Search results for "Knockout"

showing 10 items of 806 documents

B?cells are not required for T?cell priming in low zone tolerance to contact allergens and contact hypersensitivity

2004

Low zone tolerance (LZT) to contact allergens is induced by epicutaneous exposure to haptens in subsensitizing doses resulting in an inhibition of contact hypersensitivity (CHS), which, in contrast, occurs after sensitization with immunogenic doses of allergens. Performing the protocol of tolerance induction resulted in robust LZT to allergens in B cell-deficient mice in vivo, indicating that B cells are not required for the induction and effector phase of LZT. However, CHS reactions in vivo were restricted in B cell-deficient mice as compared to wild-type (WT) mice. In contrast, analysis of hapten-specific T cell activation in vitro revealed a strong proliferative response of T cells deriv…

Adoptive cell transfermedicine.medical_treatmentT cellImmunologyPriming (immunology)Picryl ChlorideCD8-Positive T-LymphocytesBiologyDermatitis ContactLymphocyte ActivationInterferon-gammaMiceAdjuvants ImmunologicImmune TolerancemedicineAnimalsImmunology and AllergySensitizationB cellCell ProliferationMice KnockoutB-Lymphocytesintegumentary systemInterleukinsOxazoloneAllergensAdoptive TransferMice Inbred C57BLTolerance inductionCytokinemedicine.anatomical_structureImmunologyLymph NodesCD8European Journal of Immunology
researchProduct

The transcription factor IFN regulatory factor–4 controls experimental colitis in mice via T cell–derived IL-6

2008

The proinflammatory cytokine IL-6 seems to have an important role in the intestinal inflammation that characterizes inflammatory bowel diseases (IBDs) such as Crohn disease and ulcerative colitis. However, little is known about the molecular mechanisms regulating IL-6 production in IBD. Here, we assessed the role of the transcriptional regulator IFN regulatory factor-4 (IRF4) in this process. Patients with either Crohn disease or ulcerative colitis exhibited increased IRF4 expression in lamina propria CD3+ T cells as compared with control patients. Consistent with IRF4 having a regulatory function in T cells, in a mouse model of IBD whereby colitis is induced in RAG-deficient mice by transp…

AdultCD4-Positive T-LymphocytesMaleAdoptive cell transferRecombinant Fusion ProteinsT-LymphocytesCD3T cellAdoptive Transfer; Adult; Animals; Apoptosis; CD4-Positive T-Lymphocytes; Colitis; Cytokines; DNA-Binding Proteins; Female; Gene Expression Regulation; Humans; Inflammatory Bowel Diseases; Interferon Regulatory Factors; Interleukin-6; Intestinal Mucosa; Male; Mice; Mice Inbred C57BL; Mice Knockout; Middle Aged; Oxazolone; Receptors Interleukin-6; Recombinant Fusion Proteins; T-Lymphocytes; Trinitrobenzenesulfonic AcidApoptosisProinflammatory cytokineMiceIntestinal mucosamedicineAnimalsHumansIntestinal MucosaColitisInterleukin 6Mice KnockoutbiologyInterleukin-6OxazoloneGeneral MedicineMiddle AgedColitisInflammatory Bowel Diseasesmedicine.diseaseAdoptive TransferReceptors Interleukin-6Ulcerative colitisDNA-Binding ProteinsMice Inbred C57BLmedicine.anatomical_structureGene Expression RegulationTrinitrobenzenesulfonic AcidInterferon Regulatory FactorsImmunologybiology.proteinCytokinesFemaleResearch ArticleJournal of Clinical Investigation
researchProduct

Posttranslationally modified proteins as mediators of sustained intestinal inflammation.

