Oncology, Adult, Male, medicine.medical_specialty, Allogeneic transplantation, Transplantation Conditioning, medicine.medical_treatment, [SDV.CAN]Life Sciences [q-bio]/Cancer, Hematopoietic stem cell transplantation, Disease-Free Survival, immune system diseases, hemic and lymphatic diseases, Internal medicine, medicine, Humans, Transplantation, Homologous, Letter to the Editor, Multiple myeloma, ComputingMilieux_MISCELLANEOUS, Aged, Hematology, business.industry, Hematopoietic Stem Cell Transplantation, [SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/Hematology, Middle Aged, medicine.disease, 3. Good health, Lymphoma, Transplantation, Leukemia, surgical procedures, operative, Treatment Outcome, Immunology, Female, Neoplasm Recurrence, Local, business, Multiple Myeloma
Abstract

Factors influencing extramedullary relapse after allogeneic transplantation for multiple myeloma

Published
2015
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3. All-trans retinoic acid (ATRA) induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity

Author

Luis Martínez-Lostao, Julián Pardo, Amélie Cornillon, Ewelina Krzywinska, Alberto Anel, Diego Sánchez-Martínez, Martin Villalba, Zhao Yang Lu, Jean François Rossi, Dietmar Fernández-Orth, Anne Saumet, Nuria Lopez-Royuela, Ariel Ramirez-Labrada, Sergio Escorza, Moeez Ghani Rathore, Charles-Henri Lecellier, Cell Immunity in Cancer, Inflammation and infection Group [Zaragoza, Spain] (Biomedical Research Center), University of Zaragoza - Universidad de Zaragoza [Zaragoza]-Fundación Agencia Aragonesa para la Investigación y el Desarrollo (ARAID)-Nanoscience Institute of Aragon - INA [Zaragoza, Spain], Cellules souches normales et cancéreuses, Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Institut de recherche en cancérologie de Montpellier (IRCM - U896 Inserm - UM1), Université Montpellier 1 (UM1)-CRLCC Val d'Aurelle - Paul Lamarque-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Apoptosis, Immunity and Cancer Group [Zaragoza, Spain] ( Department Biochemistry and Molecular and Cell Biology), University of Zaragoza - Universidad de Zaragoza [Zaragoza], Progenika Biopharma SA [Bizkaia, Spain], Institut de Génétique Moléculaire de Montpellier (IGMM), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Institut de recherche en biothérapie (IRB), Université Montpellier 1 (UM1)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), This work was supported by the program 'Chercheur d’avenir' from the Region Languedoc-Rousillon (MV), a scientific program from the 'Communauté de Travail des Pyrénées' (CTPP10/09 to MV, SE and AA), the CliNK project (SOE2/P1/E341) from Sudoe/EU (AA, J-FR and MV), the Association pour la Recherche contre le Cancer (MV), the Fondation pour la Recherche Medicale (MV), a grant FEDER Objectif competitivite (MV), l’association CIEL, l’association L’Un pour l’Autre et la fédération Ensangble (MV), Fondo Social Europeo (FSE), grants SAF2010-15341 (AA) and SAF2011-25390 (JP) Ministerio de Economía y Competitividad, Spain and fellowships from Gobierno de Aragon (DS) the ARC (MGR and EK) and Higher Education Commission, Pakistan (MGR) and La Ligue contre le Cancer (NL-R)., villalba, martin, University of Zaragoza - Universidad de Zaragoza [Zaragoza]-Nanoscience Institute of Aragon - INA [Zaragoza, Spain]-Fundación Agencia Aragonesa para la Investigación y el Desarrollo - ARAID [Zaragoza, Spain], CRLCC Val d'Aurelle - Paul Lamarque-Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 1 (UM1), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 1 (UM1)-Université de Montpellier (UM)

