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2020 |
Briand-M{é}sange, Fabienne ; Pons, V{é}ronique ; Allart, Sophie ; Masquelier, Julien ; Chicanne, Ga{ë}tan ; Beton, Nicolas ; Payrastre, Bernard ; Muccioli, Giulio G; Ausseil, J{é}r{ô}me ; Davignon, Jean Luc ; Salles, Jean Pierre ; Chap, Hugues Glycerophosphodiesterase 3 (GDE3) is a lysophosphatidylinositol-specific ectophospholipase C acting as an endocannabinoid signaling switch Journal Article Journal of Biological Chemistry, 295 (46), pp. 15767–15781, 2020, ISSN: 1083351X. @article{Briand-Mesange2020, title = {Glycerophosphodiesterase 3 (GDE3) is a lysophosphatidylinositol-specific ectophospholipase C acting as an endocannabinoid signaling switch}, author = {Briand-M{é}sange, Fabienne and Pons, V{é}ronique and Allart, Sophie and Masquelier, Julien and Chicanne, Ga{ë}tan and Beton, Nicolas and Payrastre, Bernard and Muccioli, Giulio G. and Ausseil, J{é}r{ô}me and Davignon, Jean Luc and Salles, Jean Pierre and Chap, Hugues}, doi = {10.1074/jbc.RA120.015278}, issn = {1083351X}, year = {2020}, date = {2020-11-01}, journal = {Journal of Biological Chemistry}, volume = {295}, number = {46}, pages = {15767--15781}, publisher = {American Society for Biochemistry and Molecular Biology Inc.}, abstract = {Endocannabinoid signaling plays a regulatory role in various (neuro)biological functions. 2-arachidonoylglycerol (2-AG) is the most abundant endocannabinoid, and although its canonical biosynthetic pathway involving phosphoinositide-specific phospholipase C and diacylglycerol lipase a is known, alternative pathways remain unsettled. Here, we characterize a non-canonical pathway implicating glycerophosphodiesterase 3 (GDE3, from GDPD2 gene). Human GDE3 expressed in HEK293T cell membranes catalyzed the conversion of lysophosphatidylinositol (LPI) into monoacylglycerol and inositol-1-phosphate. The enzyme was equally active against 1-acyl and 2-acyl LPI. When using 2-acyl LPI, where arachidonic acid is the predominant fatty acid, LC-MS analysis identified 2-AG as the main product of LPI hydrolysis by GDE3. Furthermore, inositol-1-phosphate release into the medium occurred upon addition of LPI to intact cells, suggesting that GDE3 is actually an ecto-lysophospholipase C. In cells expressing G-protein–coupled receptor GPR55, GDE3 abolished 1-acyl LPI–induced signaling. In contrast, upon simultaneous expression of GDE3 and cannabinoid receptor CB2, 2-acyl LPI evoked the same signal as that induced by 2-AG. These data strongly suggest that, in addition to degrading the GPR55 LPI ligand, GDE3 can act as a switch between GPR55 and CB2 signaling. Coincident with a major expression of both GDE3 and CB2 in the spleen, spleens from transgenic mice lacking GDE3 displayed doubling of LPI content compared with WT mice. Decreased production of 2-AG in whole spleen was also observed, supporting the in vivo relevance of our findings. These data thus open a new research avenue in the field of endocannabinoid generation and reinforce the view of GPR55 and LPI being genuine actors of the endocannabinoid system.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Endocannabinoid signaling plays a regulatory role in various (neuro)biological functions. 2-arachidonoylglycerol (2-AG) is the most abundant endocannabinoid, and although its canonical biosynthetic pathway involving phosphoinositide-specific phospholipase C and diacylglycerol lipase a is known, alternative pathways remain unsettled. Here, we characterize a non-canonical pathway implicating glycerophosphodiesterase 3 (GDE3, from GDPD2 gene). Human GDE3 expressed in HEK293T cell membranes catalyzed the conversion of lysophosphatidylinositol (LPI) into monoacylglycerol and inositol-1-phosphate. The enzyme was equally active against 1-acyl and 2-acyl LPI. When using 2-acyl LPI, where arachidonic acid is the predominant fatty acid, LC-MS analysis identified 2-AG as the main product of LPI hydrolysis by GDE3. Furthermore, inositol-1-phosphate release into the medium occurred upon addition of LPI to intact cells, suggesting that GDE3 is actually an ecto-lysophospholipase C. In cells expressing G-protein–coupled receptor GPR55, GDE3 abolished 1-acyl LPI–induced signaling. In contrast, upon simultaneous expression of GDE3 and cannabinoid receptor CB2, 2-acyl LPI evoked the same signal as that induced by 2-AG. These data strongly suggest that, in addition to degrading the GPR55 LPI ligand, GDE3 can act as a switch between GPR55 and CB2 signaling. Coincident with a major expression of both GDE3 and CB2 in the spleen, spleens from transgenic mice lacking GDE3 displayed doubling of LPI content compared with WT mice. Decreased production of 2-AG in whole spleen was also observed, supporting the in vivo relevance of our findings. These data thus open a new research avenue in the field of endocannabinoid generation and reinforce the view of GPR55 and LPI being genuine actors of the endocannabinoid system. |
Balbino, B; Herviou, P; o Godon,; Stackowicz, J; Goff, O R; Iannascoli, B; Sterlin, D; Brûlé, S; Millot, G A; Harris, F M; Voronina, V A; Nadeau, K C; Macdonald, L E; Murphy, A J; Bruhns, P; Reber, L L The anti-IgE mAb omalizumab induces adverse reactions by engaging Fcγ receptors. Journal Article J Clin Invest, 130 (3), pp. 1330-1335, 2020. @article{B2020, title = {The anti-IgE mAb omalizumab induces adverse reactions by engaging Fcγ receptors.}, author = {B Balbino and P Herviou and o Godon and J Stackowicz and O R Goff and B Iannascoli and D Sterlin and S Brûlé and G A Millot and F M Harris and V A Voronina and K C Nadeau and L E Macdonald and A J Murphy and P Bruhns and L L Reber}, url = {https://pubmed-ncbi-nlm-nih-gov.proxy.insermbiblio.inist.fr/31770111/}, doi = {10.1172/JCI129697}, year = {2020}, date = {2020-03-02}, journal = {J Clin Invest}, volume = {130}, number = {3}, pages = {1330-1335}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Meixiong, James ; Basso, Lilian ; Dong, Xinzhong ; Gaudenzio, Nicolas Nociceptor-Mast Cell Sensory Clusters as Regulators of Skin Homeostasis. Journal Article Trends in neurosciences, 43 (3), pp. 130–132, 2020, ISSN: 1878-108X (Electronic). @article{Meixiong2020, title = {Nociceptor-Mast Cell Sensory Clusters as Regulators of Skin Homeostasis.}, author = {Meixiong, James and Basso, Lilian and Dong, Xinzhong and Gaudenzio, Nicolas}, doi = {10.1016/j.tins.2020.01.001}, issn = {1878-108X (Electronic)}, year = {2020}, date = {2020-03-01}, journal = {Trends in neurosciences}, volume = {43}, number = {3}, pages = {130--132}, abstract = {Recent studies revealed the existence of unique functional links between mast cells and nociceptors in the skin. Here, we propose that mast cells and nociceptors form a single regulatory unit in both physiology and disease. In this model, MrgprB2/X2 signaling is a primary mechanism by which mast cells functionally interact with nociceptors to form specialized neuroimmune clusters that regulate pain, inflammation, and itch.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Recent studies revealed the existence of unique functional links between mast cells and nociceptors in the skin. Here, we propose that mast cells and nociceptors form a single regulatory unit in both physiology and disease. In this model, MrgprB2/X2 signaling is a primary mechanism by which mast cells functionally interact with nociceptors to form specialized neuroimmune clusters that regulate pain, inflammation, and itch. |
