18 results on '"Elke Schneider"'
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2. Basophil activation through TLR2 and TLR4 signaling pathways
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Manal Alkan, Fadel Sayes, Abdulraouf Ramadan, Francois Machavoine, Michel Dy, Elke Schneider, and Nathalie Thieblemont
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basophils ,PAMP ,IL-4 ,histamine ,TLR ,Immunologic diseases. Allergy ,RC581-607 - Abstract
Basophils are effector cells that respond to protease allergens and parasites, thus contributing to allergic inflammation and Th2 differentiation. However, the molecular interactions through which pathogens promote activation as well as recruitment of these cells to sites of inflammation remain poorly understood. We found that administration of extracts from Nippostrongylus brasiliensis induced both basophil recruitment into blood and liver in vivo and IL-4 and histamine production by purified bone marrow-derived basophils in vitro. Starting from this finding, we set out to identify putative pathogen-derived molecules for their capacity to activate murine basophils, using a basophil population differentiated and expanded from bone marrow cells cultured with IL-3 and sorted as a CD49b+ c-kit– subset. Among a number of Toll-like receptor (TLR) agonists tested, we found that the lipopeptide Pam2CSK4 and lipopolysaccharide (LPS) activate basophils in terms of IL-4, IL-6 and histamine production through TLR2 and TLR4, respectively. By contrast, TLR3 or TLR7 agonists had no such effect. We further identified nitric oxide (NO) as key mediator for LPS stimulation and established that in vivo administration of LPS led to basophil recruitment into the liver. Our results reveal the important contribution of MyD88 and NO signaling to antigen recognition through TLR2 and TLR4 pathways leading to activation, degranulation and release of immunoregulatory mediators.
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- 2018
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3. Mouse basophils reside in extracellular matrix-enriched bone marrow niches which control their motility.
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Salete Smaniotto, Elke Schneider, Nicolas Goudin, Rachel Bricard-Rignault, François Machavoine, Mireille Dardenne, Michel Dy, and Wilson Savino
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Medicine ,Science - Abstract
Basophils co-express FcεRIα and CD49b, the α-2 chain of integrin-type receptor VLA-2 (α2β1), which recognizes type-1 collagen as a major natural ligand. The physiological relevance of this integrin for interactions with extracellular bone marrow matrix remains unknown. Herein, we examined the expression of several receptors of this family by bone marrow-derived basophils sorted either ex-vivo or after culture with IL-3. Having established that both populations display CD49d, CD49e and CD49f (α-4, α-5 and α-6 integrins subunits, respectively), we addressed receptor functions by measuring migration, adhesion, proliferation and survival after interacting with matched natural ligands. Type I collagen, laminin and fibronectin promoted basophil migration/adhesion, the former being the most effective. None of these ligands affected basophil viability and expansion. Interactions between basophils and extracellular matrix are likely to play a role in situ, as supported by confocal 3D cell imaging of femoral bone marrow sections, which revealed basophils exclusively in type-1 collagen-enriched niches that contained likewise laminin and fibronectin. This is the first evidence for a structure/function relationship between basophils and extracellular matrix proteins inside the mouse bone marrow.
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- 2013
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4. H4 histamine receptors mediate cell cycle arrest in growth factor-induced murine and human hematopoietic progenitor cells.
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Anne-France Petit-Bertron, François Machavoine, Marie Paule Defresne, Michel Gillard, Pierre Chatelain, Prakash Mistry, Elke Schneider, and Michel Dy
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Medicine ,Science - Abstract
The most recently characterized H4 histamine receptor (H4R) is expressed preferentially in the bone marrow, raising the question of its role during hematopoiesis. Here we show that both murine and human progenitor cell populations express this receptor subtype on transcriptional and protein levels and respond to its agonists by reduced growth factor-induced cell cycle progression that leads to decreased myeloid, erythroid and lymphoid colony formation. H4R activation prevents the induction of cell cycle genes through a cAMP/PKA-dependent pathway that is not associated with apoptosis. It is mediated specifically through H4R signaling since gene silencing or treatment with selective antagonists restores normal cell cycle progression. The arrest of growth factor-induced G1/S transition protects murine and human progenitor cells from the toxicity of the cell cycle-dependent anticancer drug Ara-C in vitro and reduces aplasia in a murine model of chemotherapy. This first evidence for functional H4R expression in hematopoietic progenitors opens new therapeutic perspectives for alleviating hematotoxic side effects of antineoplastic drugs.