Subjects
Cytotoxicity, Immunologic, C–C motif chemokine, Lymphocyte, Cell, Retinoic acid, C–C chemokine receptor, NK cells, Biochemistry, Granzymes, Cathepsin C, Epstein–Barr virus, chemistry.chemical_compound, Interleukin 21, Jurkat Cells, CXCL, polyinosinic:polycytidylic acid, Cluster Analysis, ATRA, Cytotoxicity, CXCR, Cells, Cultured, C–X–C motif chemokine, miR-23a, Oligonucleotide Array Sequence Analysis, Principal Component Analysis, PCA, Reverse Transcriptase Polymerase Chain Reaction, chemokine receptor, Cell biology, Killer Cells, Natural, all-trans retinoic acid, medicine.anatomical_structure, Female, Blotting, Western, Tretinoin, [SDV.CAN]Life Sciences [q-bio]/Cancer, Biology, poly I:C, Cell Line, FDR, [SDV.CAN] Life Sciences [q-bio]/Cancer, EBV, principal components analysis, medicine, Animals, Humans, Transcriptomics, miRNA, Innate immune system, CCL, Cell Biology, CCRC, Mice, Inbred C57BL, MicroRNAs, chemistry, Granzyme, biology.protein, Interleukin-2, false discovery rate, CTSC, K562 Cells, Transcriptome
Abstract

International audience; NK cell is an innate immune system lymphocyte lineage with natural cytotoxicity. Its optimal use in the clinic requires in vitro expansion and activation. Cytokines and encounter with target cells activate NK cells and induce proliferation, and this could depend on the presence of other immune cells. Here we activated PBMCs during 5 days with IL-2, with IL-2 plus the tumor cell line K562 and with the lymphoblastoid cell line R69 and perform integrated analyses of microRNA and mRNA expression profiles of purified NK cells. The samples cluster depending on the stimuli and not on the donor, indicating that the pattern of NK cell stimulation is acutely well conserved between individuals. Regulation of mRNA expression is tighter than that of miRNA expression. All stimuli induce a common preserved genetic remodeling. In addition, encounter with target cells mainly activates pathways related to metabolism. Different target cells induce different NK cell remodeling which affects cytokine response and cytotoxicity, supporting the notion that encounter with different target cells significantly changing the activation pattern. We validate our analysis by showing that activation down regulates miR-23a, which is a negative regulator of cathepsin C (CTSC) mRNA, a gene up regulated by all stimuli. The peptidase CTSC activates the granzymes, the main effector proteases involved in NK cell cytotoxicity. All-trans retinoic acid (ATRA), which induces miR-23a expression, decreases CTSC expression and granzyme B activity leading to impaired NK cell cytotoxicity in an in vivo mouse model.

Published
2014
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4. B7-1 and 4-1BB ligand expression on a myeloma cell line makes it possible to expand autologous tumor-specific cytotoxic T cells in vitro

Author

Jean François Rossi, Marie Claude Delteil, Christophe Ferrand, Karin Tarte, Zhao-Yang Lu, L Nadal, Bernard Klein, Maud Condomines, Unité de thérapie cellulaire, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-CHU Saint-Eloi, Institut de recherche en biothérapie (IRB), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 1 (UM1)-Université de Montpellier (UM), Université Montpellier 1 - UFR de Médecine (UM1 Médecine), Université Montpellier 1 (UM1), Immunopathologie des maladies tumorales et autoimmunes, Université Montpellier 1 (UM1)-IFR76-Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'hématologie et oncologie médicale, Hôpital Lapeyronie-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Université Montpellier 1 (UM1)-Université de Montpellier (UM), Laboratoire de biologie moléculaire, EFS, Université Montpellier 1 (UM1)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Frei, Monique, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Hôpital Saint Eloi (CHRU Montpellier), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), and Université Montpellier 1 (UM1)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Hôpital Lapeyronie-Université de Montpellier (UM)

Subjects
[SDV.MHEP.HEM] Life Sciences [q-bio]/Human health and pathology/Hematology, Cancer Research, medicine.medical_treatment, chemistry.chemical_compound, 0302 clinical medicine, Transduction, Genetic, Cytotoxic T cell, 0303 health sciences, biology, [SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/Hematology, Hematology, Middle Aged, medicine.anatomical_structure, 030220 oncology & carcinogenesis, B7-1 Antigen, [SDV.IMM]Life Sciences [q-bio]/Immunology, Multiple Myeloma, medicine.drug, Interleukin 2, DNA, Complementary, [SDV.IMM] Life Sciences [q-bio]/Immunology, T cell, Genetic Vectors, [SDV.CAN]Life Sciences [q-bio]/Cancer, Article, 03 medical and health sciences, [SDV.CAN] Life Sciences [q-bio]/Cancer, Cell Line, Tumor, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Genetics, medicine, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Molecular Biology, 030304 developmental biology, CD40, Cell Biology, Immunotherapy, Molecular biology, Coculture Techniques, CTL, 4-1BB ligand, 4-1BB Ligand, Retroviridae, chemistry, Gene Expression Regulation, biology.protein, Interleukin-2, CD8, T-Lymphocytes, Cytotoxic
Abstract