Hassan, A; Wlodarczyk, M F; Benamar, M; Bassot, E; Salvioni, A; Kassem, S; Berry, A; Saoudi, A; Blanchard, N A Virus Hosted in Malaria-Infected Blood Protects against T Cell-Mediated Inflammatory Diseases by Impairing DC Function in a Type I IFN-Dependent Manner Journal Article mBio, 11 (2), 2020, (doi: 10.1128/mBio.03394-19.). @article{c, title = {A Virus Hosted in Malaria-Infected Blood Protects against T Cell-Mediated Inflammatory Diseases by Impairing DC Function in a Type I IFN-Dependent Manner}, author = {Hassan, A. and Wlodarczyk, M. F. and Benamar, M. and Bassot, E. and Salvioni, A. and Kassem, S. and Berry, A. and Saoudi, A. and Blanchard, N.}, year = {2020}, date = {2020-01-01}, journal = {mBio}, volume = {11}, number = {2}, abstract = {Coinfections shape immunity and influence the development of inflammatory diseases, resulting in detrimental or beneficial outcome. Coinfections with concurrent Plasmodium species can alter malaria clinical evolution, and malaria infection itself can modulate autoimmune reactions. Yet, the underlying mechanisms remain ill defined. Here, we demonstrate that the protective effects of some rodent malaria strains on T cell-mediated inflammatory pathologies are due to an RNA virus cohosted in malaria-parasitized blood. We show that live and extracts of blood parasitized by Plasmodium berghei K173 or Plasmodium yoelii 17X YM, protect against P. berghei ANKA-induced experimental cerebral malaria (ECM) and myelin oligodendrocyte glycoprotein (MOG)/complete Freund's adjuvant (CFA)-induced experimental autoimmune encephalomyelitis (EAE), and that protection is associated with a strong type I interferon (IFN-I) signature. We detected the presence of the RNA virus lactate dehydrogenase-elevating virus (LDV) in the protective Plasmodium stabilates and we established that LDV infection alone was necessary and sufficient to recapitulate the protective effects on ECM and EAE. In ECM, protection resulted from an IFN-I-mediated reduction in the abundance of splenic conventional dendritic cell and impairment of their ability to produce interleukin (IL)-12p70, leading to a decrease in pathogenic CD4(+) Th1 responses. In EAE, LDV infection induced IFN-I-mediated abrogation of IL-23, thereby preventing the differentiation of granulocyte-macrophage colony-stimulating factor (GM-CSF)-producing encephalitogenic CD4(+) T cells. Our work identifies a virus cohosted in several Plasmodium stabilates across the community and deciphers its major consequences on the host immune system. More generally, our data emphasize the importance of considering contemporaneous infections for the understanding of malaria-associated and autoimmune diseases.IMPORTANCE Any infection modifies the host immune status, potentially ameliorating or aggravating the pathophysiology of a simultaneous inflammatory condition. In the course of investigating how malaria infection modulates the severity of contemporaneous inflammatory diseases, we identified a nonpathogenic mouse virus in stabilates of two widely used rodent parasite lines: Plasmodium berghei K173 and Plasmodium yoelii 17X YM. We established that the protective effects of these Plasmodium lines on cerebral malaria and multiple sclerosis are exclusively due to this virus. The virus induces a massive type I interferon (IFN-I) response and causes quantitative and qualitative defects in the ability of dendritic cells to promote pathogenic T cell responses. Beyond revealing a possible confounding factor in rodent malaria models, our work uncovers some bases by which a seemingly innocuous viral (co)infection profoundly changes the immunopathophysiology of inflammatory diseases.}, note = {doi: 10.1128/mBio.03394-19.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Coinfections shape immunity and influence the development of inflammatory diseases, resulting in detrimental or beneficial outcome. Coinfections with concurrent Plasmodium species can alter malaria clinical evolution, and malaria infection itself can modulate autoimmune reactions. Yet, the underlying mechanisms remain ill defined. Here, we demonstrate that the protective effects of some rodent malaria strains on T cell-mediated inflammatory pathologies are due to an RNA virus cohosted in malaria-parasitized blood. We show that live and extracts of blood parasitized by Plasmodium berghei K173 or Plasmodium yoelii 17X YM, protect against P. berghei ANKA-induced experimental cerebral malaria (ECM) and myelin oligodendrocyte glycoprotein (MOG)/complete Freund's adjuvant (CFA)-induced experimental autoimmune encephalomyelitis (EAE), and that protection is associated with a strong type I interferon (IFN-I) signature. We detected the presence of the RNA virus lactate dehydrogenase-elevating virus (LDV) in the protective Plasmodium stabilates and we established that LDV infection alone was necessary and sufficient to recapitulate the protective effects on ECM and EAE. In ECM, protection resulted from an IFN-I-mediated reduction in the abundance of splenic conventional dendritic cell and impairment of their ability to produce interleukin (IL)-12p70, leading to a decrease in pathogenic CD4(+) Th1 responses. In EAE, LDV infection induced IFN-I-mediated abrogation of IL-23, thereby preventing the differentiation of granulocyte-macrophage colony-stimulating factor (GM-CSF)-producing encephalitogenic CD4(+) T cells. Our work identifies a virus cohosted in several Plasmodium stabilates across the community and deciphers its major consequences on the host immune system. More generally, our data emphasize the importance of considering contemporaneous infections