2006

Oxidative and carbonyl stress leads to generation of N(epsilon)-carboxymethyllysine-modified proteins (CML-mps), which are known to bind the receptor for advanced glycation end products (RAGE) and induce nuclear factor (NF)-kappaB-dependent proinflammatory gene expression. To determine the impact of CML-mps in vivo, RAGE-dependent sustained NF-kappaB activation was studied in resection gut specimens from patients with inflammatory bowel disease. Inflamed gut biopsy tissue demonstrated a significant up-regulation of RAGE and increased NF-kappaB activation. Protein extracts from the inflamed zones, but not from noninflamed resection borders, caused perpetuated NF-kappaB activation in cultured…

AdultCell ExtractsMaleReceptor for Advanced Glycation End ProductsInflammationBiologyInflammatory bowel diseasep38 Mitogen-Activated Protein KinasesPathology and Forensic MedicineProinflammatory cytokineRAGE (receptor)MiceGlycationhemic and lymphatic diseasesGene expressionmedicineAnimalsCalgranulin BHumansCalgranulin AIntestinal MucosaReceptors ImmunologicReceptorProtein Kinase InhibitorsMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3LysineNF-kappa Bnutritional and metabolic diseasesEndothelial Cellsmedicine.diseaseNFKB1Inflammatory Bowel DiseasesIntestinesDisease Models AnimalImmunologyCancer researchFemalemedicine.symptomProtein Processing Post-TranslationalRegular ArticlesThe American journal of pathology
researchProduct

Stro-1/CD44 as putative human myometrial and fibroid stem cell markers

2015

Objective To identify and characterize myometrial/fibroid stem cells by specific stem cell markers in human myometrium, and to better understand the stem cell contribution in the development of uterine fibroids. Design Prospective, experimental human and animal study. Setting University research laboratory. Patient(s)/Animal(s) Women undergoing hysterectomy for treatment of symptomatic uterine fibroids and female NOD/SCID/IL-2Rγ null mice. Intervention(s) Identification and isolation of stem cells from human fibroids and adjacent myometrium tissues using Stro-1/CD44–specific surface markers. Main Outcome Measure(s) Flow cytometry, semiquantitative polymerase chain reaction, clonogenicity as…

AdultHomeobox protein NANOGPathologymedicine.medical_specialtyMice SCIDBiologyStem cell markerArticleMiceMice Inbred NODCancer stem cellmedicineAnimalsHumansCD90Prospective StudiesProgenitor cellMice KnockoutLeiomyomaStem CellsMesenchymal stem cellObstetrics and GynecologyHematopoietic stem cellMiddle Agedfemale genital diseases and pregnancy complicationsHyaluronan Receptorsmedicine.anatomical_structureReproductive MedicineAntigens SurfaceUterine NeoplasmsMyometriumFemaleStem cellBiomarkersFertility and Sterility
researchProduct

Elevated levels of Bcl-3 inhibits Treg development and function resulting in spontaneous colitis

2017

Bcl-3 is an atypical NF-κB family member that regulates NF-κB-dependent gene expression in effector T cells, but a cell-intrinsic function in regulatory T (Treg) cells and colitis is not clear. Here we show that Bcl-3 expression levels in colonic T cells correlate with disease manifestation in patients with inflammatory bowel disease. Mice with T-cell-specific overexpression of Bcl-3 develop severe colitis that can be attributed to defective Treg cell development and function, leading to the infiltration of immune cells such as pro-inflammatory γδT cells, but not αβ T cells. In Treg cells, Bcl-3 associates directly with NF-κB p50 to inhibit DNA binding of p50/p50 and p50/p65 NF-κB dimers, t…

AdultMale0301 basic medicineP50ScienceGeneral Physics and AstronomyBiologyT-Lymphocytes RegulatoryInflammatory bowel diseaseArticleGeneral Biochemistry Genetics and Molecular BiologyYoung Adult03 medical and health sciences0302 clinical medicineImmune systemB-Cell Lymphoma 3 ProteinProto-Oncogene ProteinsGene expressionmedicineAnimalsHumansColitisMice KnockoutRegulation of gene expressionMultidisciplinaryEffectorHEK 293 cellsQNF-kappa BTranscription Factor RelANF-kappa B p50 SubunitGeneral ChemistryMiddle AgedColitismedicine.diseaseMice Inbred C57BLHEK293 Cells030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisImmunologyFemaleProtein BindingTranscription FactorsNature Communications
researchProduct