International audience; OBJECTIVE: The aim of this study was to confer an antigen-presenting cell (APC) ability on multiple myeloma cell lines (HMCLs) using B7-1 and/or 4-1BBL gene transfer. MATERIALS AND METHODS: HMCLs were retrovirally transduced with B7-1 and/or 4-1BBL cDNAs. Allogeneic or autologous T cells were stimulated by coculture with B7-1- and/or 4-1BBL-transduced HMCLs in the presence of interleukin-2. T cell clones were obtained by limiting dilution. T-cell activation was assessed by interferon-gamma Elispot assays and cytotoxicity by (51)Cr release assays. RESULTS: Neither primary multiple myeloma cells (MMCs) nor HMCLs expressed B7-1 or 4-1BBL, and these molecules could not be induced by CD40 triggering. HMCLs failed to stimulate allogeneic or autologous T cells. Transduction of HMCLs with B7-1 and/or 4-1BBL retroviruses induced a high expression of B7-1 and 4-1BBL molecules and a strong T-cell activation ability. Long-term cultured CD8(+) T-cell lines could be obtained by stimulation with the autologous B7-1/4-1BBL XG-19 HMCL. These cytotoxic T lymphocytes (CTL) efficiently killed the autologous parental XG-19 HMCL as well as autologous primary MMCs and allogeneic HMCLs. They did not kill autologous CD34 cells and autologous EBV cell line or natural killer target K562 cells. Cloned CTL could recognize allogeneic HMCLs, demonstrating that a shared anti-MMC repertoire was expanded. CONCLUSION: Transduction with B7-1 and 4-1BBL retroviruses turned HMCLs into efficient APCs. It permitted the long-term expansion of autologous anti-tumor CTL with a shared anti-MMC repertoire, for one HMCL. These data suggest developing an immunotherapy using modified tumor cells in patients with multiple myeloma.

Published
2007
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5. Low doses of GM-CSF (molgramostim) and G-CSF (filgrastim) after cyclophosphamide (4 g/m2) enhance the peripheral blood progenitor cell harvest: results of two randomized studies including 120 patients

Author

Pascal Latry, Nathalie Fegueux, Ernesto Lopez, Jean-Pierre Daurès, Bernard Klein, Zhao-Yang Lu, Carole Exbrayat, Valérie Rouille, Patrice Ceballos, Philippe Quittet, Catherine Becht, Eric Legouffe, Jean-François Rossi, Damien Pouessel, Frei, Monique, Service d'hématologie et oncologie médicale, Université Montpellier 1 (UM1)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Hôpital Lapeyronie-Université de Montpellier (UM), Unité de Thérapie Cellulaire, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Hôpital Saint Eloi (CHRU Montpellier), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Unité de Thérapie Cellulaire et Génique, Immunopathologie des maladies tumorales et autoimmunes, Université Montpellier 1 (UM1)-IFR76-Institut National de la Santé et de la Recherche Médicale (INSERM), Aide à la Décision pour une Médecine Personnalisé - Laboratoire de Biostatistique, Epidémiologie et Recherche Clinique - EA 2415 (AIDMP), Université Montpellier 1 (UM1)-Université de Montpellier (UM), Hôpital Lapeyronie-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Université Montpellier 1 (UM1)-Université de Montpellier (UM), and Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-CHU Saint-Eloi

Subjects
Male, Antigens, CD34, MESH: Multiple Myeloma, Gastroenterology, Leukocyte Count, chemistry.chemical_compound, 0302 clinical medicine, Granulocyte Colony-Stimulating Factor, MESH: Aged, MESH: Filgrastim, Hematology, MESH: Middle Aged, Middle Aged, MESH: Granulocyte-Macrophage Colony-Stimulating Factor, Recombinant Proteins, Nitrogen mustard, Granulocyte colony-stimulating factor, Granulocyte macrophage colony-stimulating factor, 030220 oncology & carcinogenesis, Drug Therapy, Combination, Female, Multiple Myeloma, medicine.drug, Adult, medicine.medical_specialty, Filgrastim, Cyclophosphamide, MESH: Leukapheresis, G-CSF, MESH: Peripheral Blood Stem Cell Transpl, Article, 03 medical and health sciences, Molgramostim, Internal medicine, medicine, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Leukapheresis, Progenitor cell, Aged, Peripheral Blood Stem Cell Transplantation, Transplantation, MESH: Humans, business.industry, Granulocyte-Macrophage Colony-Stimulating Factor, MESH: Cyclophosphamide, GM-CSF, MESH: Adult, MESH: Antigens, CD34, MESH: Male, Surgery, MESH: Drug Therapy, Combination, chemistry, MESH: Leukocyte Count, business, MESH: Female, Hematopoietic stem cells, 030215 immunology
Abstract