for the understanding of malaria-associated and autoimmune diseases.IMPORTANCE Any infection modifies the host immune status, potentially ameliorating or aggravating the pathophysiology of a simultaneous inflammatory condition. In the course of investigating how malaria infection modulates the severity of contemporaneous inflammatory diseases, we identified a nonpathogenic mouse virus in stabilates of two widely used rodent parasite lines: Plasmodium berghei K173 and Plasmodium yoelii 17X YM. We established that the protective effects of these Plasmodium lines on cerebral malaria and multiple sclerosis are exclusively due to this virus. The virus induces a massive type I interferon (IFN-I) response and causes quantitative and qualitative defects in the ability of dendritic cells to promote pathogenic T cell responses. Beyond revealing a possible confounding factor in rodent malaria models, our work uncovers some bases by which a seemingly innocuous viral (co)infection profoundly changes the immunopathophysiology of inflammatory diseases. |
Darrigues, Julie ; Santamaria, Jeremy C; Galindo-Albarrán, Ariel ; Robey, Ellen A; Joffre, Olivier P; van Meerwijk, Joost P M; Romagnoli, Paola Robust intrathymic development of regulatory T cells in young NOD mice is rapidly restrained by recirculating cells Journal Article European Journal of Immunology, 2020, ISSN: 15214141. @article{Darrigues2020b, title = {Robust intrathymic development of regulatory T cells in young NOD mice is rapidly restrained by recirculating cells}, author = {Darrigues, Julie and Santamaria, Jeremy C. and Galindo-Albarrán, Ariel and Robey, Ellen A. and Joffre, Olivier P. and van Meerwijk, Joost P.M. and Romagnoli, Paola}, url = {https://pubmed.ncbi.nlm.nih.gov/32730634/}, doi = {10.1002/eji.202048743}, issn = {15214141}, year = {2020}, date = {2020-01-01}, journal = {European Journal of Immunology}, publisher = {Wiley-VCH Verlag}, abstract = {Regulatory T lymphocytes (Treg) play a vital role in the protection of the organism against autoimmune pathology. It is therefore paradoxical that comparatively large numbers of Treg were found in the thymus of type I diabetes-prone NOD mice. The Treg population in the thymus is composed of newly developing cells and cells that had recirculated from the periphery back to the thymus. We here demonstrate that exceptionally large numbers of Treg develop in the thymus of young, but not adult, NOD mice. Once emigrated from the thymus, an unusually large proportion of these Treg is activated in the periphery, which causes a particularly abundant accumulation of recirculating Treg in the thymus. These cells then rapidly inhibit de novo development of Treg. The proportions of developing Treg thus reach levels similar to or lower than those found in most other, type 1 diabetes-resistant, inbred mouse strains. Thus, in adult NOD mice the particularly large Treg-niche is actually composed of mostly recirculating cells and only few newly developing Treg.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Regulatory T lymphocytes (Treg) play a vital role in the protection of the organism against autoimmune pathology. It is therefore paradoxical that comparatively large numbers of Treg were found in the thymus of type I diabetes-prone NOD mice. The Treg population in the thymus is composed of newly developing cells and cells that had recirculated from the periphery back to the thymus. We here demonstrate that exceptionally large numbers of Treg develop in the thymus of young, but not adult, NOD mice. Once emigrated from the thymus, an unusually large proportion of these Treg is activated in the periphery, which causes a particularly abundant accumulation of recirculating Treg in the thymus. These cells then rapidly inhibit de novo development of Treg. The proportions of developing Treg thus reach levels similar to or lower than those found in most other, type 1 diabetes-resistant, inbred mouse strains. Thus, in adult NOD mice the particularly large Treg-niche is actually composed of mostly recirculating cells and only few newly developing Treg. |
Blaize, Gaëtan ; Daniels-Treffandier, Hélène ; Aloulou, Meryem ; Rouquié, Nelly ; Yang, Cui ; Marcellin, Marlène ; Gador, Mylène ; Benamar, Mehdi ; Ducatez, Mariette ; Song, Ki-Duk ; Burlet-Schiltz, Odile ; Saoudi, Abdelhadi ; Love, Paul E; Fazilleau, Nicolas ; Gonzalez de Peredo, Anne ; Lesourne, Renaud CD5 signalosome coordinates antagonist TCR signals to control the generation of Treg cells induced by foreign antigens Journal Article Proceedings of the National Academy of Sciences of the United States of America, 2020, ISSN: 1091-6490. @article{blaize_cd5_2020, title = {CD5 signalosome coordinates antagonist TCR signals to control the generation of Treg cells induced by foreign antigens}, author = {Blaize, Gaëtan and Daniels-Treffandier, Hélène and Aloulou, Meryem and Rouquié, Nelly and Yang, Cui and Marcellin, Marlène and Gador, Mylène and Benamar, Mehdi and Ducatez, Mariette and Song, Ki-Duk and Burlet-Schiltz, Odile and Saoudi, Abdelhadi and Love, Paul E. and Fazilleau, Nicolas and Gonzalez de Peredo, Anne and Lesourne, Renaud}, doi = {10.1073/pnas.1917182117}, issn = {1091-6490}, year = {2020}, date = {2020-01-01}, journal = {Proceedings of the National Academy of Sciences of the United States of America}, abstract = {CD5 is characterized as an inhibitory coreceptor with an important regulatory role during T cell development. The molecular mechanism by which CD5 operates has been puzzling and its function in mature T cells suggests promoting rather than repressing effects on immune responses. Here, we combined quantitative mass spectrometry and genetic studies to analyze the components and the activity of the CD5 signaling machinery in primary T cells. We found that T cell receptor (TCR) engagement induces the selective phosphorylation of CD5 tyrosine 429, which serves as a docking site for proteins with adaptor functions (c-Cbl, CIN85, CRKL), connecting CD5 to positive (PI3K) and negative (UBASH3A, SHIP1) regulators of TCR signaling. c-CBL acts as a coordinator in this complex enabling CD5 to synchronize positive and negative feedbacks on TCR signaling through the other components. Disruption of CD5 signalosome in mutant mice reveals that it modulates TCR signal outputs to selectively repress the transactivation of Foxp3 and limit the inopportune induction of peripherally induced regulatory T cells during immune responses against foreign antigen. Our findings bring insights into the paradigm of coreceptor signaling, suggesting that, in addition to providing dualistic enhancing or dampening inputs, coreceptors can engage concomitant stimulatory and inhibitory signaling events, which act together to promote specific functional outcomes.