10 results on '"Julien Calvo"'
Search Results
2. Human hematopoietic stem/progenitor cells display reactive oxygen species-dependent long-term hematopoietic defects after exposure to low doses of ionizing radiations
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Vilma Barroca, Andreas Lefevre, Véronique Ménard, Marie-Laure Arcangeli, Elia Henry, Inès Souissi-Sahraoui, Françoise Pflumio, Anna Campalans, Julien Calvo, and Margaux Deynoux
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chemistry.chemical_classification ,Reactive oxygen species ,Cellular differentiation ,medicine.medical_treatment ,Hematopoietic Tissue ,Hematology ,Hematopoietic stem cell transplantation ,Cell biology ,Blood cell ,Haematopoiesis ,medicine.anatomical_structure ,chemistry ,medicine ,Stem cell ,Progenitor cell - Abstract
Hematopoietic stem cells are responsible for life-long blood cell production and are highly sensitive to exogenous stresses. The effects of low doses of ionizing radiations on radiosensitive tissues such as the hematopoietic tissue are still unknown despite their increasing use in medical imaging. Here, we study the consequences of low doses of ionizing radiations on differentiation and self-renewal capacities of human primary hematopoietic stem/progenitor cells (HSPC). We found that a single 20 mGy dose impairs the hematopoietic reconstitution potential of human HSPC but not their differentiation properties. In contrast to high irradiation doses, low doses of irradiation do not induce DNA double strand breaks in HSPC but, similar to high doses, induce a rapid and transient increase of reactive oxygen species (ROS) that promotes activation of the p38MAPK pathway. HSPC treatment with ROS scavengers or p38MAPK inhibitor prior exposure to 20 mGy irradiation abolishes the 20 mGy-induced defects indicating that ROS and p38MAPK pathways are transducers of low doses of radiation effects. Taken together, these results show that a 20 mGy dose of ionizing radiation reduces the reconstitution potential of HSPC suggesting an effect on the self-renewal potential of human hematopoietic stem cells and pinpointing ROS or the p38MAPK as therapeutic targets. Inhibition of ROS or the p38MAPK pathway protects human primary HSPC from low-dose irradiation toxicity.
- Published
- 2019
3. Hypoxia favors chemoresistance in T-ALL through an HIF1α-mediated mTORC1 inhibition loop
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Paola Ballerini, Frédéric Mazurier, Laurent Renou, Benjamin Uzan, Sara Chabi, Irina Naguibneva, André Baruchel, Lucine Fahy, Françoise Pflumio, Julien Calvo, Marie-Laure Arcangeli, Rima Haddad, Sandrine Poglio, Thierry Leblanc, Charly Le Maout, and Arnaud Petit
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Lymphoid Neoplasia ,Cell growth ,Chemistry ,Hematology ,mTORC1 ,Hypoxia (medical) ,Mitochondrion ,Mechanistic Target of Rapamycin Complex 1 ,medicine.disease ,Precursor T-Cell Lymphoblastic Leukemia-Lymphoma ,Leukemia ,medicine.anatomical_structure ,Pharmaceutical Preparations ,Drug Resistance, Neoplasm ,medicine ,Cancer research ,Tumor Microenvironment ,Humans ,Glycolysis ,Bone marrow ,medicine.symptom ,Hypoxia ,PI3K/AKT/mTOR pathway - Abstract
Resistance to chemotherapy, a major therapeutic challenge in the treatment of T-cell acute lymphoblastic leukemia (T-ALL), can be driven by interactions between leukemic cells and the microenvironment that promote survival of leukemic cells. The bone marrow, an important leukemia niche, has low oxygen partial pressures that highly participate in the regulation of normal hematopoiesis. Here we show that hypoxia inhibits T-ALL cell growth by slowing down cell cycle progression, decreasing mitochondria activity, and increasing glycolysis, making them less sensitive to antileukemic drugs and preserving their ability to initiate leukemia after treatment. Activation of the mammalian target of rapamycin (mTOR) was diminished in hypoxic leukemic cells, and treatment of T-ALL with the mTOR inhibitor rapamycin in normoxia mimicked the hypoxia effects, namely decreased cell growth and increased quiescence and drug resistance. Knocking down (KD) hypoxia-induced factor 1α (HIF-1α), a key regulator of the cellular response to hypoxia, antagonized the effects observed in hypoxic T-ALL and restored chemosensitivity. HIF-1α KD also restored mTOR activation in low O2 concentrations, and inhibiting mTOR in HIF1α KD T-ALL protected leukemic cells from chemotherapy. Thus, hypoxic niches play a protective role of T-ALL during treatments. Inhibition of HIF-1α and activation of the mTORC1 pathway may help suppress the drug resistance of T-ALL in hypoxic niches.
