0000000000462531

AUTHOR

Edward E. S. Nieuwenhuis

showing 4 related works from this author

Specific Regulation of T Helper Cell 1–mediated Murine Colitis by CEACAM1

2004

Carcinoembryonic antigen-related cellular adhesion molecule 1 (CEACAM1) is a cell surface molecule that has been proposed to negatively regulate T cell function. We have shown that CEACAM1 is associated with specific regulation of T helper cell (Th)1 pathways, T-bet–mediated Th1 cytokine signaling, and Th1-mediated immunopathology in vivo. Mice treated with anti–mouse CEACAM1-specific monoclonal antibody (mAb) CC1 during the effector phase exhibited a reduced severity of trinitrobenzene sulfonic acid colitis in association with decreased interferon (IFN)-γ production. Although oxazolone colitis has been reported as Th2 mediated, mice treated with the CC1 mAb or a CEACAM1-Fc chimeric protein…

Recombinant Fusion Proteinsmedicine.medical_treatmentT cellImmunologyBiologyArticleOxazoloneInterferon-gammaMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAntigeninflammatory bowel diseaseInterferonmedicineAnimalsImmunology and AllergyColitisCell adhesionCEACAM1030304 developmental biologyInflammationMice KnockoutMice Inbred BALB C0303 health sciencesT cell immunityOxazoloneAntibodies MonoclonalT-Lymphocytes Helper-InducerT helper cellTh1 CellsColitismedicine.diseaseMolecular biologyCarcinoembryonic AntigenImmunoglobulin Fc Fragments3. Good healthMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureCytokinechemistry030220 oncology & carcinogenesisFemaleTh1 cytokineInterleukin-1hapten-induced colitismedicine.drugJournal of Experimental Medicine
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The Transcription Factor T-bet Regulates Mucosal T Cell Activation in Experimental Colitis and Crohn's Disease

2002

The balance between pro and antiinflammatory cytokines secreted by T cells regulates both the initiation and perpetuation of inflammatory bowel diseases (IBD). In particular, the balance between interferon (IFN)-gamma/interleukin (IL)-4 and transforming growth factor (TGF)-beta activity controls chronic intestinal inflammation. However, the molecular pathways that evoke these responses are not well understood. Here, we describe a critical role for the transcription factor T-bet in controlling the mucosal cytokine balance and clinical disease. We studied the expression and function of T-bet in patients with IBD and in mucosal T cells in various T helper (Th)1- and Th2-mediated animal models …

CD4-Positive T-LymphocytesMalecolitisGenes RAG-1T-Lymphocytesmedicine.medical_treatmentMice SCIDGATA-3Polymerase Chain ReactionMiceInterleukin 210302 clinical medicineCrohn DiseaseT-Lymphocyte SubsetsImmunology and AllergyCytotoxic T cellIL-2 receptorIFN-γMice Inbred BALB C0303 health sciencesGene Transfer Techniqueshemic and immune systemsT-Lymphocytes Helper-InducerMiddle Aged3. Good healthCytokinemedicine.anatomical_structureFemaleAdultT cellImmunologychemical and pharmacologic phenomenaBiologyT-betArticleTCIRG103 medical and health sciencesmedicineAnimalsHumansColitisImmunity MucosalInterleukin 4DNA Primers030304 developmental biologyHomeodomain ProteinsBase Sequencemedicine.diseasecytokinesDisease Models AnimalGene Expression RegulationImmunologyT-Box Domain ProteinsSpleenTranscription Factors030215 immunologyJournal of Experimental Medicine
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EBV-Induced Gene 3 Transcription Is Induced by TLR Signaling in Primary Dendritic Cells via NF-κB Activation

2005

Abstract The EBV-induced gene 3 (EBI3) is expressed in dendritic cells (DCs) and part of the cytokine IL-27 that controls Th cell development. However, its regulated expression in DCs is poorly understood. In the present study we demonstrate that EBI3 is expressed in splenic CD8−, CD8+, and plasmacytoid DC subsets and is induced upon TLR signaling. Cloning and functional analysis of the EBI3 promoter using in vivo footprinting and mutagenesis showed that stimulation via TLR2, TLR4, and TLR9 transactivated the promoter in primary DCs via NF-κB and Ets binding sites at −90 and −73 bp upstream of the transcriptional start site, respectively. Furthermore, we observed that NF-κB p50/p65 and PU.1…

RNA Capsmedicine.medical_treatmentDNA Mutational AnalysisMolecular Sequence DataImmunologyAntigen-Presenting CellsReceptors Cell SurfaceBiologyCell LineMinor Histocompatibility AntigensJurkat CellsMiceCell Line TumorGene expressionmedicineAnimalsHumansImmunology and AllergyReceptors CytokinePromoter Regions GeneticGlycoproteinsMice KnockoutMembrane GlycoproteinsInnate immune systemBase SequenceToll-Like ReceptorsHEK 293 cellsNF-kappa BTLR9hemic and immune systemsEBI3Dendritic CellsMolecular biologyToll-Like Receptor 2Up-RegulationMice Inbred C57BLToll-Like Receptor 4Protein SubunitsTLR2CytokineGene Expression RegulationToll-Like Receptor 9NIH 3T3 CellsTLR4Protein BindingSignal TransductionThe Journal of Immunology
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Disruption of T helper 2-immune responses in Epstein–Barr virus-induced gene 3-deficient mice

2002

Epstein–Barr virus-induced gene 3 (EBI3) is a widely expressed IL-12p40-related protein that associates as a heterodimer with either IL-12p35 or an IL-12p35 homologue, p28, to create a new cytokine (IL-27). To define the function of EBI3in vivo, we generated knockout mice in which theebi3gene was targeted by homologous recombination. EBI3−/−mice exhibited normal numbers of both naive and mature CD4+and CD8+T cells and B cells, but markedly decreased numbers of invariant natural killer T cells (iNKT) as defined by staining with an α-galactosylceramide (αGalCer)-loaded CD1d-tetramer. iNKT cells from EBI3−/−mice exhibited decreased IL-4 and, to a lesser extent, IFN-γ production after αGalCer s…

T-Lymphocytesmedicine.medical_treatmentStimulationBiologyMinor Histocompatibility AntigensInterferon-gammaMiceTh2 CellsImmune systemmedicineAnimalsInterferon gammaReceptors CytokineInterleukin 4GlycoproteinsMultidisciplinaryInterleukinsEBI3Biological SciencesNatural killer T cellMolecular biologyMice Inbred C57BLCytokineImmunologyInterleukin-4CD8medicine.drugProceedings of the National Academy of Sciences
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