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8 results on '"MESH : Cell Communication"'

1. Viral infection prevents diabetes by inducing regulatory T cells through NKT cell-plasmacytoid dendritic cell interplay

Author

Agnès Lehuen, Roberto Mallone, Marc Dalod, Lucie Beaudoin, Julien Diana, Anna Tafuri, Vedran Brezar, Christian Boitard, Andrew L. Mellor, Matthias von Herrath, Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université Paris Descartes - Paris 5 (UPD5), Centre d'Immunologie de Marseille - Luminy (CIML), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Medical College of Georgia, Immunotherapy Center, Immunité et cancer (U932), Université Paris Descartes - Paris 5 (UPD5)-Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), La Jolla Institute for Immunology [La Jolla, CA, États-Unis], Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU), CHU Cochin [AP-HP], Université Paris Descartes - Paris 5 (UPD5)-Institut Curie-Institut National de la Santé et de la Recherche Médicale (INSERM), La Jolla Institute for Allergy and Immunology (LIA), La Jolla Institute for Allergy & Immunology, Université Paris Descartes - Paris 5 ( UPD5 ), Centre d'Immunologie de Marseille - Luminy ( CIML ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Aix Marseille Université ( AMU ) -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 ), and La Jolla Institute for Allergy and Immunology ( LIA )

Subjects
MESH: Interleukin-10, endocrine system diseases, Programmed Cell Death 1 Receptor, MESH: Membrane Glycoproteins, MESH : Membrane Glycoproteins, MESH: Lymph Nodes, Cell Communication, CD8-Positive T-Lymphocytes, Lymphocyte Activation, T-Lymphocytes, Regulatory, B7-H1 Antigen, MESH : Diabetes Mellitus, Type 1, MESH : T-Lymphocytes, Regulatory, Interleukin 21, Mice, 0302 clinical medicine, Transforming Growth Factor beta, immune system diseases, [ SDV.IMM ] Life Sciences [q-bio]/Immunology, Immunology and Allergy, Cytotoxic T cell, MESH: Animals, IL-2 receptor, MESH : Antigens, CD80, MESH : Lymph Nodes, 0303 health sciences, Membrane Glycoproteins, MESH: Dendritic Cells, MESH : Peptides, MESH: Peptides, FOXP3, hemic and immune systems, MESH : CD8-Positive T-Lymphocytes, Natural killer T cell, MESH: CD8-Positive T-Lymphocytes, 3. Good health, Interleukin-10, MESH: Virus Diseases, medicine.anatomical_structure, Virus Diseases, Antigens, Surface, B7-1 Antigen, [SDV.IMM]Life Sciences [q-bio]/Immunology, MESH: Diabetes Mellitus, Type 1, MESH : Apoptosis Regulatory Proteins, MESH : Antigens, Surface, endocrine system, MESH : Cell Communication, MESH: Antigens, Surface, T cell, Immunology, macromolecular substances, Biology, Article, 03 medical and health sciences, Islets of Langerhans, MESH: Antigens, CD80, MESH : Interleukin-10, MESH : Mice, MESH: Cell Communication, medicine, Animals, MESH : Islets of Langerhans, Antigen-presenting cell, MESH: Lymphocyte Activation, MESH: Mice, MESH : Lymphocyte Activation, MESH: Transforming Growth Factor beta, 030304 developmental biology, MESH: Apoptosis Regulatory Proteins, MESH: T-Lymphocytes, Regulatory, MESH: Islets of Langerhans, Dendritic cell, Dendritic Cells, MESH : Virus Diseases, MESH : Natural Killer T-Cells, MESH : Transforming Growth Factor beta, Diabetes Mellitus, Type 1, MESH: Natural Killer T-Cells, MESH : Dendritic Cells, Natural Killer T-Cells, MESH : Animals, Lymph Nodes, Apoptosis Regulatory Proteins, Peptides, 030215 immunology
Abstract