International audience; The use of a combination of G-CSF and GM-CSF versus G-CSF alone, after cyclophosphamide (4 g/m2) was compared in two randomized phase III studies, including 120 patients. In study A, 60 patients received 5 x 2 microg/kg/day of G-CSF and GM-CSF compared to 5 mug/kg/day of G-CSF. In study B, 60 patients received 2.5 x 2 microg/kg/day G-CSF and GM-CSF compared to G-CSF alone (5 microg/kg/day). With the aim to collect at least 5 x 10(6)/kg CD34 cells in a maximum of three large volume leukapherises (LK), 123 LK were performed in study A, showing a significantly higher number of patients reaching 10 x 10(6)/kg CD34 cells (21/29 in G+GM-CSF arm vs 11/27 in G-CSF arm, P=0.00006). In study B, 109 LK were performed, with similar results (10/27 vs 15/26, P=0.003). In both the study, the total harvest of CD34 cells/kg was twofold higher in G-CSF plus GM-CSF group (18.3 x 10(6) in study A and 15.85 x 10(6) in study B) than in G-CSF group (9 x 10(6) in study A and 8.1 x 10(6) in study B), a significant difference only seen in multiple myeloma, with no significant difference in terms of mobilized myeloma cells between G-CSF and GM-CSF groups.

Published
2006
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6. Optimizing the use of anti-interleukin-6 monoclonal antibody with dexamethasone and 140 mg/m2 of melphalan in multiple myeloma: results of a pilot study including biological aspects

Author

Philippe Quittet, Eric Legouffe, Jean-Pierre Daurès, Valérie Rouille, Marie-Cécile Bozonnat, Bernard Klein, Tarik Kanouni, Jean-François Rossi, Nathalie Fegueux, Carole Exbrayat, Ernesto Lopez, Zhao Yang Lu, John Widjenes, Robert Navarro, Service d'hématologie et oncologie médicale, Hôpital Lapeyronie-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Université Montpellier 1 (UM1)-Université de Montpellier (UM), Unité de Thérapie Cellulaire et Génique, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-CHU Saint-Eloi, Aide à la Décision pour une Médecine Personnalisé - Laboratoire de Biostatistique, Epidémiologie et Recherche Clinique - EA 2415 (AIDMP), Université Montpellier 1 (UM1)-Université de Montpellier (UM), Diaclone Research, Frei, Monique, Université Montpellier 1 (UM1)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Hôpital Lapeyronie-Université de Montpellier (UM), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Hôpital Saint Eloi (CHRU Montpellier), and Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)

Subjects
Melphalan, Male, medicine.medical_treatment, Anti-Inflammatory Agents, Pilot Projects, MESH: Multiple Myeloma, Pharmacology, Dexamethasone, autologous transplantation, MESH: Antibodies, Monoclonal, chemistry.chemical_compound, 0302 clinical medicine, Autologous stem-cell transplantation, Multiple myeloma, MESH: Aged, 0303 health sciences, MESH: Middle Aged, MESH: Mucositis, Antibodies, Monoclonal, Hematology, MESH: Pil, Middle Aged, Nitrogen mustard, 3. Good health, multiple myeloma, C-Reactive Protein, 030220 oncology & carcinogenesis, MESH: Dexamethasone, Female, medicine.drug, Adult, Mucositis, medicine.medical_specialty, MESH: Myeloablative Agonists, Transplantation, Autologous, Article, Disease-Free Survival, 03 medical and health sciences, MESH: Melphalan, Internal medicine, MESH: C-Reactive Protein, medicine, [SDV.BBM] Life Sciences [q-bio]/Biochemistry, Molecular Biology, Autologous transplantation, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, anti-interleukin-6, 030304 developmental biology, Aged, MESH: Drug Evaluation, Transplantation, Chemotherapy, MESH: Humans, business.industry, Interleukin-6, MESH: Adult, Myeloablative Agonists, medicine.disease, MESH: Interleukin-6, MESH: Male, Endocrinology, chemistry, MESH: Anti-Inflammatory Agents, MESH: Disease-Free Survival, Drug Evaluation, business, MESH: Female, Stem Cell Transplantation
Abstract

