Search results for "Knockout"

showing 10 items of 806 documents

Intrinsic TNFR2 signaling in T regulatory cells provides protection in CNS autoimmunity

2018

Significance In spite of TNF involvement in the pathogenesis of multiple sclerosis (MS), systemic TNF neutralization in MS patients was not successful. One of the possible reasons is that TNF possesses both pathogenic and protective features that may be related to TNFR1 versus TNFR2 receptor engagement. This study uncovers one of such protective functions of TNF mediated by intrinsic TNFR2 signaling in Treg cells. In mice bearing humanized TNF and TNFR2 genetic loci, TNFR2 ablation restricted to Treg cells led to reduced capacity to control Th17 cell responses, exacerbated experimental autoimmune encephalomyelitis (EAE) development, and affected the maintenance of Treg cells. These findings…

Central Nervous System0301 basic medicineEncephalomyelitis Autoimmune ExperimentalT regulatory cellsmedicine.medical_treatmentAutoimmunitychemical and pharmacologic phenomenaBiologymedicine.disease_causeT-Lymphocytes RegulatoryneuroinflammationAutoimmunityMice03 medical and health sciencesImmunology and Inflammation0302 clinical medicineImmune systemmedicineAnimalsHumansReceptors Tumor Necrosis Factor Type IIIL-2 receptorCells CulturedNeuroinflammationMice KnockoutAutoimmune diseaseMultidisciplinaryEAETumor Necrosis Factor-alphaExperimental autoimmune encephalomyelitisFOXP3hemic and immune systemsBiological Sciencesmedicine.diseaseTNF/TNFR2Mice Inbred C57BLDisease Models Animalhumanized mice030104 developmental biologyCytokineGene Expression RegulationImmunology030215 immunologyProceedings of the National Academy of Sciences
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NF-κB inducing kinase (NIK) is an essential post-transcriptional regulator of T-cell activation affecting F-actin dynamics and TCR signaling

2018

NF-κB inducing kinase (NIK) is the key protein of the non-canonical NF-κB pathway and is important for the development of lymph nodes and other secondary immune organs. We elucidated the specific role of NIK in T cells using T-cell specific NIK-deficient (NIKΔT) mice. Despite showing normal development of lymphoid organs, NIKΔT mice were resistant to induction of CNS autoimmunity. T cells from NIKΔT mice were deficient in late priming, failed to up-regulate T-bet and to transmigrate into the CNS. Proteomic analysis of activated NIK-/- T cells showed de-regulated expression of proteins involved in the formation of the immunological synapse: in particular, proteins involved in cytoskeleton dy…

Central Nervous System0301 basic medicineEncephalomyelitis Autoimmune ExperimentalT-LymphocytesT cellPrimary Cell CultureImmunologyReceptors Antigen T-CellPriming (immunology)Protein Serine-Threonine KinasesBiologyLymphocyte ActivationImmunological synapseMice03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsImmunology and AllergyProtein kinase BAdaptor Proteins Signal TransducingMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3ZAP-70 Protein-Tyrosine KinasePhospholipase C gammaGene Expression ProfilingZAP70T-cell receptorMembrane ProteinsPhosphoproteinsActinsPeptide FragmentsCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureGene Expression Regulation030220 oncology & carcinogenesisMyelin-Oligodendrocyte GlycoproteinLymph NodesSignal transductionT-Box Domain ProteinsProto-Oncogene Proteins c-aktSpleenSignal TransductionJournal of Autoimmunity
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Cannabinoids mediate analgesia largely via peripheral type 1 cannabinoid receptors in nociceptors

2007

Although endocannabinoids constitute one of the first lines of defense against pain, the anatomical locus and the precise receptor mechanisms underlying cannabinergic modulation of pain are uncertain. Clinical exploitation of the system is severely hindered by the cognitive deficits, memory impairment, motor disturbances and psychotropic effects resulting from the central actions of cannabinoids. We deleted the type 1 cannabinoid receptor (CB1) specifically in nociceptive neurons localized in the peripheral nervous system of mice, preserving its expression in the CNS, and analyzed these genetically modified mice in preclinical models of inflammatory and neuropathic pain. The nociceptor-spec…

Central Nervous SystemCannabinoid receptorCannabinoid Receptor Modulatorsmedicine.medical_treatmentCentral nervous systemPharmacologyBiologyArticleMiceReceptor Cannabinoid CB1Ganglia SpinalCannabinoid Receptor ModulatorsPeripheral Nervous SystemmedicineAnimalsNeurons AfferentAllelesDNA PrimersMice KnockoutNerve Fibers UnmyelinatedCannabinoidsGeneral NeuroscienceNociceptorsPeripheral Nervous System DiseasesEndocannabinoid systemElectrophysiologyMice Inbred C57BLmedicine.anatomical_structurenervous systemPeripheral nervous systemNeuropathic painNociceptorlipids (amino acids peptides and proteins)CannabinoidAnalgesiaNeuroscience
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Role of Sortilin in Models of Autoimmune Neuroinflammation

2015

Abstract The proneurotrophin receptor sortilin is a protein with dual functions, being involved in intracellular protein transport, as well as cellular signal transduction. The relevance of the receptor for various neuronal disorders, such as dementia, seizures, and brain injury, is well established. In contrast, little is known about the role of sortilin in immune cells and inflammatory diseases. The aim of our study was to elucidate the distribution of sortilin in different immune cell types in mice and humans and to analyze its function in autoimmune CNS inflammation. Sortilin was expressed most profoundly in murine and human macrophages and dendritic cells and to a much lesser extent in…