iNKT cell and pDC cross talk prevents type 1 diabetes by inducing T reg cells in the pancreatic lymph node during viral infection., Type 1 diabetes (T1D) is an autoimmune disease resulting from T cell–mediated destruction of insulin-producing β cells, and viral infections can prevent the onset of disease. Invariant natural killer T cells (iNKT cells) exert a regulatory role in T1D by inhibiting autoimmune T cell responses. As iNKT cell–plasmacytoid dendritic cell (pDC) cooperation controls viral replication in the pancreatic islets, we investigated whether this cellular cross talk could interfere with T1D development during viral infection. Using both virus-induced and spontaneous mouse models of T1D, we show that upon viral infection, iNKT cells induce TGF-β–producing pDCs in the pancreatic lymph nodes (LNs). These tolerogenic pDCs convert naive anti-islet T cells into Foxp3+ CD4+ regulatory T cells (T reg cells) in pancreatic LNs. T reg cells are then recruited into the pancreatic islets where they produce TGF-β, which dampens the activity of viral- and islet-specific CD8+ T cells, thereby preventing T1D development in both T1D models. These findings reveal a crucial cooperation between iNKT cells, pDCs, and T reg cells for prevention of T1D by viral infection.

Published
2011
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2. Stromal cell networks regulate thymocyte migration and dendritic cell behavior in the thymus

Author

Jonathan A. Nowak, Marc Bajénoff, Mathieu Fallet, Stephanie L. Sanos, Centre d'Immunologie de Marseille - Luminy ( CIML ), Aix Marseille Université ( AMU ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Centre d'Immunologie de Marseille - Luminy (CIML), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU)

Subjects
Chemokine, MESH: Mice, Mutant Strains, MESH : Antigens, Cell Communication, MESH: T-Lymphocyte Subsets, MESH: Mice, Knockout, MESH : Radiation Chimera, Mice, 0302 clinical medicine, Cell Movement, T-Lymphocyte Subsets, Immunology and Allergy, MESH : Cell Movement, [ SDV.IMM ] Life Sciences [q-bio]/Immunology, MESH: Animals, MESH: Cell Movement, Mice, Knockout, 0303 health sciences, MESH: Dendritic Cells, Cell biology, Thymocyte, medicine.anatomical_structure, Radiation Chimera, [SDV.IMM]Life Sciences [q-bio]/Immunology, MESH: Antigens, Thymocyte migration, Stromal cell, MESH : Cell Communication, MESH: Radiation Chimera, T cell, Immunology, Thymus Gland, MESH : Mice, Inbred C57BL, Biology, 03 medical and health sciences, MESH : Microscopy, Fluorescence, Multiphoton, MESH: Mice, Inbred C57BL, MESH: Cell Communication, MESH : Mice, medicine, Animals, MESH : Thymus Gland, Progenitor cell, Antigens, MESH: Mice, 030304 developmental biology, Dendritic cell, Dendritic Cells, MESH: Thymus Gland, Mice, Mutant Strains, MESH : T-Lymphocyte Subsets, Mice, Inbred C57BL, MESH : Mice, Mutant Strains, Microscopy, Fluorescence, Multiphoton, MESH : Stromal Cells, MESH : Dendritic Cells, T cell migration, biology.protein, MESH: Microscopy, Fluorescence, Multiphoton, MESH : Mice, Knockout, MESH : Animals, Stromal Cells, MESH: Stromal Cells, 030215 immunology
Abstract

After entry into thymus, T cell progenitors migrate in the cortex and the medulla while completing their education. Recent reports have documented the dynamic and tortuous behavior of thymocytes. However, other than chemokines and/or segregated thymic substrates, the factors contributing to the dynamic patterns of thymocyte movement are poorly characterized. By combining confocal and dynamic two-photon microscopy, we demonstrate that thymocytes continuously migrate on thymic stromal cell networks. In addition to constituting “roads” for thymocytes, we observed that these networks also provide a scaffold on which dendritic cells attach themselves. These results highlight the central role of stromal microanatomy in orchestrating the multiple cellular interactions necessary for T cell migration/development within the thymus.