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- 2009
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5. Mouse basophils reside in extracellular matrix-enriched bone marrow niches which control their motility
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Michel Dy, Wilson Savino, Mireille Dardenne, Salete Smaniotto, Elke Schneider, Rachel Bricard-Rignault, François Machavoine, Nicolas Goudin, Cytokines, hématopoïèse et réponse immune (CHRI), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS)
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Male ,Integrin ,lcsh:Medicine ,Fluorescent Antibody Technique ,Bone Marrow Cells ,chemical and pharmacologic phenomena ,Real-Time Polymerase Chain Reaction ,Extracellular matrix ,Mice ,Cell Movement ,Laminin ,Cell Adhesion ,medicine ,Extracellular ,Animals ,lcsh:Science ,Cell adhesion ,Cells, Cultured ,ComputingMilieux_MISCELLANEOUS ,Multidisciplinary ,biology ,Gene Expression Profiling ,lcsh:R ,hemic and immune systems ,Molecular biology ,Basophils ,Extracellular Matrix ,Mice, Inbred C57BL ,Fibronectin ,medicine.anatomical_structure ,biology.protein ,lcsh:Q ,Female ,Bone marrow ,Type I collagen ,Research Article - Abstract
Basophils co-express FcεRIα and CD49b, the α-2 chain of integrin-type receptor VLA-2 (α2β1), which recognizes type-1 collagen as a major natural ligand. The physiological relevance of this integrin for interactions with extracellular bone marrow matrix remains unknown. Herein, we examined the expression of several receptors of this family by bone marrow-derived basophils sorted either ex-vivo or after culture with IL-3. Having established that both populations display CD49d, CD49e and CD49f (α-4, α-5 and α-6 integrins subunits, respectively), we addressed receptor functions by measuring migration, adhesion, proliferation and survival after interacting with matched natural ligands. Type I collagen, laminin and fibronectin promoted basophil migration/adhesion, the former being the most effective. None of these ligands affected basophil viability and expansion. Interactions between basophils and extracellular matrix are likely to play a role in situ, as supported by confocal 3D cell imaging of femoral bone marrow sections, which revealed basophils exclusively in type-1 collagen-enriched niches that contained likewise laminin and fibronectin. This is the first evidence for a structure/function relationship between basophils and extracellular matrix proteins inside the mouse bone marrow.
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- 2013
6. Modulation of hematopoiesis through histamine receptor signaling
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Michel Dy, Anne-France Bertron, Elke Schneider, Cytokines, hématopoïèse et réponse immune (CHRI), 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) - Centre National de la Recherche Scientifique (CNRS), and Slama, Catherine
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Cyclin-Dependent Kinase Inhibitor p21 ,Histamine H1 receptor ,Biology ,General Biochemistry, Genetics and Molecular Biology ,Receptors, G-Protein-Coupled ,chemistry.chemical_compound ,Histamine receptor ,Mice ,Cyclic AMP ,Animals ,Humans ,Histamine H4 receptor ,Progenitor cell ,Receptor ,ComputingMilieux_MISCELLANEOUS ,Receptors, Histamine H4 ,General Immunology and Microbiology ,Cell growth ,Cell Cycle ,Imidazoles ,Thiourea ,Hematopoietic Stem Cells ,Cyclic AMP-Dependent Protein Kinases ,Cell biology ,Hematopoiesis ,chemistry ,Immunology ,Receptors, Histamine ,Signal transduction ,Histamine ,Signal Transduction - Abstract
Histamine is one of the most versatile biogenic amines targeting a variety of cells through extra- and intracellular binding sites and specific receptors, which trigger different signal transduction pathways. It has been associated with cell growth ever since G. Kahlson demonstrated that its synthesis was increased in rapidly growing tissues of plants and animals. He proposed that the newly formed amine, as opposed to its stored counterpart, might play a major role in growth processes. Later on, a number of investigators provided evidence for the contribution of histamine to the expansion of normal and malignant cells, whether of hematopoietic origin or not. These studies have generated conflicting results, revealing growth-promoting as well as inhibitory effects, most likely because the final outcome of exposure to histamine depends on the signaling pathways triggered by distinct receptors and their differential distribution among the target population. The purpose of the present review is to outline our current understanding of the regulatory functions of histamine during growth and differentiation of hematopoietic progenitors, focusing on those mediated through its H4 receptor.
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- 2011
7. Ineffective erythropoiesis with reduced red blood cell survival in serotonin-deficient mice
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Jacques Mallet, Elisa Bayard, Michel Dy, Jean-Marie Launay, Olivier Hermine, Sarah Hatia, Elke Schneider, Corinne Collet, Francine Côté, Pascal Amireault, Jacques Callebert, Florence Bernex, Cytokines, hématopoïèse et réponse immune (CHRI), 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 Logiciels Systèmes Réseaux (LSR - IMAG), Université Joseph Fourier - Grenoble 1 (UJF)-Institut National Polytechnique de Grenoble (INPG)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS), Biotechnology and biotherapy laboratory, Université Pierre et Marie Curie - Paris 6 (UPMC), Génétique Moléculaire et Cellulaire (UGMC), École nationale vétérinaire d'Alfort (ENVA)-Institut National de la Recherche Agronomique (INRA), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), l'Agence Nationale de la Recherche, la Ligue Contre le Cancer, STEM-Pole, Region Ile-de-France, Ministere Superieur de l'Enseignement et de la Recherche, Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière (CRICM), 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), École nationale vétérinaire - Alfort (ENVA)-Institut National de la Recherche Agronomique (INRA), Cytokines, hématopoïèse et réponse immune ( CHRI ), 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 Logiciels Systèmes Réseaux ( LSR - IMAG ), and Université Joseph Fourier - Grenoble 1 ( UJF ) -Institut National Polytechnique de Grenoble ( INPG ) -Centre National de la Recherche Scientifique ( CNRS )