}, keywords = {}, pubstate = {published}, tppubtype = {article} } CD5 is characterized as an inhibitory coreceptor with an important regulatory role during T cell development. The molecular mechanism by which CD5 operates has been puzzling and its function in mature T cells suggests promoting rather than repressing effects on immune responses. Here, we combined quantitative mass spectrometry and genetic studies to analyze the components and the activity of the CD5 signaling machinery in primary T cells. We found that T cell receptor (TCR) engagement induces the selective phosphorylation of CD5 tyrosine 429, which serves as a docking site for proteins with adaptor functions (c-Cbl, CIN85, CRKL), connecting CD5 to positive (PI3K) and negative (UBASH3A, SHIP1) regulators of TCR signaling. c-CBL acts as a coordinator in this complex enabling CD5 to synchronize positive and negative feedbacks on TCR signaling through the other components. Disruption of CD5 signalosome in mutant mice reveals that it modulates TCR signal outputs to selectively repress the transactivation of Foxp3 and limit the inopportune induction of peripherally induced regulatory T cells during immune responses against foreign antigen. Our findings bring insights into the paradigm of coreceptor signaling, suggesting that, in addition to providing dualistic enhancing or dampening inputs, coreceptors can engage concomitant stimulatory and inhibitory signaling events, which act together to promote specific functional outcomes. |
Lamsoul, Isabelle ; Dupré, Loïc ; Lutz, Pierre G Molecular Tuning of Filamin A Activities in the Context of Adhesion and Migration Journal Article Front Cell Dev Biol, 8 , pp. 591323, 2020, ISSN: 2296-634X. @article{lamsoul_molecular_2020, title = {Molecular Tuning of Filamin A Activities in the Context of Adhesion and Migration}, author = {Lamsoul, Isabelle and Dupré, Loïc and Lutz, Pierre G.}, doi = {10.3389/fcell.2020.591323}, issn = {2296-634X}, year = {2020}, date = {2020-01-01}, journal = {Front Cell Dev Biol}, volume = {8}, pages = {591323}, abstract = {The dynamic organization of actin cytoskeleton meshworks relies on multiple actin-binding proteins endowed with distinct actin-remodeling activities. Filamin A is a large multi-domain scaffolding protein that cross-links actin filaments with orthogonal orientation in response to various stimuli. As such it plays key roles in the modulation of cell shape, cell motility, and differentiation throughout development and adult life. The essentiality and complexity of Filamin A is highlighted by mutations that lead to a variety of severe human disorders affecting multiple organs. One of the most conserved activity of Filamin A is to bridge the actin cytoskeleton to integrins, thereby maintaining the later in an inactive state. We here review the numerous mechanisms cells have developed to adjust Filamin A content and activity and focus on the function of Filamin A as a gatekeeper to integrin activation and associated adhesion and motility.}, keywords = {}, pubstate = {published}, tppubtype = {article} } The dynamic organization of actin cytoskeleton meshworks relies on multiple actin-binding proteins endowed with distinct actin-remodeling activities. Filamin A is a large multi-domain scaffolding protein that cross-links actin filaments with orthogonal orientation in response to various stimuli. As such it plays key roles in the modulation of cell shape, cell motility, and differentiation throughout development and adult life. The essentiality and complexity of Filamin A is highlighted by mutations that lead to a variety of severe human disorders affecting multiple organs. One of the most conserved activity of Filamin A is to bridge the actin cytoskeleton to integrins, thereby maintaining the later in an inactive state. We here review the numerous mechanisms cells have developed to adjust Filamin A content and activity and focus on the function of Filamin A as a gatekeeper to integrin activation and associated adhesion and motility. |
Azar, P; Mejía, J E; Cenac, C; Shaiykova, A; Youness, A; Laffont, S; Essat, A; Izopet, J; Passaes, C; Müller-Trutwin, M; Delobel, P; Meyer, L; Guéry, J C TLR7 dosage polymorphism shapes interferogenesis and HIV-1 acute viremia in women Journal Article JCI Insight, 5 (12), 2020, ISSN: 2379-3708. @article{RN1940, title = {TLR7 dosage polymorphism shapes interferogenesis and HIV-1 acute viremia in women}, author = {Azar, P. and Mejía, J. E. and Cenac, C. and Shaiykova, A. and Youness, A. and Laffont, S. and Essat, A. and Izopet, J. and Passaes, C. and Müller-Trutwin, M. and Delobel, P. and Meyer, L. and Guéry, J. C.}, doi = {10.1172/jci.insight.136047}, issn = {2379-3708}, year = {2020}, date = {2020-01-01}, journal = {JCI Insight}, volume = {5}, number = {12}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Raymond, Stéphanie ; Piffaut, Marie ; Bigot, Jonathan ; Cazabat, Michelle ; Montes, Brigitte ; Bertrand, Kevin ; Martin-Blondel, Guillaume ; Izopet, Jacques ; Delobel, Pierre Sexual transmission of an extensively drug-resistant HIV-1 strain Journal Article The Lancet HIV, 7 (8), pp. e529–e530, 2020, ISSN: 23523018. @article{raymond_sexual_2020, title = {Sexual transmission of an extensively drug-resistant HIV-1 strain}, author = {Raymond, Stéphanie and Piffaut, Marie and Bigot, Jonathan and Cazabat, Michelle and Montes, Brigitte and Bertrand, Kevin and Martin-Blondel, Guillaume and Izopet, Jacques and Delobel, Pierre}, url = {https://linkinghub.elsevier.com/retrieve/pii/S2352301820302058}, doi = {10.1016/S2352-3018(20)30205-8}, issn = {23523018}, year = {2020}, date = {2020-01-01}, urldate = {2021-02-09}, journal = {The Lancet HIV}, volume = {7}, number = {8}, pages = {e529--e530}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Nayrac, Manon ; Requena, Mary ; Loiseau, Claire ; Cazabat, Michelle ; Suc, Bertrand ; Carrere, Nicolas ; Barange, Karl ; Alric, Laurent ; Martin-Blondel, Guillaume ; Izopet, Jacques ; Delobel, Pierre Mucosal Immunology, 14 (1), pp. 219–228, 2020, ISSN: 1933-0219, 1935-3456. @article{nayrac_th22_2020, title = {Th22 cells are efficiently recruited in the gut by CCL28 as an alternative to CCL20 but do not compensate for the loss of Th17 cells in treated HIV-1-infected individuals}, author = {Nayrac, Manon and Requena, Mary and