Published
2011
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3. Tumor Suppressor Schwannomin/Merlin Is Critical for the Organization of Schwann Cell Contacts in Peripheral Nerves

Author

Carmen Cifuentes-Diaz, Jean-Antoine Girault, Michèle Carnaud, Natalia Denisenko, Fabrice Chareyre, Marco Giovannini, Michiko Niwa-Kawakita, Laurence Goutebroze, Evelyne Benoit, Theano Irinopoulou, Institut du Fer à Moulin (IFM - Inserm U1270 - SU), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Institut du Fer à Moulin, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de Neurobiologie Alfred Fessard (INAF), Centre National de la Recherche Scientifique (CNRS), Laboratoire de neurobiologie cellulaire et moléculaire (NBCM), Génomique Fonctionnelle des Tumeurs Solides (U1162), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut de Neurobiologie Alfred Fessard ( INAF ), Centre National de la Recherche Scientifique ( CNRS ), Laboratoire de neurobiologie cellulaire et moléculaire ( NBCM ), Genomique Fonctionnelle des Tumeurs Solides, and Université Paris Diderot - Paris 7 ( UPD7 ) -IFR105-Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM )

Subjects
Cellular differentiation, [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, Cell Communication, MESH : Gene Deletion, Schwann cell proliferation, Mice, 0302 clinical medicine, Compact myelin, MESH : Cell Proliferation, MESH: Animals, Neurofibromatosis type 2, ComputingMilieux_MISCELLANEOUS, MESH : Neurofibromin 2, Neurofibromin 2, 0303 health sciences, MESH : Tumor Suppressor Proteins, General Neuroscience, MESH : Peripheral Nerves, MESH: Neurofibromin 2, Articles, MESH : Mice, Transgenic, Cell biology, medicine.anatomical_structure, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], MESH : Cell Communication, Tumor suppressor gene, MESH: Mice, Transgenic, MESH : Schwann Cells, Schwann cell, Mice, Transgenic, Biology, 03 medical and health sciences, MESH: Cell Proliferation, MESH : Mice, MESH: Cell Communication, medicine, Animals, Humans, MESH: Tumor Suppressor Proteins, Peripheral Nerves, MESH: Mice, Cell Proliferation, 030304 developmental biology, MESH: Humans, Tumor Suppressor Proteins, MESH : Humans, medicine.disease, MESH: Peripheral Nerves, Merlin (protein), nervous system, Cytoplasm, MESH: Gene Deletion, [ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Schwann Cells, MESH : Animals, MESH: Schwann Cells, Neuroscience, Gene Deletion, 030217 neurology & neurosurgery
Abstract

Schwannomin/merlin is the product of a tumor suppressor gene mutated in neurofibromatosis type 2 (NF2). Although the consequences of NF2 mutations on Schwann cell proliferation are well established, the physiological role of schwannomin in differentiated cells is not known. To unravel this role, we studied peripheral nerves in mice overexpressing in Schwann cells schwannomin with a deletion occurring in NF2 patients (P0–SCH–Δ39–121) or a C-terminal deletion. The myelin sheath and nodes of Ranvier were essentially preserved in both lines. In contrast, the ultrastructural and molecular organization of contacts between Schwann cells and axons in paranodal and juxtaparanodal regions were altered, with irregular juxtaposition of normal and abnormal areas of contact. Similar but more severe alterations were observed in mice with conditional deletion of theNf2gene in Schwann cells. The number of Schmidt–Lanterman incisures, which are cytoplasmic channels interrupting the compact myelin and characterized by distinct autotypic contacts, was increased in the three mutant lines. P0–SCH–Δ39–121 and conditionally deleted mice displayed exuberant wrapping of nonmyelinated fibers and short internodes, an abnormality possibly related to altered control of Schwann cell proliferation. In support of this hypothesis, Schwann cell number was increased along fibers before myelination in P0–SCH–Δ39–121 mice but not in those with C-terminal deletion. Schwann cell numbers were also more numerous in mice with conditional deletion. Thus, schwannomin plays an important role in the control of Schwann cell number and is necessary for the correct organization and regulation of axoglial heterotypic and glio-glial autotypic contacts.