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Ineffective erythropoiesis ,medicine.medical_specialty ,Erythrocytes ,Siderosis ,Cell Survival ,Iron ,[SDV]Life Sciences [q-bio] ,behavioral function ,Tryptophan Hydroxylase ,Biology ,medicine.disease_cause ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Bone Marrow ,Internal medicine ,medicine ,Animals ,Erythropoiesis ,Anemia, Macrocytic ,Erythroid Precursor Cells ,ComputingMilieux_MISCELLANEOUS ,Cell Proliferation ,030304 developmental biology ,0303 health sciences ,Multidisciplinary ,TPH1 ,TPH2 ,Cell Cycle ,tph ,Biological Sciences ,Tryptophan hydroxylase ,Serotonin Receptor Agonists ,serotonin ,Mice, Inbred C57BL ,Red blood cell ,Phenotype ,Endocrinology ,medicine.anatomical_structure ,Receptors, Serotonin ,Dietary Supplements ,Bone marrow ,Spleen ,030217 neurology & neurosurgery ,neurotransmitter - Abstract
Serotonin (5-HT) has long been recognized as a neurotransmitter in the central nervous system, where it modulates a variety of behavioral functions. Availability of 5-HT depends on the expression of the enzyme tryptophan hydroxylase (TPH), and the recent discovery of a dual system for 5-HT synthesis in the brain (TPH2) and periphery (TPH1) has renewed interest in studying the potential functions played by 5-HT in nonnervous tissues. Moreover, characterization of the TPH1 knockout mouse model (TPH1 −/− ) led to the identification of unsuspected roles for peripheral 5-HT, revealing the importance of this monoamine in regulating key physiological functions outside the brain. Here, we present in vivo data showing that mice deficient in peripheral 5-HT display morphological and cellular features of ineffective erythropoiesis. The central event occurs in the bone marrow where the absence of 5-HT hampers progression of erythroid precursors expressing 5-HT 2A and 5-HT 2B receptors toward terminal differentiation. In addition, red blood cells from 5-HT–deficient mice are more sensitive to macrophage phagocytosis and have a shortened in vivo half-life. The combination of these two defects causes TPH1 −/− animals to develop a phenotype of macrocytic anemia. Direct evidence for a 5-HT effect on erythroid precursors is provided by supplementation of the culture medium with 5-HT that increases the proliferative capacity of both 5-HT–deficient and normal cells. Our thorough analysis of TPH1 −/− mice provides a unique model of morphological and functional aberrations of erythropoiesis and identifies 5-HT as a key factor for red blood cell production and survival.
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- 2011
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8. Critical role of the neutrophil-associated high affinity receptor for IgE in the pathogenesis of experimental cerebral malaria
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Pierre-Henri Commere, Michel Dy, Salaheddine Mécheri, Cedric Mathieu, Jacques A. Louis, Geneviève Milon, Julien Claver, Hélène Kiefer-Biasizzo, Hajime Karasuyama, Jean-Pierre Kinet, Adeline Porcherie, Elke Schneider, Roger Peronet, Ulrich Blank, Cytokines, hématopoïèse et réponse immune (CHRI), Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS), Biologie des Interactions Hôte-Parasite, Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Immunopathologie rénale, récepteurs et inflammation, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Imagopole (CITECH), Institut Pasteur [Paris] (IP), Tokyo Medical and Dental University [Japan] (TMDU), Immunophysiologie et Parasitisme Intracellulaire, Beth Israel Deaconess Medical Center [Boston] (BIDMC), Harvard Medical School [Boston] (HMS), and Slama, Catherine
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Adoptive cell transfer ,[SDV.IMM] Life Sciences [q-bio]/Immunology ,Neutrophils ,Plasmodium berghei ,medicine.medical_treatment ,Immunology ,Population ,Malaria, Cerebral ,Immunoglobulin E ,Article ,Proinflammatory cytokine ,Pathogenesis ,03 medical and health sciences ,Mice ,0302 clinical medicine ,parasitic diseases ,medicine ,Immunology and Allergy ,Animals ,Protein Isoforms ,education ,ComputingMilieux_MISCELLANEOUS ,030304 developmental biology ,Mice, Knockout ,0303 health sciences ,education.field_of_study ,biology ,Receptors, IgE ,fungi ,biology.organism_classification ,Adoptive Transfer ,3. Good health ,Basophils ,Eosinophils ,Mice, Inbred C57BL ,Cytokine ,Cerebral Malaria ,biology.protein ,Cytokines ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,Female ,030215 immunology - Abstract
FcεR1-expressing neutrophils accumulate in the brain of mice infected with Plasmodium berghei (PbANKA) and promote the development of experimental cerebral malaria., The role of the IgE–FcεRI complex in malaria severity in Plasmodium falciparum–hosting patients is unknown. We demonstrate that mice genetically deficient for the high-affinity receptor for IgE (FcεRIα-KO) or for IgE (IgE-KO) are less susceptible to experimental cerebral malaria (ECM) after infection with Plasmodium berghei (PbANKA). Mast cells and basophils, which are the classical IgE-expressing effector cells, are not involved in disease as mast cell–deficient and basophil-depleted mice developed a disease similar to wild-type mice. However, we show the emergence of an FcεRI+ neutrophil population, which is not observed in mice hosting a non–ECM-inducing PbNK65 parasite strain. Depletion of this FcεRI+ neutrophil population prevents ECM, whereas transfer of this population into FcεRIα-KO mice restores ECM susceptibility. FcεRI+ neutrophils preferentially home to the brain and induce elevated levels of proinflammatory cytokines. These data define a new pathogenic mechanism of ECM and implicate an FcεRI-expressing neutrophil subpopulation in malaria disease severity.