Loiseau, Claire and Cazabat, Michelle and Suc, Bertrand and Carrere, Nicolas and Barange, Karl and Alric, Laurent and Martin-Blondel, Guillaume and Izopet, Jacques and Delobel, Pierre}, url = {http://www.nature.com/articles/s41385-020-0286-6}, doi = {10.1038/s41385-020-0286-6}, issn = {1933-0219, 1935-3456}, year = {2020}, date = {2020-01-01}, urldate = {2021-02-09}, journal = {Mucosal Immunology}, volume = {14}, number = {1}, pages = {219--228}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Marion, Olivier ; Lhomme, Sebastien ; Nayrac, Manon ; Dubois, Martine ; Pucelle, Mélanie ; Requena, Mary ; Migueres, Marion ; Abravanel, Florence ; Peron, Jean Marie ; Carrere, Nicolas ; Suc, Bertrand ; Delobel, Pierre ; Kamar, Nassim ; Izopet, Jacques Hepatitis E virus replication in human intestinal cells Journal Article Gut, 69 (5), pp. 901–910, 2020, ISSN: 0017-5749, 1468-3288. @article{marion_hepatitis_2020, title = {Hepatitis E virus replication in human intestinal cells}, author = {Marion, Olivier and Lhomme, Sebastien and Nayrac, Manon and Dubois, Martine and Pucelle, Mélanie and Requena, Mary and Migueres, Marion and Abravanel, Florence and Peron, Jean Marie and Carrere, Nicolas and Suc, Bertrand and Delobel, Pierre and Kamar, Nassim and Izopet, Jacques}, url = {https://gut.bmj.com/lookup/doi/10.1136/gutjnl-2019-319004}, doi = {10.1136/gutjnl-2019-319004}, issn = {0017-5749, 1468-3288}, year = {2020}, date = {2020-01-01}, urldate = {2021-02-09}, journal = {Gut}, volume = {69}, number = {5}, pages = {901--910}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Chen, Qian ; Gouilly, Jordi ; Ferrat, Yann J; Espino, Ana ; Glaziou, Quentin ; Cartron, Géraldine ; El Costa, Hicham ; Al-Daccak, Reem ; Jabrane-Ferrat, Nabila Metabolic reprogramming by Zika virus provokes inflammation in human placenta Journal Article Nature Communications, 11 (1), 2020, ISSN: 2041-1723. @article{chen_metabolic_2020, title = {Metabolic reprogramming by Zika virus provokes inflammation in human placenta}, author = {Chen, Qian and Gouilly, Jordi and Ferrat, Yann J. and Espino, Ana and Glaziou, Quentin and Cartron, Géraldine and El Costa, Hicham and Al-Daccak, Reem and Jabrane-Ferrat, Nabila}, url = {http://www.nature.com/articles/s41467-020-16754-z}, doi = {10.1038/s41467-020-16754-z}, issn = {2041-1723}, year = {2020}, date = {2020-01-01}, urldate = {2021-02-09}, journal = {Nature Communications}, volume = {11}, number = {1}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Malviya, M; Saoudi, A; Bauer, J; Fillatreau, S; Liblau, R Treatment of experimental autoimmune encephalomyelitis with engineered bi-specific Foxp3+ regulatory CD4+ T cells Journal Article J Autoimmun, 108 , pp. 102401, 2020, ISSN: 1095-9157 (Electronic) 0896-8411 (Linking). @article{RN54, title = {Treatment of experimental autoimmune encephalomyelitis with engineered bi-specific Foxp3+ regulatory CD4+ T cells}, author = {Malviya, M. and Saoudi, A. and Bauer, J. and Fillatreau, S. and Liblau, R.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/31948790}, doi = {10.1016/j.jaut.2020.102401}, issn = {1095-9157 (Electronic) 0896-8411 (Linking)}, year = {2020}, date = {2020-01-01}, journal = {J Autoimmun}, volume = {108}, pages = {102401}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2019 |
Serhan, N; Basso, L; Sibilano, R; Petitfils, C; Meixiong, J; Bonnart, C; Reber, L L; Marichal, T; Starkl, P; Cenac, N; Dong, X; Tsai, M; Galli, S J; Gaudenzio, N House dust mites activate nociceptor-mast cell clusters to drive type 2 skin inflammation Journal Article Nat Immunol, 20 (11), pp. 1435-1443, 2019. @article{N2019, title = {House dust mites activate nociceptor-mast cell clusters to drive type 2 skin inflammation}, author = {Serhan, N. and Basso, L. and Sibilano, R. and Petitfils, C. and Meixiong, J. and Bonnart, C. and Reber, L L. and Marichal, T. and Starkl, P. and Cenac, N. and Dong, X. and Tsai, M. and Galli, S J. and Gaudenzio, N.}, url = {https://pubmed-ncbi-nlm-nih-gov.proxy.insermbiblio.inist.fr/31591569/}, doi = {10.1038/s41590-019-0493-z}, year = {2019}, date = {2019-11-20}, journal = {Nat Immunol}, volume = {20}, number = {11}, pages = {1435-1443}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Adoue, V; Binet, B; Malbec, A; Fourquet, J; Romagnoli, P; van Meerwijk, J P M; Amigorena, S; Joffre, O P The Histone Methyltransferase SETDB1 Controls T Helper Cell Lineage Integrity by Repressing Endogenous Retroviruses. Journal Article Immunity, 50 , pp. 629–644, 2019. @article{Adoue2019, title = {The Histone Methyltransferase SETDB1 Controls T Helper Cell Lineage Integrity by Repressing Endogenous Retroviruses.}, author = {Adoue, V and Binet, B and Malbec, A and Fourquet, J and Romagnoli, P and van Meerwijk, J P M and Amigorena, S and Joffre, O P}, url = {https://linkinghub.elsevier.com/retrieve/pii/S1074761319300032}, doi = {10.1016/j.immuni.2019.01.003}, year = {2019}, date = {2019-01-01}, journal = {Immunity}, volume = {50}, pages = {629--644}, abstract = {Upon activation, naive CD4+ T cells differentiate into distinct T cell subsets via processes reliant on epigenetically regulated, lineage-specific developmental programs. Here, we examined the function of the histone methyltransferase SETDB1 in T helper (Th) cell differentiation. Setdb1-/- naive CD4+ T cells exhibited exacerbated Th1 priming, and when exposed to a Th1-instructive signal, Setdb1-/- Th2 cells crossed lineage boundaries and acquired a Th1 phenotype. SETDB1 did not directly control Th1 gene promoter activity but relied instead on deposition of the repressive H3K9me3 mark at a restricted and cell-type-specific set of endogenous retroviruses (ERVs) located in the vicinity of genes involved in immune processes. Refined bioinformatic analyses suggest that these retrotransposons regulate Th1 gene cis-regulatory elements or act as Th1 gene enhancers. Thus, H3K9me3 deposition by SETDB1 ensures Th cell lineage integrity by repressing a repertoire of ERVs that have been exapted into cis-regulatory modules to shape and control the Th1 gene network.}, keywords = {}, pubstate = {published}, tppubtype = {article} } Upon activation, naive CD4+ T cells differentiate into distinct T cell subsets via processes reliant on epigenetically regulated, lineage-specific developmental programs. Here, we examined the function of the histone methyltransferase SETDB1 in T helper (Th) cell differentiation. Setdb1-/- naive CD4+ T cells exhibited exacerbated Th1 priming, and when exposed to a Th1-instructive signal, Setdb1-/- Th2 cells crossed lineage boundaries and acquired a Th1 phenotype. SETDB1 did not directly control Th1 gene promoter activity but relied instead on deposition of the repressive H3K9me3 mark at a restricted and cell-type-specific set of endogenous retroviruses (ERVs) located in the vicinity of genes involved in immune processes. Refined bioinformatic analyses suggest that these retrotransposons regulate Th1 gene cis-regulatory elements or act as Th1 gene enhancers. Thus, H3K9me3 deposition by SETDB1 ensures Th cell lineage integrity by repressing a repertoire of ERVs that have been exapted into cis-regulatory modules to shape and control the Th1 gene network. |