Published
2008
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4. Cord blood-derived neurons are originated from CD133+/CD34 stem/progenitor cells in a cell-to-cell contact dependent manner

Author

Valérie Lapierre, Norbert Balon, Frédéric Deschaseaux, Claudine Versaux-Botteri, Vincent Zangiacomi, Remy Schlichter, Pierre Tiberghien, Stéphane Maddens, Laboratoire de Neurosciences Intégratives et Cliniques - UFC (EA 481) ( NEURO ), Université Bourgogne Franche-Comté [COMUE] ( UBFC ) -Université de Franche-Comté ( UFC ), Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) ( HOTE GREFFON ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Etablissement français du sang [Bourgogne-France-Comté] ( EFS [Bourgogne-France-Comté] ) -Université de Franche-Comté ( UFC ), Institut des Neurosciences Cellulaires et Intégratives ( INCI ), Université Louis Pasteur - Strasbourg I-Centre National de la Recherche Scientifique ( CNRS ), Centre de Recherche des Cordeliers ( CRC (UMR_S 872) ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Laboratoire de Neurosciences Intégratives et Cliniques - UFC (UR 481) (NEURO), Université de Franche-Comté (UFC), Université Bourgogne Franche-Comté [COMUE] (UBFC)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC (UMR INSERM 1098) (RIGHT), Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS BFC)-Université de Franche-Comté (UFC), Institut des Neurosciences Cellulaires et Intégratives (INCI), Université Louis Pasteur - Strasbourg I-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche des Cordeliers (CRC (UMR_S 872)), Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Neurosciences Intégratives et Cliniques - UFC (EA 481) (NEURO), Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement français du sang [Bourgogne-Franche-Comté] (EFS [Bourgogne-Franche-Comté])-Université de Franche-Comté (UFC), Université Paris Descartes - Paris 5 (UPD5)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Neurosciences Intégratives et Cliniques - UFC ( NEURO ), Université Bourgogne Franche-Comté ( UBFC ) -Université de Franche-Comté ( UFC ), Interactions hôte-greffon-tumeur, ingénierie cellulaire et génique - UFC ( HOTE GREFFON ), and Saas, Philippe

Subjects
MESH : Cell Line, Cellular differentiation, CD34, MESH: Neurons, Antigens, CD34, Cell Communication, 0302 clinical medicine, [ SDV.IMM ] Life Sciences [q-bio]/Immunology, AC133 Antigen, MESH: Antigens, CD, Neurons, 0303 health sciences, MESH: Peptides, MESH : Peptides, Stem Cells, Cell Differentiation, Hematology, Fetal Blood, 3. Good health, Cell biology, Endothelial stem cell, medicine.anatomical_structure, Cord blood, MESH : Antigens, CD34, MESH : Stem Cells, [SDV.IMM]Life Sciences [q-bio]/Immunology, Stem cell, MESH : Cell Differentiation, Adult stem cell, Subcellular Fractions, MESH: Cell Differentiation, [SDV.IMM] Life Sciences [q-bio]/Immunology, MESH : Cell Communication, MESH: Glycoproteins, MESH: Stem Cells, Biology, MESH : Subcellular Fractions, MESH : Neurons, Cell Line, 03 medical and health sciences, Antigens, CD, MESH: Cell Communication, medicine, MESH : Antigens, CD, Humans, MESH: Fetal Blood, Progenitor cell, 030304 developmental biology, Glycoproteins, MESH : Fetal Blood, MESH: Humans, MESH : Humans, Cell Biology, MESH: Antigens, CD34, MESH : Glycoproteins, MESH: Cell Line, nervous system, MESH: Subcellular Fractions, Immunology, Neuron, Peptides, 030217 neurology & neurosurgery, Developmental Biology
Abstract