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- 2011
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9. Histamine, immune cells and autoimmunity
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Elke Schneider, Michel Dy, Maria Leite-de-Moraes, Slama, Catherine, Robin L. Thurmond, Cytokines, hématopoïèse et réponse immune (CHRI), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS)
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0303 health sciences ,Innate immune system ,Antigen presentation ,Histamine H1 receptor ,Biology ,Mast cell ,Histidine decarboxylase ,3. Good health ,03 medical and health sciences ,chemistry.chemical_compound ,Histamine receptor ,0302 clinical medicine ,medicine.anatomical_structure ,Immune system ,chemistry ,Immunology ,medicine ,Histamine ,030304 developmental biology ,030215 immunology - Abstract
Histamine is one ofthe most versatile biogenic amines with multiple roles during the immune response and in allergic disorders. With four distinct G protein-coupled receptors (H1R, HER, H3R and H4R), intracellular histamine binding sites (most likely members of the cytochrome P450 family) as well as a membrane transporter (Organic Cation Transporter; OCT3) expressed in various immunocompetent cells, it can entertain a complex network of interactions. These signaling pathways are expressed differentially, depending on the stage of differentiation or activation of target cells, thus adding a further degree of complexity to the system. For this reason, published data are sometimes conflicting and varying according to the particular cell type or responses analyzed and the experimental approaches used. On the other hand, histamine is generated by several cells during the immune response, not only through release of intracellular stores in mast cells or basophils in response to IgE-dependent or -independent stimuli, but also through neosynthesis catalyzed by histidine decarboxylase (HDC) in a number ofhematopoietic cells that secrete the amine immediately without prior storage. These features enable histamine to tune the fine balance between immunity and tolerance by affecting dendritic cells, immunoregulatory cells, T-cell polarization and cytokine production, making the way for new pharmacological strategies to control immune reactivity during immune disorders, such as autoimmunity.
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- 2010
10. The pro-Th2 cytokine IL-33 directly interacts with invariant NKT and NK cells to induce IFN-gamma production
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Michel Samson, Elvire Bourgeois, Pierre Gourdy, Séverine Diem, Stéphane Roga, Elke Schneider, Michel Dy, Linh Pham Van, Jean-Philippe Girard, Anne Barra, André Herbelin, Jean-Marc Gombert, Cytokines, hématopoïèse et réponse immune (CHRI), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Signalisation et Réponses aux Agents Infectieux et Chimiques (SeRAIC), Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES), Détoxication et réparation tissulaire, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Rennes 1 (UR1), Laboratoire d'immunologie [CHU Poitiers], Centre hospitalier universitaire de Poitiers (CHU Poitiers), Institut de pharmacologie et de biologie structurale (IPBS), Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Descartes - Paris 5 (UPD5), CNRS, Université de Paris Descartes, Ligue Nationale contre le Cancer, la Chancellerie des Universités de Paris, Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-IFR140, Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-IFR140-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), Slama, Catherine, Université de Rennes (UR), Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université de Toulouse (UT)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS), Université de Toulouse (UT)-Université de Toulouse (UT)- Institut Fédératif de Recherche Bio-médicale Institution (IFR150)-Institut National de la Santé et de la Recherche Médicale (INSERM), Cytokines, hématopoïèse et réponse immune ( CHRI ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Signalisation et Réponses aux Agents Infectieux et Chimiques ( SeRAIC ), Université de Rennes 1 ( UR1 ), Université de Rennes ( UNIV-RENNES ) -Université de Rennes ( UNIV-RENNES ) -IFR140, Université de Rennes ( UNIV-RENNES ) -Université de Rennes ( UNIV-RENNES ) -IFR140-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Centre hospitalier universitaire de Poitiers ( CHU Poitiers ), Institut de pharmacologie et de biologie structurale ( IPBS ), Centre National de la Recherche Scientifique ( CNRS ) -Université Toulouse III - Paul Sabatier ( UPS ), Institut des Maladies Métaboliques et Cardiovasculaires ( I2MC ), Université Toulouse III - Paul Sabatier ( UPS ), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Hôpital de Rangueil, CHU Toulouse [Toulouse]-CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut de médecine moléculaire de Rangueil ( I2MR ), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Université Paris Descartes - Paris 5 ( UPD5 ), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS)
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MESH: Interleukin-12 ,MESH: Spleen ,medicine.medical_treatment ,MESH: Mice, Knockout ,Interleukin 21 ,Mice ,0302 clinical medicine ,Immunology and Allergy ,[ SDV.IMM ] Life Sciences [q-bio]/Immunology ,MESH : Female ,MESH: Animals ,IL-2 receptor ,ComputingMilieux_MISCELLANEOUS ,Mice, Knockout ,0303 health sciences ,Mice, Inbred BALB C ,ZAP70 ,Natural killer T cell ,Interleukin-12 ,Killer Cells, Natural ,Cytokine ,Liver ,Interleukin 12 ,Cytokines ,Natural killer cells ,Natural killer T cells ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,Female ,MESH : Killer Cells, Natural ,MESH : Spleen ,MESH: Killer Cells, Natural ,MESH: Interleukins ,MESH: Interferon-gamma ,Immunology ,MESH: Mice, Inbred BALB C ,MESH : Mice, Inbred C57BL ,Biology ,MESH : Interleukin-4 ,03 medical and health sciences ,Interferon-gamma ,Th2 Cells ,MESH: Mice, Inbred C57BL ,MESH: Th2 Cells ,MESH : Mice ,medicine ,MESH : Interleukin-12 ,Animals ,Humans ,MESH: Mice ,MESH : Mice, Inbred BALB C ,MESH : Interferon-gamma ,030304 developmental biology ,Inflammation ,Lymphokine-activated killer cell ,MESH: Humans ,Interleukins ,MESH : Humans ,MESH : Liver ,MESH: Interleukin-4 ,Interleukin-33 ,MESH : Natural Killer T-Cells ,MESH : Th2 Cells ,Interleukin 33 ,Mice, Inbred C57BL ,MESH: Natural Killer T-Cells ,Natural Killer T-Cells ,MESH : Mice, Knockout ,Th1/Th2 cells ,Interleukin-4 ,MESH : Animals ,MESH : Interleukins ,MESH: Female ,Spleen ,030215 immunology ,MESH: Liver - Abstract
International audience; IL-33 has recently been identified as a cytokine endowed with pro-Th2 functions, raising the question of its effect on invariant natural killer T cell (iNKT), which are potent IL-4 producers. Here, we report a two-fold increase of iNKT-cell counts in spleen and liver after a 7-day treatment of mice with IL-33, which results from a direct effect, given that purified iNKT cells express the T1/ST2 receptor constitutively and respond to IL-33 by in vitro expansion and functional activation. Conversely to the expected pro-Th2 effect, IL-33 induced a preferential increase in IFN-gamma rather than IL-4 production upon TCR engagement that depended on endogenous IL-12. Moreover, in combination with the pro-inflammatory cytokine IL-12, IL-33 enhanced IFN-gamma production by both iNKT and NK cells. Taken together these data support the conclusion that IL-33 can contribute as a co-stimulatory factor to innate cellular immune responses.