A constitutive BCL2 down-regulation aggravates the phenotype of PKD1-mutant-induced polycystic kidney disease

2017

IF 5.340; International audience; The main identified function of BCL2 protein is to prevent cell death by apoptosis. Mice knock-out for Bcl2 demonstrate growth retardation, severe polycystic kidney disease (PKD), gray hair and lymphopenia, and die prematurely after birth. Here, we report a 40-year-old male referred to for abdominal and thoracic aortic dissection with associated aortic root aneurysm, PKD, lymphocytopenia with a history of T cell lymphoblastic lymphoma, white hair since the age of 20, and learning difficulties. PKD, which was also detected in the father and sister, was related to an inherited PKD1 mutation. The combination of PKD with gray hair and lymphocytopenia was also r…

AdultMale0301 basic medicineTRPP Cation Channelsphenotypebcl2 geneBiologymicro rnaMice03 medical and health sciencesdown-regulationsymptom aggravating factorshemic and lymphatic diseasest-lymphocyteGene expressionGeneticsmedicinePolycystic kidney diseaseAnimalsHumansGenetic Predisposition to Disease[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsgenesMolecular BiologyGeneGenetics (clinical)Exome sequencingMice KnockoutPKD1apoptosisExonsGeneral MedicinePolycystic Kidney Autosomal Dominantmedicine.diseasePhenotypePedigreeUp-Regulation3. Good healthMicroRNAs030104 developmental biologyMRNA SequencingProto-Oncogene Proteins c-bcl-2[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsImmunologyCancer researchLymphocytopeniapolycystic kidney diseasesbcl-2 proteinHuman Molecular Genetics
researchProduct

Stromal SPARC contributes to the detrimental fibrotic changes associated with myeloproliferation whereas its deficiency favors myeloid cell expansion.

2012

Abstract In myeloid malignancies, the neoplastic clone outgrows normal hematopoietic cells toward BM failure. This event is also sustained by detrimental stromal changes, such as BM fibrosis and osteosclerosis, whose occurrence is harbinger of a dismal prognosis. We show that the matricellular protein SPARC contributes to the BM stromal response to myeloproliferation. The degree of SPARC expression in BM stromal elements, including CD146+ mesenchymal stromal cells, correlates with the degree of stromal changes, and the severity of BM failure characterizing the prototypical myeloproliferative neoplasm primary myelofibrosis. Using Sparc−/− mice and BM chimeras, we demonstrate that SPARC contr…

AdultMalePathologymedicine.medical_specialtyMyeloidStromal cellImmunologyAdenomatous Polyposis Coli ProteinGene ExpressionCD146 AntigenBiologyBiochemistryMiceBone MarrowMyeloproliferationmedicineAnimalsHumansMyeloid CellsOsteonectinMyelofibrosisMyeloproliferative neoplasmCells CulturedAgedCell ProliferationAged 80 and overMice KnockoutMesenchymal stem cellMesenchymal Stem CellsPMF SPARC MYELOFIBROSISCell BiologyHematologyMiddle Agedmedicine.diseaseTransplantationHaematopoiesismedicine.anatomical_structureThrombopoietinLeukemia MyeloidPrimary MyelofibrosisFemaleSPARC stroma
researchProduct

Identification of a gene-pathway associated with non-alcoholic steatohepatitis.