International audience; Previous studies described that neurons could be generated in vitro from human umbilical cord blood cells. However, there are few data concerning their origin. Notably, cells generating neurons are not well characterized. The present study deals with the origin of cord blood cells generating neurons and mechanisms allowing the neuronal differentiation. We studied neuronal markers of both total fractions of cord blood and stem/progenitor cord blood cells before and after selections and cultures. We also compared neuronal commitment of cord blood cells to that observed for the neuronal cell line SK-N-BE(2). Before cultures, neuronal markers are found within the total fraction of cord blood cells. In CD133+ stem/progenitor cell fraction only immature neuronal markers are detected. However, CD133+ cells are unable to give rise to neurons in cultures, whereas this is achieved when total fraction of cord blood cells is used. In fact, mature functional neurons can be generated from CD133+ cells only in cell-to-cell close contact with either CD133- fraction or a neurogenic epithelium. Furthermore, since CD133+ fraction is heterogenous, we used several selections to precisely identify the phenotype of cord blood-derived neuronal stem/progenitor cells. Results reveal that only CD34- cells from CD133+ fraction possess neuronal potential. These data show the phenotype of cord blood neuronal stem/progenitor cells and the crucial role of direct cell-to-cell contact to achieve their commitment. Identifying the neuron supporting factors may be beneficial to the use of cord blood neuronal stem/progenitor cells for regenerative medicine.

Published
2008
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5. Transforming growth factor beta controls the directional migration of hepatocyte cohorts by modulating their adhesion to fibronectin

Author

Urszula Hibner, Fabien Binamé, Patrice Lassus, Institut de Génétique Moléculaire de Montpellier ( IGMM ), Université de Montpellier ( UM ) -Centre National de la Recherche Scientifique ( CNRS ), Institut de Génétique Moléculaire de Montpellier (IGMM), and Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM)

Subjects
rac1 GTP-Binding Protein, MESH : Cell Line, MESH : Protein Subunits, Apoptosis, Cell Communication, Integrin alpha5, MESH : Hepatocytes, Epithelium, Mesoderm, MESH: Hepatocytes, Mice, 0302 clinical medicine, Cell Movement, Transforming Growth Factor beta, MESH: Fibronectins, MESH : Cell Movement, MESH : Fibronectins, MESH: Animals, MESH: Cell Movement, MESH: Mesoderm, 0303 health sciences, MESH : Gene Expression Regulation, MESH: Cell Surface Extensions, MESH : Mesoderm, Articles, Adhesion, MESH: Protein Subunits, MESH: Gene Expression Regulation, Cell biology, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Hepatocyte, MESH: Integrin alpha5, MESH : Cell Communication, MESH : Cell Membrane, MESH : Cell Surface Extensions, Biology, Cell Line, MESH: Cell Adhesion, MESH: Gene Expression Profiling, 03 medical and health sciences, MESH : rac1 GTP-Binding Protein, MESH : Integrin alpha5, MESH: Cell Communication, MESH : Mice, Cell Adhesion, medicine, Animals, Humans, [SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH: Mice, Molecular Biology, [ SDV.BBM ] Life Sciences [q-bio]/Biochemistry, Molecular Biology, MESH: Transforming Growth Factor beta, 030304 developmental biology, MESH: Humans, MESH: rac1 GTP-Binding Protein, Gene Expression Profiling, MESH: Apoptosis, MESH : Gene Expression Profiling, Cell Membrane, MESH : Humans, Cell Biology, MESH : Epithelium, Fibronectins, MESH: Cell Line, Fibronectin, Protein Subunits, MESH: Epithelium, MESH : Cell Adhesion, MESH : Transforming Growth Factor beta, Gene Expression Regulation, Hepatocytes, biology.protein, Cell Surface Extensions, MESH : Animals, MESH : Apoptosis, MESH: Cell Membrane, Transforming growth factor
Abstract

International audience; Transforming growth factor beta (TGF-beta) has a strong impact on liver development and physiopathology, exercised through its pleiotropic effects on growth, differentiation, survival, and migration. When exposed to TGF-beta, the mhAT3F cells, immortalized, highly differentiated hepatocytes, maintained their epithelial morphology and underwent dramatic alterations of adhesion, leading to partial or complete detachment from a culture plate, followed by readhesion and spreading. These alterations of adhesive behavior were caused by sequential changes in expression of the alpha5beta1 integrin and of its ligand, the fibronectin. The altered specificity of anchorage to the extracellular matrix gave rise to changes in cells' collective motility: cohorts adhering to fibronectin maintained a persistent, directional motility, with ezrin-rich pathfinder cells protruding from the tips of the cohorts. The absence of adhesion to fibronectin prevented the appearance of polarized pathfinders and lead to random, oscillatory motility. Our data suggest a novel role for TGF-beta in the control of collective migration of epithelial cohorts.