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- 2009
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11. IL-33 activates unprimed murine basophils directly in vitro and induces their in vivo expansion indirectly by promoting hematopoietic growth factor production
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Mélanie Levasseur, Elke Schneider, Rachel Bricard, Abdelrauf Ramadan, Michel Dy, André Herbelin, Anne-France Petit-Bertron, Jean-Philippe Girard, Cytokines, hématopoïèse et réponse immune (CHRI), 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)-Centre National de la Recherche Scientifique (CNRS), and Slama, Catherine
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Transcriptional Activation ,medicine.medical_treatment ,Hematopoietic growth factor ,Immunology ,Bone Marrow Cells ,Basophil ,Biology ,Mice ,chemistry.chemical_compound ,Colony-Stimulating Factors ,In vivo ,medicine ,Animals ,Immunology and Allergy ,ComputingMilieux_MISCELLANEOUS ,Cell Proliferation ,Interleukin 3 ,Mice, Knockout ,Interleukins ,Growth factor ,Granulocyte-Macrophage Colony-Stimulating Factor ,Interleukin-33 ,Basophils ,Cell biology ,Interleukin 33 ,medicine.anatomical_structure ,chemistry ,Interleukin-3 ,Bone marrow ,Interleukin-5 ,Histamine - Abstract
IL-33, a new member of the IL-1 family, has been described as an important inducer of Th2 cytokines and mediator of inflammatory responses. In this study, we demonstrate that murine basophils sorted directly from the bone marrow, without prior exposure to IL-3 or FcεR cross-linking, respond to IL-33 alone by producing substantial amounts of histamine, IL-4, and IL-6. These cells express ST2 constitutively and generate a cytokine profile that differs from their IL-3-induced counterpart by a preferential production of IL-6. In vivo, IL-33 promotes basophil expansion in the bone marrow (BM) through an indirect mechanism of action depending on signaling through the βc chain shared by receptors for IL-3, GM-CSF, and IL-5. IL-3 can still signal through its specific βIL-3 chain in these mutant mice, which implies that it is not the unique growth-promoting mediator in this setup, but requires IL-5 and/or GMCSF. Our results support a major role of the latter growth factor, which is readily generated by total BM cells as well as sorted basophils in response to IL-33 along with low amounts of IL-3. Furthermore, GM-CSF amplifies IL-3-induced differentiation of basophils from BM cells, whereas IL-5 that is also generated in vivo, affects neither their functions nor their growth in vitro or in vivo. In conclusion, our data provide the first evidence that IL-33 not only activates unprimed basophils directly, but also promotes their expansion in vivo through induction of GM-CSF and IL-3.
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- 2009
12. Comparison of the effect of 4-methyl histamine on human and mouse basophil activation
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Elke Schneider, Michel Dy, F. Machavoine, J. Sainte-Laudy, A. F. Bertron, Cytokines, hématopoïèse et réponse immune (CHRI), 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) - Centre National de la Recherche Scientifique (CNRS), and Slama, Catherine
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Allergy ,Immunology ,Pharmacology toxicology ,Mouse Basophil ,Pharmacology ,CD13 Antigens ,Receptors, G-Protein-Coupled ,chemistry.chemical_compound ,Mice ,Histamine Hydrochloride ,medicine ,Animals ,Humans ,Receptors, Histamine H2 ,Histamine H4 receptor ,Pyrophosphatases ,ComputingMilieux_MISCELLANEOUS ,Receptors, Histamine H4 ,Chemistry ,Phosphoric Diester Hydrolases ,Methylhistamines ,N-methylhistamine ,Immunoglobulin E ,medicine.disease ,Basophils ,N-Formylmethionine Leucyl-Phenylalanine ,Receptors, Histamine ,Interleukin-4 ,Histamine ,Human basophil - Abstract
International audience
- Published
- 2008
13. Critical role of ROR-γT in a new thymic pathway leading to IL-17-producing invariant NKT cell differentiation
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Elke Schneider, Michel Dy, Matthias Lochner, Maria Leite-de-Moraes, Gérard Eberl, Daniella Arêas Mendes-da-Cruz, Marie-Laure Michel, Alexandre C. Keller, Cytokines, hématopoïèse et réponse immune (CHRI), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Slama, Catherine, ProdInra, Migration, and Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS)
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Male ,Receptors, Retinoic Acid ,[SDV]Life Sciences [q-bio] ,Cellular differentiation ,Green Fluorescent Proteins ,Cell ,Galactosylceramides ,Mice, Transgenic ,Thymus Gland ,Lymphocyte Activation ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Immune system ,medicine ,Animals ,ComputingMilieux_MISCELLANEOUS ,030304 developmental biology ,0303 health sciences ,Receptors, Thyroid Hormone ,Multidisciplinary ,biology ,Cell growth ,Interleukin-17 ,Cell Differentiation ,Nuclear Receptor Subfamily 1, Group F, Member 3 ,Biological Sciences ,Natural killer T cell ,Fetal Thymic Organ Culture ,Cell biology ,[SDV] Life Sciences [q-bio] ,medicine.anatomical_structure ,CD1D ,Immunology ,biology.protein ,Natural Killer T-Cells ,Interleukin 17 ,030215 immunology - Abstract
