Search results for "Knockout"

showing 10 items of 806 documents

Thymus-derived regulatory T cells are positively selected on natural self-antigen through cognate interactions of high functional avidity

2016

Regulatory T (Treg) cells expressing Foxp3 transcripton factor are essential for immune homeostasis. They arise in the thymus as a separate lineage from conventional CD4+Foxp3- T (Tconv) cells. Here, we show that the thymic development of Treg cells depends on the expression of their endogenous cognate self-antigen. The formation of these cells was impaired in mice lacking this self-antigen, while Tconv cell development was not negatively affected. Thymus-derived Treg cells were selected by self-antigens in a specific manner, while autoreactive Tconv cells were produced through degenerate recognition of distinct antigens. These distinct modes of development were associated with the expressi…

0301 basic medicineCell typeCancer ResearchEncephalomyelitis Autoimmune ExperimentalMultiple Sclerosis[SDV]Life Sciences [q-bio]ImmunologyReceptors Antigen T-CellEndogenyT-Cell Antigen Receptor Specificitychemical and pharmacologic phenomenaThymus GlandBiologymedicine.disease_causeAutoantigensT-Lymphocytes RegulatoryAutoimmunity03 medical and health sciencesMice0302 clinical medicineAntigenT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsHumansAvidityCTLA-4 AntigenReceptorClonal Selection Antigen-MediatedCells CulturedMice KnockoutCell growthFOXP3Forkhead Transcription Factorshemic and immune systemsPeptide Fragments[SDV] Life Sciences [q-bio]Mice Inbred C57BL030104 developmental biologyInfectious DiseasesImmunologyMyelin-Oligodendrocyte Glycoprotein030215 immunology
researchProduct

Cell-Type-Specific Responses to Interleukin-1 Control Microbial Invasion and Tumor-Elicited Inflammation in Colorectal Cancer.

2017

Summary Chronic inflammation drives the progression of colorectal cancer (CRC). Increased expression of interleukin (IL)-17A is associated with poor prognosis, and IL-17A blockade curbs tumor progression in preclinical models of CRC. Here we examined the impact of IL-1 signaling, a key regulator of the IL-17 pathway, in different cell types within the CRC microenvironment. Genetic deletion of the IL-1 receptor (IL-1R1) in epithelial cells alleviated tumorigenesis in the APC model of CRC, demonstrating a cell-autonomous role for IL-1 signaling in early tumor seed outgrowth. T cell specific ablation of IL-1R1 decreased tumor-elicited inflammation dependent on IL-17 and IL-22, thereby reducing…

0301 basic medicineCell typeColorectal cancerCarcinogenesisNeutrophilsmedicine.medical_treatmentImmunologyMedizinInflammationBiologymedicine.disease_causeArticle03 medical and health sciencesMice0302 clinical medicineSalmonellamedicineTumor MicroenvironmentImmunology and AllergyAnimalsHumansCells CulturedInflammationMice KnockoutTumor microenvironmentSalmonella Infections AnimalInterleukinsInterleukin-17InterleukinReceptors Interleukin-1medicine.disease030104 developmental biologyInfectious DiseasesCytokineTumor progressionOrgan Specificity030220 oncology & carcinogenesisCancer researchmedicine.symptomCarcinogenesisColorectal NeoplasmsInterleukin-1Signal TransductionImmunity
researchProduct

Tnfaip3 expression in pulmonary conventional type 1 Langerin‐expressing dendritic cells regulates T helper 2‐mediated airway inflammation in mice

2020

Abstract Background Conventional type 1 dendritic cells (cDC1s) control anti‐viral and anti‐tumor immunity by inducing antigen‐specific cytotoxic CD8+ T‐cell responses. Controversy exists whether cDC1s also control CD4+ T helper 2 (Th2) cell responses, since suppressive and activating roles have been reported. DC activation status, controlled by the transcription factor NF‐κB, might determine the precise outcome of Th‐cell differentiation upon encounter with cDC1s. To investigate the role of activated cDC1s in Th2‐driven immune responses, pulmonary cDC1s were activated by targeted deletion of A20/Tnfaip3, a negative regulator of NF‐κB signaling. Methods To target pulmonary cDC1s, Cd207 (Lan…