Published
2008
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6. ZAP-70 kinase regulates HIV cell-to-cell spread and virological synapse formation

Author

Françoise Porrot, Céline Trouillet, Marion Sourisseau, Nathalie Sol-Foulon, Maria-Isabel Thoulouze, Olivier Schwartz, Andrés Alcover, Fabien Blanchet, Cinzia Nobile, Vincenzo Di Bartolo, Claire Hivroz, Nelly Noraz, Naomi Taylor, Virus et Immunité, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Biologie Cellulaire des Lymphocytes (BIOCELLY), Immunité et cancer, Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Curie [Paris], Institut de Génétique Moléculaire de Montpellier (IGMM), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), Institut Pasteur [Paris]-Centre National de la Recherche Scientifique ( CNRS ), Biologie Cellulaire des Lymphocytes ( BIOCELLY ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -INSTITUT CURIE, Institut de Génétique Moléculaire de Montpellier ( IGMM ), Université de Montpellier ( UM ) -Centre National de la Recherche Scientifique ( CNRS ), Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), and Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
MESH : Hela Cells, T-Lymphocytes, MESH : HIV, Cell Communication, Virus Replication, Jurkat cells, Immunological synapse, Jurkat Cells, MESH: Jurkat Cells, Cells, Cultured, MESH : Jurkat Cells, 0303 health sciences, ZAP-70 Protein-Tyrosine Kinase, Immunological synapse formation, Kinase, MESH: HIV, General Neuroscience, 030302 biochemistry & molecular biology, MESH : Infant, hemic and immune systems, Immunological Synapses, MESH: Infant, 3. Good health, Cell biology, MESH : Virus Replication, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, Intracellular, MESH: Cells, Cultured, Cell signaling, MESH : Cell Communication, Biology, [ SDV.MP.VIR ] Life Sciences [q-bio]/Microbiology and Parasitology/Virology, General Biochemistry, Genetics and Molecular Biology, Article, 03 medical and health sciences, MESH : ZAP-70 Protein-Tyrosine Kinase, MESH : Cells, Cultured, MESH: Cell Communication, Humans, Molecular Biology, 030304 developmental biology, MESH : T-Lymphocytes, MESH: Humans, General Immunology and Microbiology, MESH : Humans, MESH: Virus Replication, HIV, Infant, MESH: ZAP-70 Protein-Tyrosine Kinase, Virology, MESH: Hela Cells, MESH: T-Lymphocytes, Viral replication, HeLa Cells
Abstract

International audience; HIV efficiently spreads in lymphocytes, likely through virological synapses (VSs). These cell-cell junctions share some characteristics with immunological synapses, but cellular proteins required for their constitution remain poorly characterized. We have examined here the role of ZAP-70, a key kinase regulating T-cell activation and immunological synapse formation, in HIV replication. In lymphocytes deficient for ZAP-70, or expressing a kinase-dead mutant of the protein, HIV replication was strikingly delayed. We have characterized further this replication defect. ZAP-70 was dispensable for the early steps of viral cycle, from entry to expression of viral proteins. However, in the absence of ZAP-70, intracellular Gag localization was impaired. ZAP-70 was required in infected donor cells for efficient cell-to-cell HIV transmission to recipients and for formation of VSs. These results bring novel insights into the links that exist between T-cell activation and HIV spread, and suggest that HIV usurps components of the immunological synapse machinery to ensure its own spread through cell-to-cell contacts.