Invariant natural killer T (iNKT) cells constitute a subpopulation of T cells that recognize glycolipids presented by CD1d molecules. They are characterized by their prompt production of interleukin-4 (IL-4) and interferon-γ (IFN-γ), which enables them to modulate diverse immune responses. Recently, we enlarged this concept by identifying a distinct IL-17-producing iNKT cell subset, named iNKT17 cells. The mechanisms leading to the acquisition of this new iNKT cell activity are unknown. Herein we show that IL-17-producing iNKT cells are already present in the thymus, predominantly among a subset regarded so far as an immature stage of thymic iNKT cell development, the CD1d tetramer pos CD44 pos NK1.1 neg CD4 neg cells. Using EGFP reporter mice, we demonstrate that the transcription factor ROR-γt is critical for the thymic differentiation of this subset because only ROR-γt pos iNKT cells are capable of massively secreting IL-17. Moreover, IL-17-producing CD1d tetramer pos CD44 pos NK1.1 neg CD4 neg thymic iNKT cells have reached a mature differentiation stage because they fail to generate other cell subsets in fetal thymic organ culture. Conversely, thymic ROR-γt neg iNKT cell precursors give rise to progeny, but acquire neither ROR-γt expression nor the ability to secrete IL-17. In conclusion, our findings demonstrate an alternative thymic pathway leading to the development of iNKT17 cells that requires ROR-γt expression.
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- 2008
- Full Text
- View/download PDF
14. The Pro-Th1 cytokine IL-12 enhances IL-4 production by invariant NKT cells: relevance for T cell-mediated hepatitis
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Diane Damotte, Luiza M Araujo, André Herbelin, Michel Dy, Emilie Philadelphe, Elke Schneider, Michel Samson, Séverine Diem, Jordan Denizeau, Ren Zhu, Aude Aumeunier, Pierre Gourdy, Cytokines, hématopoïèse et réponse immune (CHRI), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Service d'anatomo-pathologie [CHU HEGP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Détoxication et réparation tissulaire, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES), Hormones, facteurs de croissance et physiopathologie vasculaire, IFR 31 Louis Bugnard (IFR 31), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Toulouse [Toulouse]-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Toulouse [Toulouse]-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Cytokines, hématopoïèse et réponse immune ( CHRI ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Européen Georges Pompidou [APHP] ( HEGP ), Université de Rennes 1 ( UR1 ), Université de Rennes ( UNIV-RENNES ) -Université de Rennes ( UNIV-RENNES ) -IFR140-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Université Toulouse III - Paul Sabatier ( UPS ), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR 31 Louis Bugnard ( IFR 31 ), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ) -CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Samson, Michel, Université de Toulouse (UT)-Université de Toulouse (UT)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), and Université de Toulouse (UT)-Université de Toulouse (UT)-Centre Hospitalier Universitaire de Toulouse (CHU Toulouse)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)
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MESH: Interleukin-12 ,MESH: Mice, Mutant Strains ,MESH : Cytokines ,MESH: T-Lymphocyte Subsets ,Hepatitis, Animal ,Mice ,0302 clinical medicine ,T-Lymphocyte Subsets ,Concanavalin A ,MESH : Th1 Cells ,Immunology and Allergy ,[ SDV.IMM ] Life Sciences [q-bio]/Immunology ,MESH: Animals ,MESH: Interleukin-12 Receptor beta 1 Subunit ,MESH : Concanavalin A ,NOD mice ,0303 health sciences ,education.field_of_study ,MESH: Cytokines ,MESH: Hepatitis, Animal ,Natural killer T cell ,Interleukin-12 ,3. Good health ,Killer Cells, Natural ,medicine.anatomical_structure ,MESH : Interleukin-12 Receptor beta 1 Subunit ,Interleukin 12 ,Cytokines ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,MESH : Killer Cells, Natural ,MESH: Killer Cells, Natural ,[SDV.IMM] Life Sciences [q-bio]/Immunology ,T cell ,Immunology ,Population ,MESH: Concanavalin A ,Biology ,MESH : Interleukin-4 ,03 medical and health sciences ,Immune system ,MESH : Mice ,Interleukin-12 Receptor beta 1 Subunit ,medicine ,MESH : Interleukin-12 ,Animals ,Secretion ,education ,MESH: Mice ,Interleukin 4 ,030304 developmental biology ,Th1 Cells ,MESH: Interleukin-4 ,MESH : Disease Models, Animal ,Mice, Mutant Strains ,MESH : T-Lymphocyte Subsets ,MESH : Mice, Mutant Strains ,Disease Models, Animal ,MESH: Th1 Cells ,Interleukin-4 ,MESH : Animals ,MESH: Disease Models, Animal ,MESH : Hepatitis, Animal ,030215 immunology - Abstract
IL-12 is essential for invariant NKT (iNKT) cells because it can maintain a functionally active population and promote a cytokine profile that is assumed to be mainly of the pro-Th1 type. We used the murine concanavalin A (Con A)-induced hepatitis model, in which iNKT cells, IL-12, IL-4, and IFN-γ are equally requisite, to reevaluate this issue. We demonstrate that IL-12 interacts directly with iNKT cells, contributes to their recruitment to the liver, and enhances their IL-4 production, which is essential for disease onset. IL-12-deficient mice were less susceptible to experimental hepatitis and their iNKT cells produced less IL-4 than their wild-type counterpart. A normal response could be restored by IL-12 injection, revealing its importance as endogenous mediator. In accordance with this observation, we found that iNKT cells expressed the IL-12R constitutively, in contrast to conventional T cells. Furthermore, the physiological relevance of our data is supported by the lower susceptibility to disease induction of NOD mice, known for their inherent functional and numerical abnormalities of iNKT cells associated with decreased iNKT cell-derived IL-4 production and low IL-12 secretion. Taken together, our findings provide the first evidence that IL-12 can enhance the immune response through increased IL-4 production by iNKT cells, underscoring once more the functional plasticity of this subset.