2007

Background/Aims We have integrated gene expression profiling of liver biopsies of NASH patients with liver samples of a mouse model of steatohepatitis (MAT1A-KO) to identify a gene-pathway associated with NASH. Methods Affymetrix U133 Plus 2.0 microarrays were used to evaluate nine patients with NASH, six patients with steatosis, and six control subjects; Affymetrix MOE430A microarrays were used to evaluate wild-type and MAT1A-KO mice at 15 days, 1, 3, 5 and 8 months after birth. Transcriptional profiles of patients with NASH and MAT1A-KO mice were compared with those of their proficient controls. Results We identified a gene-pathway associated with NASH, that accurately distinguishes betwe…

AdultMalePathologymedicine.medical_specialtySp1 Transcription FactorGene ExpressionHyperphosphorylationBiologyBioinformaticsdigestive systemSp1MiceGene-pathwayGene expressionmedicineAnimalsHumansPhosphorylationPromoter Regions GeneticGeneNon-alcoholic steatohepatitisMice KnockoutS-adenosylmethionineHepatologyMicroarray analysis techniquesGene Expression Profilingnutritional and metabolic diseasesMethionine AdenosyltransferaseMiddle AgedMicroarray Analysismedicine.diseasedigestive system diseasesFatty LiverGene expression profilingLiverFemaleSteatosisSteatohepatitisDNA microarray
researchProduct

Genetic risk prediction and neurobiological understanding of alcoholism.

2014

We have used a translational Convergent Functional Genomics (CFG) approach to discover genes involved in alcoholism, by gene-level integration of genome-wide association study (GWAS) data from a German alcohol dependence cohort with other genetic and gene expression data, from human and animal model studies, similar to our previous work in bipolar disorder and schizophrenia. A panel of all the nominally significant P-value SNPs in the top candidate genes discovered by CFG  (n=135 genes, 713 SNPs) was used to generate a genetic  risk prediction score (GRPS), which showed a trend towards significance (P=0.053) in separating  alcohol dependent individuals from controls in an independent German…

AdultMaleRiskCandidate geneAlcohol abuseContext (language use)Single-nucleotide polymorphismGenome-wide association studyBioinformaticsPolymorphism Single NucleotideMice03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineGermanyAnimalsHumansMedicineGenetic Predisposition to DiseaseBiological Psychiatry030304 developmental biologyMice KnockoutGenetics0303 health sciencesbusiness.industryAlcohol dependenceGenomics16. Peace & justicemedicine.diseaseUnited States3. Good healthAlcoholismDisease Models AnimalPsychiatry and Mental healthBehavioral medicineCohortOriginal ArticleFemaleCorrigendumbusiness030217 neurology & neurosurgeryGenome-Wide Association Study
researchProduct

Transglutaminase Type II Plays a Protective Role in Hepatic Injury

2003

The up-regulation of "tissue" transglutaminase (TG2) gene has been shown to occur in various pathologies and can lead to severe liver injury; however, its role in the onset of liver damage has not yet been clarified. To address this issue, we have used two experimental settings: carbon tetrachloride (CCl(4))-induced liver injury in wild-type and TG2 knockout mice; and liver biopsies obtained from a large cohort of hepatitis C virus (HCV)-infected patients. Mice lacking TG2 failed to clear the hepatic necrotic tissue formed in response to prolonged CCl(4) exposure (5 weeks) and 60% of them died before the end of the treatment. By contrast, wild-type mice were able to recover after the toxic …

AdultPathologymedicine.medical_specialtyNecrosisGenotypeTissue transglutaminaseHepatitis C virusCCL4medicine.disease_causeGene Expression Regulation EnzymologicPathology and Forensic MedicineExtracellular matrixMiceNecrosisGTP-Binding ProteinsmedicineAnimalsHumansProtein Glutamine gamma Glutamyltransferase 2Mice KnockoutHepatitisLiver injuryTransglutaminasesbiologyCarbon Tetrachloride PoisoningHepatitis C ChronicMiddle Agedmedicine.diseaseMice Inbred C57BLLiverKnockout mousebiology.proteinmedicine.symptomRegular ArticlesThe American Journal of Pathology
researchProduct