Published
2007
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7. Stromal cell networks regulate lymphocyte entry, migration, and territoriality in lymph nodes

Author

Ronald N. Germain, Frédéric Brau, Nicolas Glaichenhaus, Jackson G. Egen, Lily Koo, Marc Bajénoff, Jean Pierre Laugier, Lymphocyte Biology Section ( NIAID ), National Institutes of Health, Immunologie des Maladies Infectieuses Allergiques et Autoimmunes, Université Nice Sophia Antipolis ( UNS ), Université Côte d'Azur ( UCA ) -Université Côte d'Azur ( UCA ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Centre Commun de Microscopie Appliquée ( CCMA ), Université Côte d'Azur ( UCA ) -Université Côte d'Azur ( UCA ), Institut de pharmacologie moléculaire et cellulaire ( IPMC ), Université Côte d'Azur ( UCA ) -Université Côte d'Azur ( UCA ) -Centre National de la Recherche Scientifique ( CNRS ), Intramural Research Program of NIAID, NIH, DHHS, Institut de la Santé et de la Recherche Médicale (INSERM), Lymphocyte Biology Section (NIAID), Université Nice Sophia Antipolis (... - 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), Centre Commun de Microscopie Appliquée (CCMA), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA), Institut de pharmacologie moléculaire et cellulaire (IPMC), and COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Pathology, Adoptive cell transfer, Lymphocyte, MESH : Immunohistochemistry, MESH : Diagnostic Imaging, MESH : Lymphocytes, MESH: Chemotaxis, Leukocyte, MESH: Lymph Nodes, Cell Communication, Mice, 0302 clinical medicine, Reticular cell, MESH: Microscopy, Confocal, Immunology and Allergy, [ SDV.IMM ] Life Sciences [q-bio]/Immunology, MESH: Animals, Lymphocytes, MESH : Lymph Nodes, 0303 health sciences, Microscopy, Confocal, MESH : Adoptive Transfer, Cell migration, MESH : Chemotaxis, Leukocyte, Adoptive Transfer, Immunohistochemistry, Cell biology, Chemotaxis, Leukocyte, medicine.anatomical_structure, Infectious Diseases, MESH : Microscopy, Electron, Transmission, MESH: Microscopy, Electron, Transmission, [SDV.IMM]Life Sciences [q-bio]/Immunology, Diagnostic Imaging, MESH : Microscopy, Electron, Scanning, medicine.medical_specialty, Stromal cell, Naive T cell, MESH: Microscopy, Electron, Scanning, MESH : Cell Communication, T cell, Immunology, MESH : Mice, Inbred C57BL, Biology, 03 medical and health sciences, Microscopy, Electron, Transmission, MESH: Mice, Inbred C57BL, MESH: Cell Communication, MESH : Mice, medicine, Animals, MESH : Microscopy, Confocal, MESH: Mice, 030304 developmental biology, Follicular dendritic cells, MESH: Diagnostic Imaging, MESH: Immunohistochemistry, Mice, Inbred C57BL, MESH: Adoptive Transfer, CELLIMMUNO, MESH : Stromal Cells, Microscopy, Electron, Scanning, CELLBIO, MESH: Lymphocytes, Lymph Nodes, MESH : Animals, Stromal Cells, MESH: Stromal Cells, 030215 immunology
Abstract

SummaryAfter entry into lymph nodes (LNs), B cells migrate to follicles, whereas T cells remain in the paracortex, with each lymphocyte type showing apparently random migration within these distinct areas. Other than chemokines, the factors contributing to this spatial segregation and to the observed patterns of lymphocyte movement are poorly characterized. By combining confocal, electron, and intravital microscopy, we showed that the fibroblastic reticular cell network regulated naive T cell access to the paracortex and also supported and defined the limits of T cell movement within this domain, whereas a distinct follicular dendritic cell network similarly served as the substratum for movement of follicular B cells. These results highlight the central role of stromal microanatomy in orchestrating cell migration within the LN.