- Published
- 2007
15. Identification of an IL-17-producing NK1.1(neg) iNKT cell population involved in airway neutrophilia
- Author
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Michel Dy, Chi-Huey Wong, Maria Leite-de-Moraes, Marie-Laure Michel, François Trottein, Elke Schneider, Alexandre C. Keller, Christophe Paget, Paul B. Savage, Masakazu Fujio, Cytokines, hématopoïèse et réponse immune (CHRI), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Schistosomiase, paludisme et inflammation, Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé, Institut Fédératif de Recherche 142, Institut Fédératif de Recherche, Scripps Research Institute, Department of chemistry and Biochemistry (DCB), Brigham Young University (BYU), The Scripps Research Institute [La Jolla, San Diego], and ProdInra, Migration
- Subjects
medicine.medical_treatment ,[SDV]Life Sciences [q-bio] ,Immunology ,Population ,Galactosylceramides ,Biology ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Antigen ,Interferon ,medicine ,Immunology and Allergy ,Animals ,Antigens, Ly ,Lectins, C-Type ,education ,Lung ,Cells, Cultured ,030304 developmental biology ,0303 health sciences ,education.field_of_study ,Innate immune system ,Interleukin-17 ,Brief Definitive Report ,Interleukin ,Antibodies, Monoclonal ,Flow Cytometry ,Neutrophilia ,Lymphocyte Subsets ,[SDV] Life Sciences [q-bio] ,Killer Cells, Natural ,Mice, Inbred C57BL ,Cytokine ,Neutrophil Infiltration ,Antigens, Surface ,Brief Definitive Reports ,Interleukin 17 ,medicine.symptom ,Glycolipids ,Bronchoalveolar Lavage Fluid ,030215 immunology ,medicine.drug ,NK Cell Lectin-Like Receptor Subfamily B - Abstract
International audience; Invariant natural killer T (iNKT) cells are an important source of both T helper type 1 (Th1) and Th2 cytokines, through which they can exert beneficial, as well as deleterious, effects in a variety of inflammatory diseases. This functional heterogeneity raises the question of how far phenotypically distinct subpopulations are responsible for such contrasting activities. In this study, we identify a particular set of iNKT cells that lack the NK1.1 marker (NK1.1(neg)) and secrete high amounts of interleukin (IL)-17 and low levels of interferon (IFN)-gamma and IL-4. NK1.1(neg) iNKT cells produce IL-17 upon synthetic (alpha-galactosylceramide [alpha-GalCer] or PBS-57), as well as natural (lipopolysaccharides or glycolipids derived from Sphingomonas wittichii and Borrelia burgdorferi), ligand stimulation. NK1.1(neg) iNKT cells are more frequent in the lung, which is consistent with a role in the natural immunity to inhaled antigens. Indeed, airway neutrophilia induced by alpha-GalCer or lipopolysaccharide instillation was significantly reduced in iNKT-cell-deficient Jalpha18(-/-) mice, which produced significantly less IL-17 in their bronchoalveolar lavage fluid than wild-type controls. Furthermore, airway neutrophilia was abolished by a single treatment with neutralizing monoclonal antibody against IL-17 before alpha-GalCer administration. Collectively, our findings reveal that NK1.1(neg) iNKT lymphocytes represent a new population of IL-17-producing cells that can contribute to neutrophil recruitment through preferential IL-17 secretion.