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- 2020
4. Fratricide-resistant CD1a-specific CAR T cells for the treatment of cortical T-cell acute lymphoblastic leukemia
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María L. Toribio, José Luis Fuster, Clara Bueno, Julien Calvo, Francisco Gutierrez-Agüera, Jan Cools, Benjamin Uzan, Manuel Ramírez-Orellana, Françoise Pflumio, Sara González-García, Talia Velasco-Hernandez, Montserrat Torrebadell, Matteo Libero Baroni, O. Blanch-Lombarte, Pablo Menendez, Diego Sánchez-Martínez, Julia G. Prado, Jordi Juncà, Mireia Camós, and Heleia Roca-Ho
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Immunobiology and Immunotherapy ,MONOCLONAL-ANTIBODY ,T-Lymphocytes ,medicine.medical_treatment ,CD34 ,CHILDREN ,Precursor T-Cell Lymphoblastic Leukemia-Lymphoma ,Biochemistry ,Jurkat cells ,Immunotherapy, Adoptive ,Antigens, CD1 ,Jurkat Cells ,Mice ,0302 clinical medicine ,hemic and lymphatic diseases ,Medicine ,CYTOGENETIC ABNORMALITIES ,0303 health sciences ,Receptors, Chimeric Antigen ,integumentary system ,THYMECTOMY ,SAFETY SWITCH ,HUMAN THYMUS ,Hematology ,CHIMERIC ANTIGEN RECEPTOR ,3. Good health ,medicine.anatomical_structure ,IMMUNE FUNCTION ,Life Sciences & Biomedicine ,EXPRESSION ,T cell ,Immunology ,MESENCHYMAL STEM-CELLS ,03 medical and health sciences ,Antigen ,Animals ,Humans ,Progenitor cell ,030304 developmental biology ,Science & Technology ,business.industry ,Cell Biology ,Immunotherapy ,Xenograft Model Antitumor Assays ,Chimeric antigen receptor ,Cell culture ,Drug Resistance, Neoplasm ,Cancer research ,business ,Automobiles ,030215 immunology - Abstract
Relapsed/refractory T-cell acute lymphoblastic leukemia (T-ALL) has a dismal outcome, and no effective targeted immunotherapies for T-ALL exist. The extension of chimeric antigen receptor (CAR) T cells (CARTs) to T-ALL remains challenging because the shared expression of target antigens between CARTs and T-ALL blasts leads to CART fratricide. CD1a is exclusively expressed in cortical T-ALL (coT-ALL), a major subset of T-ALL, and retained at relapse. This article reports that the expression of CD1a is mainly restricted to developing cortical thymocytes, and neither CD34+ progenitors nor T cells express CD1a during ontogeny, confining the risk of on-target/off-tumor toxicity. We thus developed and preclinically validated a CD1a-specific CAR with robust and specific cytotoxicity in vitro and antileukemic activity in vivo in xenograft models of coT-ALL, using both cell lines and coT-ALL patient-derived primary blasts. CD1a-CARTs are fratricide resistant, persist long term in vivo (retaining antileukemic activity in re-challenge experiments), and respond to viral antigens. Our data support the therapeutic and safe use of fratricide-resistant CD1a-CARTs for relapsed/refractory coT-ALL. ispartof: BLOOD vol:133 issue:21 pages:2291-2304 ispartof: location:United States status: published
- Published
- 2018
5. DNMT3AR882H mutant and Tet2 inactivation cooperate in the deregulation of DNA methylation control to induce lymphoid malignancies in mice
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Cécile K. Lopez, Kristian Helin, Elena Mylonas, Michaela Fontenay, Enguerran Mouly, Françoise Pflumio, P. Gaulard, Marianne Terndrup Pedersen, M'Boyba Diop, Michael Weber, Laurianne Scourzic, Lucile Couronné, Nathalie Droin, O. Bernard, Julien Calvo, Patrice Dubreuil, Ambre Bender, Philippe Dessen, N Martin, V Della Valle, Sylvain Guibert, Thomas Mercher, Biotechnologie et signalisation cellulaire (BSC), Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)-Institut de recherche de l'Ecole de biotechnologie de Strasbourg (IREBS), Hématopoïèse normale et pathologique ( U1170 Inserm ), Université Paris-Sud - Paris 11 ( UP11 ) -Institut Gustave Roussy ( IGR ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut Gustave Roussy ( IGR ), Génétique des tumeurs ( U985 ), Institut Gustave Roussy ( IGR ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Norwegian Defence Intelligence School [Oslo] ( NDUC ), Centre de recherche en économie et management ( CREM ), Université de Caen Normandie ( UNICAEN ), Normandie Université ( NU ) -Normandie Université ( NU ) -Université de Rennes 1 ( UR1 ), Université de Rennes ( UNIV-RENNES ) -Université de Rennes ( UNIV-RENNES ) -Centre National de la Recherche Scientifique ( CNRS ), Centro de Aplicaciones de Tecnologías de Avanzada ( CENATAV ), CENATAV, Laboratoire Ligérien de Linguistique ( LLL ), Bibliothèque nationale de France ( BnF ) -Université d'Orléans ( UO ) -Université de Tours-Centre National de la Recherche Scientifique ( CNRS ), Université Paris Descartes - Faculté de Médecine ( UPD5 Médecine ), Université Paris Descartes - Paris 5 ( UPD5 ), The Unilever Centre for Molecular Science Informatics, Department of Chemistry, University of Cambridge [UK] ( CAM ), Département de pathologie [Mondor], Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 ), Institut Mondor de Recherche Biomédicale ( IMRB ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 ( UPEC UP12 ), Images et Modèles, Centre de Recherche en Acquisition et Traitement de l'Image pour la Santé ( CREATIS ), Université Jean Monnet [Saint-Étienne] ( UJM ) -Hospices Civils de Lyon ( HCL ) -Institut National des Sciences Appliquées de Lyon ( INSA Lyon ), Université de Lyon-Institut National des Sciences Appliquées ( INSA ) -Université de Lyon-Institut National des Sciences Appliquées ( INSA ) -Université Claude Bernard Lyon 1 ( UCBL ), Université de Lyon-Centre National de la Recherche Scientifique ( CNRS ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Université Jean Monnet [Saint-Étienne] ( UJM ) -Hospices Civils de Lyon ( HCL ) -Institut National des Sciences Appliquées de Lyon ( INSA Lyon ), and Université de Lyon-Centre National de la Recherche Scientifique ( CNRS ) -Institut National de la Santé et de la Recherche Médicale ( INSERM )
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0301 basic medicine ,Cancer Research ,Myeloid ,Cellular differentiation ,Notch signaling pathway ,Biology ,Sciences du Vivant [q-bio]/Biochimie, Biologie Moléculaire ,medicine.disease_cause ,Article ,[ SDV.CAN ] Life Sciences [q-bio]/Cancer ,DNA Methyltransferase 3A ,Dioxygenases ,03 medical and health sciences ,Mice ,Proto-Oncogene Proteins ,medicine ,Animals ,Genes, Tumor Suppressor ,[SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology ,DNA (Cytosine-5-)-Methyltransferases ,Mutation ,Receptors, Notch ,Myeloid leukemia ,Cell Differentiation ,Hematology ,DNA Methylation ,Lymphoproliferative Disorders ,Transplantation ,Gene expression profiling ,DNA-Binding Proteins ,030104 developmental biology ,medicine.anatomical_structure ,Oncology ,embryonic structures ,DNA methylation ,Immunology ,Cancer research - Abstract
International audience; TEN-ELEVEN-TRANSLOCATION-2 (TET2) and DNA-METHYLTRANSFERASE-3A (DNMT3A), both encoding proteins involved in regulating DNA methylation, are mutated in hematological malignancies affecting both myeloid and lymphoid lineages. We previously reported an association of TET2 and DNMT3A mutations in progenitors of patients with angioimmunoblastic T-cell lymphomas (AITL). Here, we report on the cooperative effect of Tet2 inactivation and DNMT3A mutation affecting arginine 882 (DNMT3A(R882H)) using a murine bone marrow transplantation assay. Five out of eighteen primary recipients developed hematological malignancies with one mouse developing an AITL-like disease, two mice presenting acute myeloid leukemia (AML)-like and two others T-cell acute lymphoblastic leukemia (T-ALL)-like diseases within 6 months following transplantation. Serial transplantations of DNMT3A(R882H) Tet2(-/-) progenitors led to a differentiation bias toward the T-cell compartment, eventually leading to AITL-like disease in 9/12 serially transplanted recipients. Expression profiling suggested that DNMT3A(R882H) Tet2(-/-) T-ALLs resemble those of NOTCH1 mutant. Methylation analysis of DNMT3A(R882H) Tet2(-/-) T-ALLs showed a global increase in DNA methylation affecting tumor suppressor genes and local hypomethylation affecting genes involved in the Notch pathway. Our data confirm the transformation potential of DNMT3A(R882H) Tet2(-/-) progenitors and represent the first cooperative model in mice involving Tet2 inactivation driving lymphoid malignancies.
