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3 results on '"European Project: 39516,MUGEN"'

1. A novel pathway down-modulating T cell activation involves HPK-1–dependent recruitment of 14-3-3 proteins on SLP-76

Author

Julien Fourtane, Olivier Schwartz, Oreste Acuto, Florent Carrette, Mogjiborahman Salek, Britta Jungwirth, Nathalie Sol-Foulon, Benjamin Montagne, Vincenzo Di Bartolo, Frédérique Michel, Wolf D. Lehmann, Immunologie Moléculaire, Institut Pasteur [Paris] - Centre National de la Recherche Scientifique (CNRS), Central Spectroscopy German Cancer Research Center (DKFZ) (CENTRAL SPECTROSCOPY), German Cancer Research Center DKFZ, Virus et Immunité, Centre National de la Recherche Scientifique (CNRS)-Institut Pasteur [Paris], Central Spectroscopy, German Cancer Research Center, German Cancer Research Center - Deutsches Krebsforschungszentrum [Heidelberg] (DKFZ), Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), This work was supported by grants from the Institut Pasteur, the CNRS, the Association pour la Recherche sur le Cancer, the Ligue Contre le Cancer-Comité Ile-de-France, and the European Union (MUGEN Network of Excellence, contract no. LSGH-CT-2005-005203)., European Project: 39516,MUGEN, and Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS)

Subjects
genetic structures, T-Lymphocytes, [SDV]Life Sciences [q-bio], Immunology, Down-Regulation, Protein Serine-Threonine Kinases, Biology, Lymphocyte Activation, Jurkat cells, Article, Phosphorylation cascade, Serine, Jurkat Cells, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Chlorocebus aethiops, Animals, Humans, Immunology and Allergy, Protein phosphorylation, Phosphorylation, Adaptor Proteins, Signal Transducing, 030304 developmental biology, 0303 health sciences, T-cell receptor, Tyrosine phosphorylation, Articles, Phosphoproteins, equipment and supplies, Molecular biology, eye diseases, Cell biology, 14-3-3 Proteins, chemistry, [SDV.IMM.IA] Life Sciences [q-bio]/Immunology/Adaptive immunology, COS Cells, sense organs, Signal transduction, Protein Binding, Signal Transduction, 030215 immunology
Abstract

International audience; The SH2 domain-containing leukocyte protein of 76 kD (SLP-76) is a pivotal element of the signaling machinery controlling T cell receptor (TCR)-mediated activation. Here, we identify 14-3-3epsilon and zeta proteins as SLP-76 binding partners. This interaction was induced by TCR ligation and required phosphorylation of SLP-76 at serine 376. Ribonucleic acid interference and in vitro phosphorylation experiments showed that serine 376 is the target of the hematopoietic progenitor kinase 1 (HPK-1). Interestingly, either S376A mutation or HPK-1 knockdown resulted in increased TCR-induced tyrosine phosphorylation of SLP-76 and phospholipase C-gamma1. Moreover, an SLP-76-S376A mutant induced higher interleukin 2 gene transcription than wild-type SLP-76. These data reveal a novel negative feedback loop involving HPK-1-dependent serine phosphorylation of SLP-76 and 14-3-3 protein recruitment, which tunes T cell activation.

Published
2007
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2. Mouse and human neutrophils induce anaphylaxis