- Published
- 2007
- Full Text
- View/download PDF
16. Fas receptor signaling is requisite for B cell differentiation
- Author
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Florence Vasseur, Flora Zavala, Valérie Pasqualetto, Sophie Ezine, Elke Schneider, Université Paris Descartes - Paris 5 (UPD5), Differenciation Thymique et Physiologie des Lymphocytes T (U591), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Diabète de Type 1 : mécanismes et traitements immunologiques, Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), and Cytokines, hématopoïèse et réponse immune (CHRI)
- Subjects
Fas Ligand Protein ,Genotype ,Immunology ,Spleen ,CD8-Positive T-Lymphocytes ,Biology ,Fas ligand ,Mice ,03 medical and health sciences ,Chimera (genetics) ,0302 clinical medicine ,medicine ,Animals ,Immunology and Allergy ,Cell Lineage ,fas Receptor ,B cell ,Cell Proliferation ,030304 developmental biology ,B-Lymphocytes ,0303 health sciences ,Membrane Glycoproteins ,Tumor Necrosis Factor-alpha ,Cell Differentiation ,Cell Biology ,Marginal zone ,Fas receptor ,Cell biology ,Mice, Inbred C57BL ,Haematopoiesis ,medicine.anatomical_structure ,Radiation Chimera ,Tumor Necrosis Factors ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,Bone marrow ,Signal Transduction ,030215 immunology - Abstract
The Fas/Fas ligand (FasL) pathway has been largely implicated in the homeostasis of mature cells. However, it is still unclear whether it plays a role at the progenitor level. To address this issue, we created chimeric mice by transferring C57BL/6 bone marrow (BM) cells of the lpr (Fas−FasL+) or gld (Fas+FasL−) genotype into Rag-2−/− hosts of the same genetic background. In this model, the consequences of a deficient Fas/FasL pathway on lymphoid differentiation could be evaluated without endogenous competition. Analysis of the chimerism revealed a differential sensitivity of hematopoietic lineages to the lack of Fas receptor signaling. While donor-derived myelo-monocytic cells were similarly distributed in all chimeric mice, mature B cells were deleted in the BM and the spleen of lpr chimera, leading to the absence of the marginal zone (MZ) as detected by immunohistology. In contrast, B cell hematopoiesis was complete in gld chimera but MZ macrophages undetectable. These defects suggest a direct and determinant dual role of FasL regulation in negative selection of B cells and in maintenance of the MZ.
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- 2005
- Full Text
- View/download PDF
17. Trends in histamine research: new functions during immune responses and hematopoiesis
- Author
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Malvyne Rolli-Derkinderen, Michel Arock, Elke Schneider, Michel Dy, Universität Klangenfurt, Alpen-Adria-Universität Klagenfurt [Klagenfurt, Austria], Laboratoire d'Informatique et d'Intelligence Artificielle, Institut National des Sciences Appliquées - Strasbourg ( INSA Strasbourg ), Institut National des Sciences Appliquées ( INSA ) -Institut National des Sciences Appliquées ( INSA ) -Université Louis Pasteur - Strasbourg I, Institute for Process control and Robotics, Universität Karlsruhe (TH), Cytokines, hématopoïèse et réponse immune ( CHRI ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Physiopathologie et pharmacologie cellulaires et moléculaires, Université de Nantes ( UN ) -IFR26-Institut National de la Santé et de la Recherche Médicale ( INSERM ), Laboratoire de Biologie et de Pharmacologie Appliquée ( LBPA ), École normale supérieure - Cachan ( ENS Cachan ) -Centre National de la Recherche Scientifique ( CNRS ), Institut National des Sciences Appliquées - Strasbourg (INSA Strasbourg), Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Université Louis Pasteur - Strasbourg I, Cytokines, hématopoïèse et réponse immune (CHRI), 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 de Nantes (UN)-IFR26-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire de Biologie et de Pharmacologie Appliquée (LBPA), and École normale supérieure - Cachan (ENS Cachan)-Centre National de la Recherche Scientifique (CNRS)
- Subjects
MESH: Hematopoiesis ,MESH: Receptors, G-Protein-Coupled ,MESH: Basophils ,Receptors, G-Protein-Coupled ,chemistry.chemical_compound ,Histamine receptor ,0302 clinical medicine ,Immunology and Allergy ,[ SDV.IMM ] Life Sciences [q-bio]/Immunology ,MESH: Animals ,Mast Cells ,Receptor ,0303 health sciences ,MESH: Mast Cells ,MESH : Research ,Mast cell ,3. Good health ,Basophils ,MESH : Histamine ,Haematopoiesis ,medicine.anatomical_structure ,MESH: Research ,030220 oncology & carcinogenesis ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,Receptors, Histamine ,MESH : Receptors, G-Protein-Coupled ,MESH : Basophils ,MESH : Mast Cells ,MESH: Histamine ,Histamine ,Immunology ,Histamine H1 receptor ,Biology ,Basophil degranulation ,MESH : Receptors, Histamine ,03 medical and health sciences ,Immune system ,medicine ,Animals ,Humans ,030304 developmental biology ,Receptors, Histamine H4 ,MESH: Humans ,Research ,MESH : Humans ,Hematopoiesis ,MESH : Hematopoiesis ,MESH: Receptors, Histamine ,chemistry ,MESH : Animals - Abstract
Histamine is a bioamine with multiple physiological activities. In the immune system, it not only mediates the deleterious effects accompanying allergic reactions, but it acts also in a more subtle way by modulating the T helper 1 (Th1)–Th2 balance and possibly hematopoiesis. The histamine required for Th-cell polarization is provided by mast cell or basophil degranulation, as well as being newly synthesized and immediately released by other hematopoietic cells, in response to molecules generated during the immune response. Its global effect depends on the subtype and distribution of histamine receptors on target cells. The recent discovery of a novel H 4 receptor, which is expressed preferentially on immunocompetent cells, will have important consequences for the understanding of the regulatory functions of histamine during the immune response.
- Published
- 2002
18. Dyslexia and Foreign Language Learning
- Author
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Elke Schneider, Margaret Crombie, Elke Schneider, and Margaret Crombie
- Subjects
- LB1050.5
- Abstract
Offering strategies and techniques for teaching modern foreign languages - an often severely challenging subject for pupils with dyslexia - this book is specifically designed to meet the needs of the busy subject specialist teacher looking for guidance on supporting pupils.
- Published
- 2003
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