0301 basic medicineCellDUSTCD8-Positive T-LymphocytesINHALED ANTIGENTh2&#8208Mice0302 clinical medicineTnfaip3Medicine and Health SciencesCytotoxic T cellImmunology and AllergyInterferon gammaLungSensitizationMice KnockoutCONSTITUTIVE EXPRESSIONIFN-GAMMAbiologyCD8(+) T cellsType 1 conventional dendritic cellsIMMUNE-RESPONSES3. Good healthmedicine.anatomical_structureA20Original Articlemedicine.drugLangerinImmunologyCD8+ T cells03 medical and health sciencesImmune systemTh2 CellsImmunitymedicineAnimalsdriven airway inflammationCD103(+)InflammationBiology and Life SciencesTH2 RESPONSESA20/Tnfaip3Dendritic CellsTh2‐driven airway inflammationMice Inbred C57BL030104 developmental biologyinterferon gamma030228 respiratory systemImmunologybiology.proteinASTHMABasic and Translational Allergy ImmunologyORIGINAL ARTICLESCD8LUNGAllergy
researchProduct

The activation of Wnt signaling by a STAT6-dependent macrophage phenotype promotes mucosal repair in murine IBD

2016

The complete repair of the mucosa constitutes a key goal in inflammatory bowel disease (IBD) treatment. The Wnt signaling pathway mediates mucosal repair and M2 macrophages that coordinate efficient healing have been related to Wnt ligand expression. Signal transducer and activator of transcription 6 (STAT6) mediates M2 polarization in vitro and we hypothesize that a STAT6-dependent macrophage phenotype mediates mucosal repair in acute murine colitis by activating the Wnt signaling pathway. Our results reveal an impaired mucosal expression of M2 macrophage-associated genes and delayed wound healing in STAT6(-/-) mice treated with 2,4,6-trinitrobenzenesulfonic acid (TNBS). These mice also ex…

0301 basic medicineCellular differentiationImmunologyBiology03 medical and health sciencesMice0302 clinical medicineImmunology and AllergyAnimalsHumansIntestinal MucosaCells CulturedSTAT6Mice KnockoutMice Inbred BALB CWound HealingWnt signaling pathwayLGR5LRP5Cell DifferentiationColitisInflammatory Bowel DiseasesCell biologyWnt Proteins030104 developmental biologyPhenotypeTrinitrobenzenesulfonic AcidImmunologySTAT proteinMacrophages PeritonealSignal transductionWound healingSTAT6 Transcription Factor030215 immunologySignal Transduction
researchProduct

E-Cadherin is Dispensable to Maintain Langerhans Cells in the Epidermis.

2019

The cell adhesion molecule E-cadherin is a major component of adherens junctions and marks Langerhans cells (LC), the only dendritic cell (DC) population of the epidermis. LC form a dense network and attach themselves to the surrounding keratinocytes via homophilic E-cadherin binding. LC activation, mobilization, and migration require a reduction in LC E-cadherin expression. To determine whether E-cadherin plays a role in regulating LC homeostasis and function, we generated CD11c-specific E-cadherin knockout mice (CD11c-Ecaddel). In the absence of E-cadherin−mediated cell adhesion, LC numbers remained stable and similar as in control mice, even in aged animals. Intriguingly, E-cadherin−defi…

0301 basic medicineCellular differentiationPopulationDermatologyDermatitis ContactBiochemistryAdherens junction03 medical and health sciencesMice0302 clinical medicineCell MovementAnimalsHomeostasisHumansPsoriasisCell adhesioneducationMolecular BiologyCell ShapeCells CulturedMice Knockouteducation.field_of_studyImiquimodEpidermis (botany)CadherinCell adhesion moleculeChemistryCell DifferentiationCell BiologyDendritic cellCadherinsCell biologyCD11c AntigenDisease Models Animal030104 developmental biology030220 oncology & carcinogenesisLangerhans CellsEpidermisThe Journal of investigative dermatology
researchProduct

IL-17 controls central nervous system autoimmunity through the intestinal microbiome