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- 2016
6. Single cell assays unveil functional and transcriptional heterogeneity of human hemopoietic lympho-myeloid progenitors
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Jessica Doondeea, Andreas Reinisch, Zahra Aboukhalil, Fiona K. Hamey, Françoise Pflumio, Marina Samitsch, Georg W. Otto, Bilyana Stoilova, Berthold Göttgens, Lynn Quek, Ravindra Majeti, Emmanouela Repapi, Catherine Porcher, Julien Calvo, Paresh Vyas, Batchimeg Usukhbayar, Nicolas Goardon, Emmanuelle Six, Stephen S. Taylor, and Dimitris Karamitros
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Cancer Research ,Haematopoiesis ,Myeloid ,medicine.anatomical_structure ,Cell ,Genetics ,medicine ,Cell Biology ,Hematology ,Biology ,Progenitor cell ,Molecular Biology ,Cell biology - Published
- 2017
7. Assessment of Human Multi-Potent Hematopoietic Stem/Progenitor Cell Potential Using a Single In Vitro Screening System
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Julien Calvo, Aissa Benyoucef, Marie-Christine Rouyez, Jan Baijer, and Françoise Pflumio
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Cellular differentiation ,Blotting, Western ,CD34 ,lcsh:Medicine ,Gene Expression ,Antigens, CD34 ,Biology ,Stem cell marker ,Cell Line ,Molecular Genetics ,03 medical and health sciences ,0302 clinical medicine ,Molecular Cell Biology ,Genetics ,Humans ,Progenitor cell ,lcsh:Science ,030304 developmental biology ,Interleukin 3 ,0303 health sciences ,Multidisciplinary ,Stem Cells ,lcsh:R ,Calcium-Binding Proteins ,Computational Biology ,Membrane Proteins ,Cell Differentiation ,Hematology ,Hematopoietic Stem Cells ,Flow Cytometry ,ADP-ribosyl Cyclase 1 ,Cell biology ,Hematopoiesis ,Endothelial stem cell ,030220 oncology & carcinogenesis ,Medicine ,Intercellular Signaling Peptides and Proteins ,lcsh:Q ,Stem cell ,Cellular Types ,Adult stem cell ,Research Article ,Developmental Biology - Abstract
Hematopoietic stem cells are responsible for the generation of the entire blood system through life. This characteristic relies on their ability to self renew and on their multi-potentiality. Thus quantification of the number of hematopoietic stem cells in a given cell population requires to show both properties in the studied cell populations. Although xenografts models that support human hematopoietic stem cells have been described, such in vivo experimental systems remain restrictive for high throughput screening purposes for example. In this work we developed a conditional tetracycline inducible system controlling the expression of the human NOTCH ligand Delta-like 1 in the murine stromal MS5 cells. We cultured hematopoietic immature cells enriched in progenitor/stem cells in contact with MS5 cells that conditionally express Delta-like 1, in conditions designed to generate multipotential lineage differentiation. We show that upon induction or repression of DL1 expression during co-culture, human immature CD34(+)CD38(-/low)(CD45RA(-)CD90(+)) cells can express their B, T, NK, granulo/monocytic and erythroid potentials in a single well, and at the single cell level. We also document the interference of low NOTCH activation with human B and myelo/erythroid lymphoid differentiation. This system represents a novel tool to precisely quantify human hematopoietic immature cells with both lymphoid and myeloid potentials.