Author

Hajime Karasuyama, Nico van Rooijen, David A. Mancardi, Marc Daëron, Takao Shimizu, Yoshihiro Kita, Bruno Iannascoli, Pierre Bruhns, Friederike Jönsson, Allergologie Moléculaire et Cellulaire, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), The University of Tokyo (UTokyo), Department of Immune Regulation [Tokyo, Japan], Graduate School of Medical and Dental Sciences [Tokyo, Japan]-Tokyo Medical and Dental University [Japan] (TMDU), Department of Molecular Cell Biology [Amsterdam UMC], Vrije Universiteit Medical Centre (VUMC), Vrije Universiteit Amsterdam [Amsterdam] (VU)-Vrije Universiteit Amsterdam [Amsterdam] (VU), This work was supported by the Institut Pasteur, the Institut National de la Santé et de la Recherche Médicale (INSERM), the Agence Nationale de la Recherche (ANR) (grants 05-JCJC-0236-01 and GENOPAT-09-GENO-014-01), the Fondation pour la Recherche Médicale (FRM) (Programme Allergie 2007), by funding under the Sixth Research Framework Programme of the European Union, Project MUGEN (MUGEN LSHG-CT-2005-005203), by the Société Française d’Allergologie (SFA) (Soutien de la recherche en allergologie 2010) and the Balsan company. F. Jönsson was financially supported by ANR, MUGEN, and is currently a recipient of a fellowship from the FRM. D.A. Mancardi was financially supported by FRM and is currently a recipient of a fellowship from the Institut Pasteur (Bourse Roux). T. Shimizu and Y. Kita are supported in part by Grants-in-Aid from the Ministry of Education, Science, Culture, Sports and Technology of Japan., ANR-05-JCJC-0236,FcR & Allergy,Roles and interactions of human FcR in allergic symptoms induced by human immunoglobulins and allergens: construction of a ' humanized ' mouse model.(2005), ANR-09-GENO-0014,InflammAbs,Contrôle de l'inflammation par les RFc humains dans des modèles murins d'allergie et d'autoimmunité.(2009), European Project: 39516,MUGEN, Martin, Marie, Jeunes chercheuses et jeunes chercheurs - Roles and interactions of human FcR in allergic symptoms induced by human immunoglobulins and allergens: construction of a ' humanized ' mouse model. - - FcR & Allergy2005 - ANR-05-JCJC-0236 - JCJC - VALID, Physiopathologie moléculaire: des maladies rares aux maladies communes - Contrôle de l'inflammation par les RFc humains dans des modèles murins d'allergie et d'autoimmunité. - - InflammAbs2009 - ANR-09-GENO-0014 - GENO - VALID, INTEGRATED FUNCTIONAL GENOMICS IN MUTANT MOUSE MODELS AS TOOLS TO INVESTIGATE THE COMPLEXITY OF HUMAN IMMUNOLOGICAL DISEASE - MUGEN - 39516 - OLD, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Molecular cell biology and Immunology, and CCA - Immuno-pathogenesis

Subjects
Male, MESH: Mice, Inbred NOD, Neutrophils, MESH: Neutrophils, Immunoglobulin E, MESH: Mice, Knockout, Immunoglobulin G, Neutrophil Activation, MESH: Basophils, chemistry.chemical_compound, Mice, 0302 clinical medicine, Mice, Inbred NOD, Medicine, MESH: Animals, [SDV.IMM.ALL]Life Sciences [q-bio]/Immunology/Allergology, Receptor, Mice, Knockout, MESH: Immunoglobulin G, 0303 health sciences, biology, MESH: Neutrophil Activation, General Medicine, 3. Good health, Basophils, [SDV.IMM]Life Sciences [q-bio]/Immunology, Antibody, Histamine, Anaphylaxis, [SDV.IMM.ALL] Life Sciences [q-bio]/Immunology/Allergology, Research Article, [SDV.IMM] Life Sciences [q-bio]/Immunology, MESH: Mice, Transgenic, Mice, Transgenic, MESH: Receptors, IgG, 03 medical and health sciences, Species Specificity, MESH: Mice, Inbred C57BL, Animals, Humans, MESH: Species Specificity, Platelet Activating Factor, MESH: Mice, 030304 developmental biology, MESH: Platelet Activating Factor, MESH: Humans, Platelet-activating factor, business.industry, Receptors, IgG, medicine.disease, MESH: Male, Mice, Inbred C57BL, MESH: Anaphylaxis, chemistry, Immunology, biology.protein, IgG deficiency, business, 030215 immunology
Abstract