Domingo, Cristina ; Fraissinet, Juliane ; Ansah, Patrick O; Kelly, Corey ; Bhat, Niranjan ; Sow, Samba O; Mejía, José E Long-term immunity against yellow fever in children vaccinated during infancy: a longitudinal cohort study Journal Article Lancet Infect Dis, 2019, ISSN: 1473-3099. @article{RN3090, title = {Long-term immunity against yellow fever in children vaccinated during infancy: a longitudinal cohort study}, author = {Domingo, Cristina and Fraissinet, Juliane and Ansah, Patrick O. and Kelly, Corey and Bhat, Niranjan and Sow, Samba O. and Mejía, José E.}, doi = {10.1016/S1473-3099(19)30323-8}, issn = {1473-3099}, year = {2019}, date = {2019-01-01}, journal = {Lancet Infect Dis}, abstract = {Background. A single dose of vaccine against yellow fever is routinely administered to infants aged 9–12 months under the Expanded Programme on Immunization, but the long-term outcome of vaccination in this age group is unknown. We aimed to evaluate the long-term persistence of neutralising antibodies to yellow fever virus following routine vaccination in infancy. Methods. We did a longitudinal cohort study, using a microneutralisation assay to measure protective antibodies against yellow fever in Malian and Ghanaian children vaccinated around age 9 months and followed up for 4·5 years (Mali), or 2·3 and 6·0 years (Ghana). Healthy children with available day-0 sera, a complete follow-up history, and no record of yellow fever revaccination were included; children seropositive for yellow fever at baseline were excluded. We standardised antibody concentrations with reference to the yellow fever WHO International Standard. Findings. We included 587 Malian and 436 Ghanaian children vaccinated between June 5, 2009, and Dec 26, 2012. In the Malian group, 296 (50·4%, 95% CI 46·4–54·5) were seropositive (antibody concentration ≥0·5 IU/mL) 4·5 years after vaccination. Among the Ghanaian children, 121 (27·8%, 23·5–32·0) were seropositive after 2·3 years. These results show a large decrease from the proportions of seropositive infants 28 days after vaccination, 96·7% in Mali and 72·7% in Ghana, reported by a previous study of both study populations. The number of seropositive children increased to 188 (43·1%, 95% CI 38·5–47·8) in the Ghanaian group 6·0 years after vaccination, but this result might be confounded by unrecorded revaccination or natural infection with wild yellow fever virus during a 2011–12 outbreak in northern Ghana. Interpretation. Rapid waning of immunity during the early years after vaccination of 9-month-old infants argues for a revision of the single-dose recommendation for this target population in endemic countries. The short duration of immunity in many vaccinees suggests that booster vaccination is necessary to meet the 80% population immunity threshold for prevention of yellow fever outbreaks. }, keywords = {}, pubstate = {published}, tppubtype = {article} } Background. A single dose of vaccine against yellow fever is routinely administered to infants aged 9–12 months under the Expanded Programme on Immunization, but the long-term outcome of vaccination in this age group is unknown. We aimed to evaluate the long-term persistence of neutralising antibodies to yellow fever virus following routine vaccination in infancy. Methods. We did a longitudinal cohort study, using a microneutralisation assay to measure protective antibodies against yellow fever in Malian and Ghanaian children vaccinated around age 9 months and followed up for 4·5 years (Mali), or 2·3 and 6·0 years (Ghana). Healthy children with available day-0 sera, a complete follow-up history, and no record of yellow fever revaccination were included; children seropositive for yellow fever at baseline were excluded. We standardised antibody concentrations with reference to the yellow fever WHO International Standard. Findings. We included 587 Malian and 436 Ghanaian children vaccinated between June 5, 2009, and Dec 26, 2012. In the Malian group, 296 (50·4%, 95% CI 46·4–54·5) were seropositive (antibody concentration ≥0·5 IU/mL) 4·5 years after vaccination. Among the Ghanaian children, 121 (27·8%, 23·5–32·0) were seropositive after 2·3 years. These results show a large decrease from the proportions of seropositive infants 28 days after vaccination, 96·7% in Mali and 72·7% in Ghana, reported by a previous study of both study populations. The number of seropositive children increased to 188 (43·1%, 95% CI 38·5–47·8) in the Ghanaian group 6·0 years after vaccination, but this result might be confounded by unrecorded revaccination or natural infection with wild yellow fever virus during a 2011–12 outbreak in northern Ghana. Interpretation. Rapid waning of immunity during the early years after vaccination of 9-month-old infants argues for a revision of the single-dose recommendation for this target population in endemic countries. The short duration of immunity in many vaccinees suggests that booster vaccination is necessary to meet the 80% population immunity threshold for prevention of yellow fever outbreaks. |
Piliponsky, A M; Shubin, N J; Lahiri, A K; Truong, P; Clauson, M; Niino, K; Tsuha, A L; Nedospasov, S A; Karasuyama, H; Reber, L L; Tsai, M; Mukai, K; Galli, S J Basophil-derived tumor necrosis factor can enhance survival in a sepsis model in mice Journal Article Nat Immunol, 20 (2), pp. 129-140, 2019, ISSN: 1529-2916 (Electronic) 1529-2908 (Linking). @article{RN1b, title = {Basophil-derived tumor necrosis factor can enhance survival in a sepsis model in mice}, author = {Piliponsky, A. M. and Shubin, N. J. and Lahiri, A. K. and Truong, P. and Clauson, M. and Niino, K. and Tsuha, A. L. and Nedospasov, S. A. and Karasuyama, H. and Reber, L. L. and Tsai, M. and Mukai, K. and Galli, S. J.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/30664762}, doi = {10.1038/s41590-018-0288-7}, issn = {1529-2916 (Electronic) 1529-2908 (Linking)}, year = {2019}, date = {2019-01-01}, journal = {Nat Immunol}, volume = {20}, number = {2}, pages = {129-140}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2018 |