International audience; Interleukin-6 (IL-6) is a major survival factor for multiple myeloma (MM) cells preventing apoptosis induced by dexamethasone (DEX) or chemotherapy. In all, 24 consecutive patients with MM in first-line therapy received DEX for 4 days, followed by melphalan (HDM: 140 mg/m2) and autologous stem cell transplantation (ASCT). The anti-IL-6 monoclonal antibody (mAb) (B-E8) was given till haematological recovery, starting 1 day before DEX. Results were historically compared to MM patients treated with HDM 140 and 200 mg/m2. Our results show (1) that B-E8 was able to fully neutralize IL-6 activity in vivo before and after HDM as shown by inhibition of C reactive protein (CRP) production; (2) no haematological toxicity; (3) a significant reduction of mucositis and fever; (4) a median event-free survival of 35 months and an overall survival of 68.2% at 5 years with a median follow-up of 72 months; and (5) the overall daily IL-6 production progressively increased on and after 7 days post-HDM, with the increased serum CRP levels. In the 5/24 patients with uncontrolled CRP production, a large IL-6 production was detected (320 microg/day) that could not possibly be neutralized by B-E8. These data show the feasibility to neutralize IL-6 in vivo with anti-IL-6 mAb in the context of HDM.

Published
2005
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7. Kaposi's sarcoma-associated herpesvirus is not detected with immunosuppression in multiple myeloma

Author

Jean-François Rossi, Bernard Klein, Yuan Chang, Sonja J. Olsen, Karin Tarte, Michel Jourdan, Eric Legouffe, Zhao-Yang Lu, Microenvironnement et cancer (MiCa), Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Institut de biologie et chimie des protéines [Lyon] (IBCP), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), Institut de Génétique Moléculaire de Montpellier (IGMM), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), and Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM)

Subjects
viruses, medicine.medical_treatment, Immunology, medicine.disease_cause, Biochemistry, Peripheral blood mononuclear cell, infection hhv-8, Pathogenesis, 03 medical and health sciences, 0302 clinical medicine, Acquired immunodeficiency syndrome (AIDS), medicine, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Kaposi's sarcoma-associated herpesvirus, Multiple myeloma, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, 0303 health sciences, business.industry, virus diseases, Immunosuppression, Cell Biology, Hematology, medicine.disease, Virology, 3. Good health, Therapeutic immunosuppression, 030220 oncology & carcinogenesis, Sarcoma, business
Abstract

To the Editor: Kaposi’s sarcoma-associated herpesvirus (KSHV) is involved in the pathogenesis of all forms of Kaposi’s sarcoma (KS).[1][1] In acquired immunodeficiency syndrome (AIDS)-associated KS, KSHV detection in peripheral blood mononuclear cells increases with immunosuppression.[2][2]

Published
1998
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8. Large scale and clinical grade purification of syndecan-1 plus malignant plasma cells

Author

John Wijdenes, Catherine Hertog, Jean-François Rossi, Bernard Klein, Jean Brochier, Zhao-Yang Lu, Ren-Xiao Sun, Institut de Génétique Moléculaire de Montpellier (IGMM), and Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM)

Subjects
Pathology, medicine.medical_specialty, Syndecans, medicine.drug_class, medicine.medical_treatment, Immunology, Plasma Cells, Chymopapain, Plasma cell, Monoclonal antibody, Syndecan 1, 03 medical and health sciences, 0302 clinical medicine, Antigen, Cancer immunotherapy, Immunology and Allergy, Medicine, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, 030304 developmental biology, 0303 health sciences, Membrane Glycoproteins, biology, business.industry, Immunomagnetic Separation, multiple myelomatosis plasma cell syndecan-1 bone-marrow transplantation multiple-myeloma progenitor cells peripheral-blood expression lymphocytes resistance apoptosis therapy, Clinical grade, Multiple myelomatosis, 3. Good health, medicine.anatomical_structure, biology.protein, Proteoglycans, Syndecan-1, business, Multiple Myeloma, 030215 immunology
Abstract

For cancer immunotherapy, it is usually necessary to obtain a large number of tumor cells from patients. We have previously reported that syndecan-1 is present only on malignant plasma cells in samples from patients with multiple myelomatosis. We report here that this antigen is cleaved by chymopapain. This makes it possible to develop a rapid and clinical grade procedure to purify large numbers of myeloma cells using anti-syndecan-1 mAb, magnetic beads and chymopapain. (C) 1997 Elsevier Science B.V.