International audience; Anaphylaxis is a life-threatening hyperacute immediate hypersensitivity reaction. Classically, it depends on IgE, FcεRI, mast cells, and histamine. However, anaphylaxis can also be induced by IgG antibodies, and an IgG1-induced passive type of systemic anaphylaxis has been reported to depend on basophils. In addition, it was found that neither mast cells nor basophils were required in mouse models of active systemic anaphylaxis. Therefore, we investigated what antibodies, receptors, and cells are involved in active systemic anaphylaxis in mice. We found that IgG antibodies, FcγRIIIA and FcγRIV, platelet-activating factor, neutrophils, and, to a lesser extent, basophils were involved. Neutrophil activation could be monitored in vivo during anaphylaxis. Neutrophil depletion inhibited active, and also passive, systemic anaphylaxis. Importantly, mouse and human neutrophils each restored anaphylaxis in anaphylaxis-resistant mice, demonstrating that neutrophils are sufficient to induce anaphylaxis in mice and suggesting that neutrophils can contribute to anaphylaxis in humans. Our results therefore reveal an unexpected role for IgG, IgG receptors, and neutrophils in anaphylaxis in mice. These molecules and cells could be potential new targets for the development of anaphylaxis therapeutics if the same mechanism is responsible for anaphylaxis in humans.

Published
2011
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3. c cytokines condition the progressive differentiation of CD4+ T cells

Author

James P. Di Santo, Helene Strick-Marchand, Erwan Corcuff, Olivier Lantz, Guillemette X. Masse, Anna Tafuri-Bladt, Delphine Guy-Grand, Matthew L. Albert, Cytokines et Développement Lymphoïde, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Lymphopoïèse, Immunité et cancer, Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Curie [Paris], Immunobiologie des Cellules Dendritiques, This work received financial support from the Institut Pasteur, the Institut National de la Santé et de la Recherche Médicale, the Ligue Nationale Contre le Cancer, the Université Paris 7, the Fondation de la Recherche Médicale, and the European Community to the MUGEN Network of Excellence (Grant LSHG-CT-2005-005203)., European Project: 39516,MUGEN, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
CD4-Positive T-Lymphocytes, Male, T cell, Mice, Transgenic, Biology, Granzymes, 03 medical and health sciences, Interleukin 21, Interferon-gamma, Mice, 0302 clinical medicine, medicine, Cytotoxic T cell, Animals, Humans, IL-2 receptor, L-Selectin, Receptors, Immunologic, Antigen-presenting cell, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, Interleukin-15, 0303 health sciences, Multidisciplinary, ZAP70, Cell Differentiation, Biological Sciences, NKG2D, Natural killer T cell, Cell biology, Interleukin-2 Receptor beta Subunit, medicine.anatomical_structure, Hyaluronan Receptors, NK Cell Lectin-Like Receptor Subfamily K, Immunology, Cytokines, Receptors, Natural Killer Cell, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, 030215 immunology
Abstract

After their initial antigen encounter in the secondary lymphoid organs, activated T cells must receive additional signals in the peripheral tissues to fully differentiate. Here, we provide evidence that γccytokines are critical during this process. Using the Marilyn (Ml) T cell antigen receptor (TCR) transgenic model, we show that male skin grafts are tolerated in the absence of γc, but that Ml CD4+T cells proliferate normally in response to antigen, traffic to the graft site and recruit an inflammatory response [including natural killer (NK) cells, neutrophils, and macrophages] that is independent of T cell γcexpression. Whereas wild-type T cells demonstrate a progressive differentiation phenotype from the spleen to the tissues, skin-infiltrating effector T cells (CD44hiCD62Llo) from γc−mice were phenotypically abnormal with reduced ICOS, NKG2D, granzyme B, and IFN-γ expression. These defects could be mapped to deficiencies in IL-2 and, surprisingly, IL-15. These results define a late checkpoint in T cell differentiation in the tissues where γccytokines, including IL-15, authenticate CD4+T cell effector functions.

Published
2007
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