Published
2006
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8. Involvement of connexin 43 in human trophoblast cell fusion and differentiation

Author

Frendo, Jean-Louis, Cronier, Laurent, Bertin, Gwladys, Guibourdenche, Jean, Vidaud, Michel, Evain-Brion, Danièle, Malassiné, André, Développement humain : Croissance et différenciation, Institut des sciences du Médicament -Toxicologie - Chimie - Environnement (IFR71), Institut de Recherche pour le Développement (IRD)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-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 Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de Biomembranes et Signalisation Cellulaire (LBSC), Université de Poitiers-Centre National de la Recherche Scientifique (CNRS), Service de biochimie-hormonologie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Robert Debré-Université Paris Diderot - Paris 7 (UPD7), Laboratoire de génétique moléculaire, Université Paris Descartes - Paris 5 (UPD5)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Paris Descartes - Paris 5 (UPD5)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut des sciences du Médicament -Toxicologie - Chimie - Environnement ( IFR71 ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL ( ENSCP ) -Centre National de la Recherche Scientifique ( CNRS ) -Institut de Recherche pour le Développement ( IRD ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL ( ENSCP ) -Centre National de la Recherche Scientifique ( CNRS ) -Institut de Recherche pour le Développement ( IRD ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Laboratoire de Biomembranes et Signalisation cellulaire, Université de Poitiers, Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Robert Debré-Université Paris Diderot - Paris 7 ( UPD7 ), and Université Paris Descartes - Paris 5 ( UPD5 ) -Centre National de la Recherche Scientifique ( CNRS )

Subjects
MESH : Cell Communication, MESH: Cytoskeletal Proteins, MESH: Gap Jun, MESH : Fluorescence Recovery After Photobleaching, MESH : Desmoplakins, MESH: Desmoplakins, MESH: Chorionic Gonadotropin, MESH : Cells, Cultured, MESH: Cell Communication, MESH : Connexin 43, MESH : Female, MESH : Gap Jun, reproductive and urinary physiology, MESH : Chorionic Gonadotropin, MESH : Cell Fusion, MESH : Endogenous Retroviruses, MESH : Cytoskeletal Proteins, [SDV.BDLR]Life Sciences [q-bio]/Reproductive Biology, female genital diseases and pregnancy complications, MESH: Connexin 43, [ SDV.BDLR ] Life Sciences [q-bio]/Reproductive Biology, MESH : Chorionic Gonadotropin, beta Subunit, Human, MESH: Cell Fusion, embryonic structures, MESH: Chorionic Gonadotropin, beta Subunit, Human, sense organs, MESH: Female, MESH: Fluorescence Recovery After Photobleaching, MESH: Endogenous Retroviruses, MESH: Cells, Cultured
Abstract

The syncytiotrophoblast is the principal component of the human placenta involved in feto-maternal exchanges and hormone secretion. The syncytiotrophoblast arises from the fusion of villous cytotrophoblasts. We recently showed that functional gap junctional intercellular communication (GJIC) is an important prerequisite for syncytiotrophoblast formation and that connexin 43 (Cx43) is present in cytotrophoblasts and in the syncytiotrophoblast. To determine whether Cx43 is directly involved in trophoblast fusion, we used an antisense strategy in primary cultures of human villous cytotrophoblasts that spontaneously differentiate into the syncytiotrophoblast by cell fusion. We assessed the morphological and functional differentiation of trophoblasts by desmoplakin immunostaining, by quantifying hCG (human chorionic gonadotropin) production and by measuring the expression of specific trophoblast genes (hCG and HERV-W). Furthermore, we used the gap-FRAP (fluorescence recovery after photobleaching) method to investigate functional GJIC. Cytotrophoblasts treated with Cx43 antisense aggregated and fused poorly. Furthermore, less HERV-W env mRNA, hCGbeta mRNA and hCG secretion were detected in Cx43 antisense-treated cytotrophoblasts than in cells treated with scrambled antisense. Treatment with Cx43 antisense dramatically reduced the percentage of coupled trophoblast cells. Taken together, these results suggest that Cx43 is directly involved in human trophoblast cell-cell communication, fusion and differentiation.

Published
2003
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