2021

Interleukin-17A- (IL-17A) and IL-17F-producing CD4(+) T helper cells (T(H)17 cells) are implicated in the development of chronic inflammatory diseases, such as multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). T-H 17 cells also orchestrate leukocyte invasion of the central nervous system (CNS) and subsequent tissue damage. However, the role of IL-17A and IL-17F as effector cytokines is still confused with the encephalitogenic function of the cells that produce these cytokines, namely, T-H 17 cells, fueling a long-standing debate in the neuroimmunology field. Here, we demonstrated that mice deficient for IL-17A/F lose their susceptibility to EAE, which…

0301 basic medicineCentral Nervous SystemMaleEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisreceptorImmunologyCentral nervous system610 Medicine & healthGut flora10263 Institute of Experimental Immunologymedicine.disease_causeAutoimmunityinterleukin-1703 medical and health sciencesMice0302 clinical medicinemedicinecytokineAnimalsHumanscnst-cellsMice Knockout2403 Immunologybiologygut microbiotaMultiple sclerosisExperimental autoimmune encephalomyelitisGeneral MedicineFecal Microbiota Transplantationneutralizationmedicine.diseasebiology.organism_classificationAdoptive Transfer3. Good healthGut EpitheliumGastrointestinal Microbiome030104 developmental biologyNeuroimmunologymedicine.anatomical_structureImmunology2723 Immunology and Allergy570 Life sciences; biologyTh17 CellssequencesFemaleInterleukin 17030217 neurology & neurosurgery
researchProduct

Opposing Effects of CREBBP Mutations Govern the Phenotype of Rubinstein-Taybi Syndrome and Adult SHH Medulloblastoma

2018

Recurrent mutations in chromatin modifiers are specifically prevalent in adolescent or adult patients with Sonic hedgehog-associated medulloblastoma (SHH MB). Here, we report that mutations in the acetyltransferase CREBBP have opposing effects during the development of the cerebellum, the primary site of origin of SHH MB. Our data reveal that loss of Crebbp in cerebellar granule neuron progenitors (GNPs) during embryonic development of mice compromises GNP development, in part by downregulation of brain-derived neurotrophic factor (Bdnf). Interestingly, concomitant cerebellar hypoplasia was also observed in patients with Rubinstein-Taybi syndrome, a congenital disorder caused by germline mu…

0301 basic medicineCerebellumCrebbp protein mousemetabolism [Cerebellar Neoplasms]acetyltransferase; cerebellum; CREBBP; development; Rubinstein-Taybi syndrome; SHH medulloblastomagenetics [Hedgehog Proteins]MiceNeurotrophic factorsmetabolism [CREB-Binding Protein]Mice KnockoutNeuronsRubinstein-Taybi Syndromepathology [Rubinstein-Taybi Syndrome]CREBBPCREB-Binding ProteinPhenotypegenetics [CREB-Binding Protein]3. Good healthpathology [Cerebellar Neoplasms]acetyltransferasePhenotypemedicine.anatomical_structuregenetics [Rubinstein-Taybi Syndrome]Femalemetabolism [Hedgehog Proteins]Signal TransductionSHH medulloblastomaAdultcerebellumBiologyGeneral Biochemistry Genetics and Molecular BiologyCREBBP; Rubinstein-Taybi syndrome; SHH medulloblastoma; acetyltransferase; cerebellum; development.03 medical and health sciencesGermline mutationAcetyltransferasesmetabolism [Medulloblastoma]medicineAnimalsHumansgenetics [Cerebellar Neoplasms]Hedgehog Proteinsddc:610Cerebellar NeoplasmsdevelopmentMolecular BiologyMedulloblastomaRubinstein–Taybi syndromegenetics [Medulloblastoma]metabolism [Rubinstein-Taybi Syndrome]pathology [Medulloblastoma]Cell Biologymedicine.disease030104 developmental biologyMutationphysiology [CREB-Binding Protein]Cancer researchSHH protein humanCerebellar hypoplasia (non-human)metabolism [Acetyltransferases]CREBBP protein humanMedulloblastomaDevelopmental BiologyCongenital disorderDevelopmental Cell
researchProduct

Loss of organic cation transporter 3 (Oct3) leads to enhanced proliferation and hepatocarcinogenesis