Published
1997
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9. Interleukin-6 in human multiple myeloma

Author

Zhao-Yang Lu, Régis Bataille, Xue Guang Zhang, Bernard Klein, Institut de Génétique Moléculaire de Montpellier (IGMM), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), School of Earth and Space Sciences [Beijing], and Peking University [Beijing]

Subjects
Myeloma protein, medicine.medical_treatment, Immunology, Biochemistry, 03 medical and health sciences, 0302 clinical medicine, Text mining, Immunopathology, Medicine, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Interleukin 6, Multiple myeloma, biology, business.industry, Bone Marrow/physiology/physiopathology Hematopoietic Stem Cells/*physiology Humans Interleukin-6/*physiology Models, Cell Biology, Hematology, medicine.disease, medicine.anatomical_structure, Cytokine, 030220 oncology & carcinogenesis, biology.protein, Biological Multiple Myeloma/blood/*immunology Plasma Cells/immunology/*physiology Signal Transduction, Bone marrow, Signal transduction, business, 030215 immunology
Published
1995
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10. Interleukin-10 is a proliferation factor but not a differentiation factor for human myeloma cells

Author

Xue-Guang Zhang, Bernard Klein, Régis Bataille, Zhao Yang Lu, Brigitte Morel-Fournier, John Wijdenes, Jean-François Rossi, Zong-Jiang Gu, Carmen Rodríguez, Jean Luc Harousseau, School of Earth and Space Sciences [Beijing], Peking University [Beijing], Institut de Génétique Moléculaire de Montpellier (IGMM), and Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM)

Subjects
Cell Differentiation/drug effects Cell Division/drug effects Enzyme-Linked Immunosorbent Assay Humans Interleukin-10/blood/*pharmacology Interleukin-6/biosynthesis Leukemia, medicine.medical_specialty, medicine.medical_treatment, Cellular differentiation, Immunology, Plasma cell, Interleukin/antagonists & inhibitors/physiology Receptors, Biochemistry, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, medicine, Cultured/drug effects, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, Multiple myeloma, Plasma cell leukemia, biology, Growth factor, Cell Biology, Hematology, medicine.disease, Molecular biology, 3. Good health, Interleukin 10, Endocrinology, medicine.anatomical_structure, Cytokine, Plasma Cell/blood/pathology Middle Aged Multiple Myeloma/blood/*pathology Myeloma Proteins/biosynthesis Neoplasm Proteins/biosynthesis/blood Plasma Cells/drug effects/metabolism Polymerase Chain Reaction Receptors, 030220 oncology & carcinogenesis, Interleukin-6 Recombinant Proteins/pharmacology Tumor Cells, biology.protein, Antibody, 030215 immunology
Abstract

Because interleukin-10 (IL-10) is a potent differentiation factor of human B cells into mature plasma cells, we investigated its effect on human malignant plasma cells. IL-10 did not induce any differentiation and increase in Ig synthesis in four human IL-6-dependent malignant plasma cell lines. However, it stimulated the proliferation of two of four cytokine-dependent cell lines in the absence of IL-6 and IL-10-dependent myeloma cell lines have been obtained. The myeloma cell growth activity of IL-10 was unaffected by anti-IL-6 and anti-IL-6R antibodies. Similarly, IL-10 stimulated (P = .001) the proliferation of freshly-explanted myeloma cells in IL-6-deprived cultures of tumor samples from patients with active multiple myeloma (MM) and produced twice as many myeloma cells in these cultures. Again, this cytokine was unable to induce further differentiation (assessed by rate of Ig production) of fresh myeloma cells. A very sensitive enzyme-linked immunosorbent assay (ELISA; 1 pg/mL) only rarely detected IL-10 in the sera of MM patients (3 of 89). On the contrary, serum IL-10 was detected in 60% of patients with plasma cell leukemia (12 of 20). These data show that IL-10 is an IL-6-unrelated growth factor for malignant plasmablastic cells. This cytokine could be involved in the late phase of MM in vivo.

Published
1995
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