Rosa, N; Triffaux, E; Robert, V; Mars, M; Klein, M; Bouchaud, G; Canivet, A; Magnan, A; Guery, J C; Pelletier, L; Savignac, M J Allergy Clin Immunol, 142 (3), pp. 892-903, 2018, ISSN: 1097-6825 (Electronic) 0091-6749 (Linking). @article{RN24, title = {The beta and alpha2delta auxiliary subunits of voltage-gated calcium channel 1 (Cav1) are required for TH2 lymphocyte function and acute allergic airway inflammation}, author = {Rosa, N. and Triffaux, E. and Robert, V. and Mars, M. and Klein, M. and Bouchaud, G. and Canivet, A. and Magnan, A. and Guery, J. C. and Pelletier, L. and Savignac, M.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29129580 https://www.sciencedirect.com/science/article/pii/S0091674917317402}, doi = {10.1016/j.jaci.2017.09.045}, issn = {1097-6825 (Electronic) 0091-6749 (Linking)}, year = {2018}, date = {2018-09-01}, journal = {J Allergy Clin Immunol}, volume = {142}, number = {3}, pages = {892-903}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Souyris, M; Cenac, C; Azar, P; Daviaud, D; Canivet, A; Grunenwald, S; Pienkowski, C; Chaumeil, J; Mejia, J E; Guery, J C TLR7 escapes X chromosome inactivation in immune cells Journal Article Sci Immunol, 3 (19), 2018, ISSN: 2470-9468 (Electronic) 2470-9468 (Linking), (In the top 5% of all research outputs scored by Altmetric. http://www.altmetric.com/details/32261033). @article{RN25b, title = {TLR7 escapes X chromosome inactivation in immune cells}, author = {Souyris, M. and Cenac, C. and Azar, P. and Daviaud, D. and Canivet, A. and Grunenwald, S. and Pienkowski, C. and Chaumeil, J. and Mejia, J. E. and Guery, J. C.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29374079}, doi = {10.1126/sciimmunol.aap8855}, issn = {2470-9468 (Electronic) 2470-9468 (Linking)}, year = {2018}, date = {2018-01-26}, journal = {Sci Immunol}, volume = {3}, number = {19}, note = {In the top 5% of all research outputs scored by Altmetric. http://www.altmetric.com/details/32261033}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Turner, M; Diaz-Munoz, M D RNA-binding proteins control gene expression and cell fate in the immune system Journal Article Nat Immunol, 19 (2), pp. 120-129, 2018, ISSN: 1529-2916 (Electronic) 1529-2908 (Linking). @article{RN1b, title = {RNA-binding proteins control gene expression and cell fate in the immune system}, author = {Turner, M. and Diaz-Munoz, M. D.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29348497}, doi = {10.1038/s41590-017-0028-4}, issn = {1529-2916 (Electronic) 1529-2908 (Linking)}, year = {2018}, date = {2018-01-01}, journal = {Nat Immunol}, volume = {19}, number = {2}, pages = {120-129}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Eissmann, M F; Dijkstra, C; Wouters, M A; Baloyan, D; Mouradov, D; Nguyen, P M; Davalos-Salas, M; Putoczki, T L; Sieber, O M; Mariadason, J M; Ernst, M; Masson, F Interleukin 33 Signaling Restrains Sporadic Colon Cancer in an Interferon-gamma-Dependent Manner Journal Article Cancer Immunol Res, 6 (4), pp. 409-421, 2018, ISSN: 2326-6074 (Electronic) 2326-6066 (Linking). @article{RN1b, title = {Interleukin 33 Signaling Restrains Sporadic Colon Cancer in an Interferon-gamma-Dependent Manner}, author = {Eissmann, M. F. and Dijkstra, C. and Wouters, M. A. and Baloyan, D. and Mouradov, D. and Nguyen, P. M. and Davalos-Salas, M. and Putoczki, T. L. and Sieber, O. M. and Mariadason, J. M. and Ernst, M. and Masson, F.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29463593}, doi = {10.1158/2326-6066.CIR-17-0218}, issn = {2326-6074 (Electronic) 2326-6066 (Linking)}, year = {2018}, date = {2018-01-01}, journal = {Cancer Immunol Res}, volume = {6}, number = {4}, pages = {409-421}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Houmadi, R; Guipouy, D; Rey-Barroso, J; Vasconcelos, Z; Cornet, J; Manghi, M; Destainville, N; Valitutti, S; Allart, S; Dupre, L The Wiskott-Aldrich Syndrome Protein Contributes to the Assembly of the LFA-1 Nanocluster Belt at the Lytic Synapse Journal Article Cell Rep, 22 (4), pp. 979-991, 2018, ISSN: 2211-1247 (Electronic). @article{RN3b, title = {The Wiskott-Aldrich Syndrome Protein Contributes to the Assembly of the LFA-1 Nanocluster Belt at the Lytic Synapse}, author = {Houmadi, R. and Guipouy, D. and Rey-Barroso, J. and Vasconcelos, Z. and Cornet, J. and Manghi, M. and Destainville, N. and Valitutti, S. and Allart, S. and Dupre, L.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29386139}, doi = {10.1016/j.celrep.2017.12.088}, issn = {2211-1247 (Electronic)}, year = {2018}, date = {2018-01-01}, journal = {Cell Rep}, volume = {22}, number = {4}, pages = {979-991}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Gaud, G; Lesourne, R; Love, P E Regulatory mechanisms in T cell receptor signalling Journal Article Nat Rev Immunol, 2018, ISSN: 1474-1741 (Electronic) 1474-1733 (Linking). @article{RN1b, title = {Regulatory mechanisms in T cell receptor signalling}, author = {Gaud, G. and Lesourne, R. and Love, P. E.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29789755}, doi = {10.1038/s41577-018-0020-8}, issn = {1474-1741 (Electronic) 1474-1733 (Linking)}, year = {2018}, date = {2018-01-01}, journal = {Nat Rev Immunol}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Betourne, A; Szelechowski, M; Thouard, A; Abrial, E; Jean, A; Zaidi, F; Foret, C; Bonnaud, E M; Charlier, C M; Suberbielle, E; Malnou, C E; Granon, S; Rampon, C; Gonzalez-Dunia, D Hippocampal expression of a virus-derived protein impairs memory in mice Journal Article Proc Natl Acad Sci U S A, 115 (7), pp. 1611-1616, 2018, ISSN: 1091-6490 (Electronic) 0027-8424 (Linking). @article{RN108, title = {Hippocampal expression of a virus-derived protein impairs memory in mice}, author = {Betourne, A. and Szelechowski, M. and Thouard, A. and Abrial, E. and Jean, A. and Zaidi, F. and Foret, C. and Bonnaud, E. M. and Charlier, C. M. and Suberbielle, E. and Malnou, C. E. and Granon, S. and Rampon, C. and Gonzalez-Dunia, D.