2017

// Johanna Vollmar 1 , Anja Lautem 2 , Ellen Closs 3 , Detlef Schuppan 4 , Yong Ook Kim 4 , Daniel Grimm 1 , Jens U. Marquardt 1 , Peter Fuchs 1 , Beate K. Straub 5 , Arno Schad 5 , Dirk Grundemann 6 , Jorn M. Schattenberg 1 , Nadine Gehrke 1 , Marcus A. Worns 1 , Jan Baumgart 7 , Peter R. Galle 1 and Tim Zimmermann 1 1 Department of Internal Medicine, Gastroenterology and Hepatology, University Medical Center, Johannes Gutenberg-University Mainz, Mainz, Germany 2 Department of Hepatobiliary and Transplantation Surgery, University Medical Center, Johannes Gutenberg-University Mainz, Mainz, Germany 3 Department of Pharmacology, University Medical Center, Johannes Gutenberg-University Mainz, …

0301 basic medicineCyclin DSLC22A303 medical and health sciences0302 clinical medicinemedicineUniversity medicalSLC22A3OCT3 knockoutSLC22A1Organic cation transport proteinsbiologyTumor sizeKinasebusiness.industryhepatocarcinogenesisorganic cation transportermedicine.diseaseMolecular biologyhumanities030104 developmental biologyOncology030220 oncology & carcinogenesisHepatocellular carcinomabiology.proteinbusinessAfter treatmentResearch PaperOncotarget
researchProduct

STAT1 Isoforms Differentially Regulate NK Cell Maturation and Anti-tumor Activity

2020

Natural killer (NK) cells are important components of the innate immune defense against infections and cancers. Signal transducer and activator of transcription 1 (STAT1) is a transcription factor that is essential for NK cell maturation and NK cell-dependent tumor surveillance. Two alternatively spliced isoforms of STAT1 exist: a full-length STAT1α and a C-terminally truncated STAT1β isoform. Aberrant splicing is frequently observed in cancer cells and several anti-cancer drugs interfere with the cellular splicing machinery. To investigate whether NK cell-mediated tumor surveillance is affected by a switch in STAT1 splicing, we made use of knock-in mice expressing either only the STAT1α (S…

0301 basic medicineCytotoxicity ImmunologicLymphomaNK cellsCell MaturationMice0302 clinical medicineInterferonImmunology and AllergyProtein IsoformsSTAT1Immunologic SurveillanceOriginal ResearchBone Marrow TransplantationReceptors InterferonInterleukin-15Mice KnockoutLymphopoiesisinterferonInterferon-Stimulated Gene Factor 3Cell biologySpecific Pathogen-Free OrganismsKiller Cells NaturalSTAT1 Transcription FactorOrgan SpecificityMHC class ISignal transductionsignal transductionmedicine.druglcsh:Immunologic diseases. AllergyLymphoid TissueImmunologyBiologyLymphocyte Depletion03 medical and health sciencesInterleukin-15 Receptor alpha SubunitCell Line TumormedicineAnimalsTranscription factorInnate immune systemisoformsMice Inbred C57BL030104 developmental biologyCancer cellSTAT proteinbiology.proteinlcsh:RC581-607IL-15RαSpleen030215 immunologyFrontiers in Immunology
researchProduct

The activation of NMDA receptors alters the structural dynamics of the spines of hippocampal interneurons

2017

N-Methyl-d-Aspartate receptors (NMDARs) are present in both pyramidal neurons and interneurons of the hippocampus. These receptors play a key role in the structural plasticity of excitatory neurons, but to date little is known about their influence on the remodeling of interneurons. Among hippocampal interneurons, the somatostatin expressing cells in the CA1 stratum oriens are of special interest because of their functional importance and structural characteristics: they display dendritic spines, which change their density in response to different stimuli. In order to understand the role of NMDAR activation on the structural dynamics of the spines of somatostatin expressing interneurons in …

0301 basic medicineDendritic spineDendritic SpinesHippocampusHippocampal formationBiologyHippocampusReceptors N-Methyl-D-Aspartate03 medical and health sciences0302 clinical medicineInterneuronsAnimalsReceptorCells CulturedMice KnockoutPyramidal Cellsmusculoskeletal neural and ocular physiologyGeneral NeuroscienceLong-term potentiationSpine030104 developmental biologySomatostatinnervous systemExcitatory postsynaptic potentialNMDA receptorSomatostatinNeuroscience030217 neurology & neurosurgeryNeuroscience Letters
researchProduct