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- 2012
8. NOTCH is a key regulator of human T-cell acute leukemia initiating cell activity
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Judith Landman-Parker, Philippe Brunet de la Grange, Bastien Gerby, Paul-Henri Romeo, Nicolas Boissel, Michaela Fontenay, Françoise Pflumio, Julien Calvo, André Baruchel, Florence Armstrong, Paola Ballerini, Hervé Dombret, Marie-Christine Rouyez, 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), Service d'hématologie-oncologie adultes, Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Université Paris Diderot - Paris 7 (UPD7)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), Service d'hématologie pédiatrique, Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Université Paris Diderot - Paris 7 (UPD7), Université Pierre et Marie Curie - Paris 6 (UPMC), Service d'hématologie-immunologie-oncologie pédiatrique [CHU Trousseau], Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Trousseau [APHP], Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Université Paris Diderot - Paris 7 (UPD7), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Université Paris Diderot - Paris 7 (UPD7)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), CHU Trousseau [APHP], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)
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Cellular immunity ,Stromal cell ,[SDV]Life Sciences [q-bio] ,Immunology ,Notch signaling pathway ,Regulator ,Cell Culture Techniques ,[SDV.CAN]Life Sciences [q-bio]/Cancer ,Cell Communication ,Mice, SCID ,Biology ,Precursor T-Cell Lymphoblastic Leukemia-Lymphoma ,Biochemistry ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Mice, Inbred NOD ,Calcium-binding protein ,Precursor cell ,Tumor Cells, Cultured ,Animals ,Humans ,Receptor, Notch1 ,Receptor ,ComputingMilieux_MISCELLANEOUS ,030304 developmental biology ,0303 health sciences ,Cell growth ,Calcium-Binding Proteins ,Genes, T-Cell Receptor gamma ,Membrane Proteins ,Cell Biology ,Hematology ,Coculture Techniques ,Cell biology ,030220 oncology & carcinogenesis ,Intercellular Signaling Peptides and Proteins ,Amyloid Precursor Protein Secretases ,Stromal Cells ,Oligopeptides ,Neoplasm Transplantation ,Signal Transduction - Abstract
Understanding the pathways that regulate the human T-cell acute lymphoblastic leukemia (T-ALL) initiating cells (T-LiC) activity has been hampered by the lack of biologic assays in which this human disease can be studied. Here we show that coculture of primary human T-ALL with a mouse stromal cell line expressing the NOTCH ligand delta-like-1 (DL1) reproducibly allowed maintenance of T-LiC and long-term growth of blast cells. Human T-ALL mutated or not on the NOTCH receptor required sustained activation of the NOTCH pathway via receptor/ligand interaction for growth and T-LiC activity. On the reverse, inhibition of the NOTCH pathway during primary cultures abolished in vitro cell growth and in vivo T-LiC activity. Altogether, these results demonstrate the major role of the NOTCH pathway activation in human T-ALL development and in the maintenance of leukemia-initiating cells.