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29378968}, doi = {10.1073/pnas.1711977115}, issn = {1091-6490 (Electronic) 0027-8424 (Linking)}, year = {2018}, date = {2018-01-01}, journal = {Proc Natl Acad Sci U S A}, volume = {115}, number = {7}, pages = {1611-1616}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Colin, P; Zhou, Z; Staropoli, I; Garcia-Perez, J; Gasser, R; Armani-Tourret, M; Benureau, Y; Gonzalez, N; Jin, J; Connell, B J; Raymond, S; Delobel, P; Izopet, J; Lortat-Jacob, H; Alcami, J; Arenzana-Seisdedos, F; Brelot, A; Lagane, B CCR5 structural plasticity shapes HIV-1 phenotypic properties Journal Article PLoS Pathog, 14 (12), pp. e1007432, 2018, ISSN: 1553-7374 (Electronic) 1553-7366 (Linking). @article{RN859, title = {CCR5 structural plasticity shapes HIV-1 phenotypic properties}, author = {Colin, P. and Zhou, Z. and Staropoli, I. and Garcia-Perez, J. and Gasser, R. and Armani-Tourret, M. and Benureau, Y. and Gonzalez, N. and Jin, J. and Connell, B. J. and Raymond, S. and Delobel, P. and Izopet, J. and Lortat-Jacob, H. and Alcami, J. and Arenzana-Seisdedos, F. and Brelot, A. and Lagane, B.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/30521629}, doi = {10.1371/journal.ppat.1007432}, issn = {1553-7374 (Electronic) 1553-7366 (Linking)}, year = {2018}, date = {2018-01-01}, journal = {PLoS Pathog}, volume = {14}, number = {12}, pages = {e1007432}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
2017 |
Tauber, Maïthé; Boulanouar, Kader; Diene, Gwenaelle; Çabal-Berthoumieu, Sophie; Ehlinger, Virginie; Fichaux-Bourin, Pascale; Molinas, Catherine; Faye, Sandy; Valette, Marion; Pourrinet, Jeanne; Cessans, Catie; Viaux-Sauvelon, Sylvie; Bascoul, Céline; Guedeney, Antoine; Delhanty, Patric; Geenen, Vincent; Martens, Henri; Muscatelli, Françoise; Cohen, David; Consoli, Angèle; Payoux, Pierre; Arnaud, Catherine; Salles, Jean-Pierre The Use of Oxytocin to Improve Feeding and Social Skills in Infants With Prader–Willi Syndrome Journal Article PEDIATRICS, 139 (2), pp. e2 0162976, 2017. @article{RN10b, title = {The Use of Oxytocin to Improve Feeding and Social Skills in Infants With Prader–Willi Syndrome}, author = {Maïthé Tauber and Kader Boulanouar and Gwenaelle Diene and Sophie Çabal-Berthoumieu and Virginie Ehlinger and Pascale Fichaux-Bourin and Catherine Molinas and Sandy Faye and Marion Valette and Jeanne Pourrinet and Catie Cessans and Sylvie Viaux-Sauvelon and Céline Bascoul and Antoine Guedeney and Patric Delhanty and Vincent Geenen and Henri Martens and Françoise Muscatelli and David Cohen and Angèle Consoli and Pierre Payoux and Catherine Arnaud and Salles, Jean-Pierre}, year = {2017}, date = {2017-01-01}, journal = {PEDIATRICS}, volume = {139}, number = {2}, pages = {e2 0162976}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Asrir, A; Aloulou, M; Gador, M; Perals, C; Fazilleau, N Interconnected subsets of memory follicular helper T cells have different effector functions Journal Article Nat Commun, 8 (1), pp. 847, 2017, ISSN: 2041-1723 (Electronic) 2041-1723 (Linking). @article{RN2b, title = {Interconnected subsets of memory follicular helper T cells have different effector functions}, author = {Asrir, A. and Aloulou, M. and Gador, M. and Perals, C. and Fazilleau, N.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29018187}, doi = {10.1038/s41467-017-00843-7}, issn = {2041-1723 (Electronic) 2041-1723 (Linking)}, year = {2017}, date = {2017-01-01}, journal = {Nat Commun}, volume = {8}, number = {1}, pages = {847}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Duguet, F; Locard-Paulet, M; Marcellin, M; Chaoui, K; Bernard, I; Andreoletti, O; Lesourne, R; Burlet-Schiltz, O; Gonzalez de Peredo, A; Saoudi, A Proteomic Analysis of Regulatory T Cells Reveals the Importance of Themis1 in the Control of Their Suppressive Function Journal Article Mol Cell Proteomics, 16 (8), pp. 1416-1432, 2017, ISSN: 1535-9484 (Electronic) 1535-9476 (Linking). @article{RN4b, title = {Proteomic Analysis of Regulatory T Cells Reveals the Importance of Themis1 in the Control of Their Suppressive Function}, author = {Duguet, F. and Locard-Paulet, M. and Marcellin, M. and Chaoui, K. and Bernard, I. and Andreoletti, O. and Lesourne, R. and Burlet-Schiltz, O. and Gonzalez de Peredo, A. and Saoudi, A.}, url = {http://www.ncbi.nlm.nih.gov/pubmed/28373295}, doi = {10.1074/mcp.M116.062745}, issn = {1535-9484 (Electronic) 1535-9476 (Linking)}, year = {2017}, date = {2017-01-01}, journal = {Mol Cell Proteomics}, volume = {16}, number = {8}, pages = {1416-1432}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Laffont, Sophie; Blanquart, Eve; Savignac, Magali; Cenac, Claire; Laverny, Gilles; Metzger, Daniel; Girard, Jean-Philippe; Belz, Gabrielle T; Pelletier, Lucette; Seillet, Cyril; Guery, Jean-Charles Androgen signaling negatively controls group 2 innate lymphoid cells Journal Article J Exp Med, 214 (6), pp. 1581-1592, 2017, ISSN: 1540-9538 (Electronic) 0022-1007 (Linking). @article{RN3, title = {Androgen signaling negatively controls group 2 innate lymphoid cells}, author = {Sophie Laffont and Eve Blanquart and Magali Savignac and Claire Cenac and Gilles Laverny and Daniel Metzger and Jean-Philippe Girard and Gabrielle T Belz and Lucette Pelletier and Cyril Seillet and Jean-Charles Guery}, url = {https://www.ncbi.nlm.nih.gov/pubmed/28484078}, doi = {10.1084/jem.20161807}, issn = {1540-9538 (Electronic) 0022-1007 (Linking)}, year = {2017}, date = {2017-01-01}, journal = {J Exp Med}, volume = {214}, number = {6}, pages = {1581-1592}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Yshii, L M; Hohlfeld, R; Liblau, R S Inflammatory CNS disease caused by immune checkpoint inhibitors: status and perspectives Journal Article Nat Rev Neurol, 13 (12), pp. 755-763, 2017, ISSN: 1759-4766 (Electronic) 1759-4758 (Linking). @article{RN5b, title = {Inflammatory CNS disease caused by immune checkpoint inhibitors: status and perspectives}, author = {Yshii, L. M. and Hohlfeld, R. and Liblau, R. S.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/29104289}, doi = {10.1038/nrneurol.2017.144}, issn = {1759-4766 (Electronic) 1759-4758 (Linking)}, year = {2017}, date = {2017-01-01}, journal = {Nat Rev Neurol}, volume = {13}, number = {12}, pages = {755-763}, keywords = {}, pubstate = {published}, tppubtype = {article} } |
Joulia, R; Mailhol, C; Valitutti, S; Didier, A; Espinosa, E Direct monitoring of basophil degranulation by using avidin-based probes Journal Article J Allergy Clin Immunol, 2017, ISSN: 1097-6825 (Electronic) 0091-6749 (Linking). @article{RN16, title = {Direct monitoring of basophil degranulation by using avidin-based probes}, author = {Joulia, R. and Mailhol, C. and Valitutti, S. and Didier, A. and Espinosa, E.}, url = {https://www.ncbi.nlm.nih.gov/pubmed/28433691}, doi = {10.1016/j.jaci.2017.03.030}, issn = {1097-6825 (Electronic) 0091-6749 (Linking)}, year = {2017}, date = {2017-01-01}, journal = {J Allergy Clin Immunol}, keywords = {}, pubstate = {published}, tppubtype = {article} } |