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- 2009
9. Primary infection with simian immunodeficiency virus: plasmacytoid dendritic cell homing to lymph nodes, type I interferon, and immune suppression
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Pierre Lebon, Thibault Andrieu, Patricia Brochard, Benjamin Manéglier, Ingrid Karlsson, Leïla Perié, Anne Hosmalin, Bruno Vaslin, Odile Spreux-Varoquaux, Roger Le Grand, Michelina Nascimbeni, Benoit Malleret, Benoit Delache, Julien Calvo, Service de virologie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Saint-Vincent de Paul, Institut Cochin (UMR_S567 / UMR 8104), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Immunopathologie Expérimentale, Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Laboratoire d'Immuno-Pathologie Expérimentale, Service de Neurovirologie, Université Paris-Sud - Paris 11 (UP11)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-CRSSA, Laboratoire de Neuro-Immuno-Virologie, Service de Neurovirologie EMI E-01 (UMR E01), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay, Assistance publique - Hôpitaux de Paris (AP-HP) - Hôpital Saint-Vincent de Paul, Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS), Université Paris-Sud - Paris 11 (UP11) - École pratique des hautes études (EPHE) - Commissariat à l'énergie atomique et aux énergies alternatives (CEA) - CRSSA, Université Paris-Sud - Paris 11 (UP11) - Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Université Paris-Sud - Paris 11 (UP11)-École Pratique des Hautes Études (EPHE), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Saint-Vincent de Paul, Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5), Université Paris-Sud - Paris 11 (UP11)-École pratique des hautes études (EPHE)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-CRSSA, and Université Paris-Sud - Paris 11 (UP11)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)
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CD4-Positive T-Lymphocytes ,[SDV.IMM] Life Sciences [q-bio]/Immunology ,Immunology ,Simian Acquired Immunodeficiency Syndrome ,Plasmacytoid dendritic cell ,Biology ,CD8-Positive T-Lymphocytes ,medicine.disease_cause ,Biochemistry ,03 medical and health sciences ,0302 clinical medicine ,Immune system ,Cell Movement ,medicine ,Immune Tolerance ,Animals ,Indoleamine-Pyrrole 2,3,-Dioxygenase ,Viremia ,Antigen-presenting cell ,Acute-Phase Reaction ,030304 developmental biology ,0303 health sciences ,Interleukin-18 ,Interleukin-2 Receptor alpha Subunit ,FOXP3 ,Cell Biology ,Hematology ,Dendritic cell ,Dendritic Cells ,Simian immunodeficiency virus ,Acquired immune system ,Virology ,3. Good health ,Macaca fascicularis ,Interferon Type I ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,Simian Immunodeficiency Virus ,Lymph Nodes ,Interferon type I ,030215 immunology ,medicine.drug - Abstract
Plasmacytoid dendritic cells (pDCs) are antigen-presenting cells that develop into type-I interferon (IFN-I)–producing cells in response to pathogens. Their role in human immunodeficiency virus (HIV) pathogenesis needs to be understood. We analyzed their dynamics in relation to innate and adaptive immunity very early during the acute phase of simian immunodeficiency virus (SIV) infection in 18 macaques. pDC counts decreased in blood and increased in peripheral lymph nodes, consistent with early recruitment in secondary lymphoid tissues. These changes correlated with the kinetic and intensity of viremia and were associated with a peak of plasma IFN-I. IFN-I and viremia were positively correlated with functional activity of the immune suppression associated enzyme indoleamine-2,3-dioxygenase (IDO) and FoxP3+CD8+ T cells, which both negatively correlated with SIV-specific T-cell proliferation and CD4+ T-cell activation. These data suggest that pDCs and IFN-I play a key role in shaping innate and adaptive immunity toward suppressive pathways during the acute phase of SIV/HIV primary infection.
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- 2008
10. Declined Presentation
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Naïs Prade, Jacques Ghysdael, André Baruchel, Paola Ballerini, Frederic Baleydier, Judith Landman-Parker, Arnaud Petit, Xavier Cahu, Sandrine Poglio, Françoise Pflumio, Benjamin Uzan, Julien Calvo, Eric Delabesse, and Thierry Leblanc
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Cancer Research ,T cell ,Lymphoblastic Leukemia ,Cell Biology ,Hematology ,Biology ,medicine.anatomical_structure ,Adipogenesis ,Immunology ,Genetics ,medicine ,Bone marrow ,Presentation (obstetrics) ,Molecular Biology - Published
- 2014
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