Central Nervous SystemCell typeEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisT-LymphocytesEncephalomyelitisImmunologyAutoimmunityBiologyMiceImmune systemmedicineAnimalsHumansImmunology and AllergyReceptorNeuroinflammationMice KnockoutAutoimmune diseaseAntigen PresentationMacrophagesExperimental autoimmune encephalomyelitisDendritic Cellsmedicine.diseaseImmunity InnateMice Inbred C57BLAdaptor Proteins Vesicular TransportBrain InjuriesImmunologyNeurogenic InflammationSignal transductionSignal Transduction
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OTUB1 inhibits CNS autoimmunity by preventing IFN-γ-induced hyperactivation of astrocytes.

2019

Astrocytes are critical regulators of neuroinflammation in multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). Growing evidence indicates that ubiquitination of signaling molecules is an important cell‐intrinsic mechanism governing astrocyte function during MS and EAE. Here, we identified an upregulation of the deubiquitinase OTU domain, ubiquitin aldehyde binding 1 (OTUB1) in astrocytes during MS and EAE. Mice with astrocyte‐specific OTUB1 ablation developed more severe EAE due to increased leukocyte accumulation, proinflammatory gene transcription, and demyelination in the spinal cord as compared to control mice. OTUB1‐deficient astrocytes were hy…

Central Nervous SystemEncephalomyelitis Autoimmune ExperimentalNeuroimmunomodulationmedicine.medical_treatmentexperimental autoimmune encephalomyelitisAutoimmunityBiologymultiple sclerosisubiquitinationGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineneuroinflammationInterferon-gammaMice03 medical and health sciences0302 clinical medicineastrocytemedicineAnimalsMolecular BiologyCells CulturedNeuroinflammation030304 developmental biologyMice Knockout0303 health sciencesGeneral Immunology and MicrobiologySuppressor of cytokine signaling 1General NeuroscienceExperimental autoimmune encephalomyelitisArticlesmedicine.disease3. Good healthCell biologyMice Inbred C57BLCysteine EndopeptidasesCytokinemedicine.anatomical_structureAnimals NewbornAstrocytesSTAT proteinOTUB1FemaleNeurogenic InflammationJanus kinase030217 neurology & neurosurgeryAstrocyte
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T helper cell- and CD40-dependent germline IgM prevents chronic virus-induced demyelinating disease

2012

Generation of antiviral IgM is usually considered as a marker of a short-lived initial antibody response that is replaced by hypermutated and more-efficient IgG. However, once viruses have established a particular niche for their persistence (e.g., within the CNS), the immune system has to specifically mobilize a broad range of antimicrobial effectors to contain the pathogen in the long term. Infection of the CNS with the mouse hepatitis virus (MHV) provides a unique model situation in which the extent of inflammatory CNS disease is determined by the balance between antiviral immune control, viral replication, and immune-mediated damage. We show here that whereas antibody- or B cell-defici…

Central Nervous SystemEnzyme-Linked Immunospot AssayFluorescent Antibody TechniqueVirusMice03 medical and health sciences0302 clinical medicineImmune systemCytidine DeaminaseActivation-induced (cytidine) deaminaseDemyelinating diseasemedicineAnimalsCD40 Antigens030304 developmental biologyMice KnockoutAnalysis of VarianceB-LymphocytesMurine hepatitis virus0303 health sciencesMultidisciplinaryCD40biologyT-Lymphocytes Helper-InducerT helper cellBiological SciencesFlow Cytometrymedicine.diseaseVirology3. Good healthmedicine.anatomical_structureImmunoglobulin MViral replicationImmunologybiology.proteinAntibodyDemyelinating Diseases030215 immunologyProceedings of the National Academy of Sciences
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Role of the cellular prion protein in oligodendrocyte precursor cell proliferation and differentiation in the developing and adult mouse CNS

2012

There are numerous studies describing the signaling mechanisms that mediate oligodendrocyte precursor cell (OPC) proliferation and differentiation, although the contribution of the cellular prion protein (PrP c) to this process remains unclear. PrP c is a glycosyl-phosphatidylinositol (GPI)-anchored glycoprotein involved in diverse cellular processes during the development and maturation of the mammalian central nervous system (CNS). Here we describe how PrP c influences oligodendrocyte proliferation in the developing and adult CNS. OPCs that lack PrP c proliferate more vigorously at the expense of a delay in differentiation, which correlates with changes in the expression of oligodendrocyt…

Central Nervous SystemTelencephalonMouseCellular differentiationanimal diseasesGene ExpressionHippocampusMice0302 clinical medicineNeural Stem CellsGene expressionMolecular Cell BiologyNeurobiology of Disease and RegenerationCell proliferationNeuronsCerebral CortexMice Knockout0303 health sciencesProliferació cel·lularMultidisciplinaryNeurogenesisQRCell DifferentiationAnimal ModelsNeural stem cell3. Good healthCell biologyOligodendrogliamedicine.anatomical_structureKnockout mouseMedicineFemaleBiologia del desenvolupamentCellular TypesCell DivisionResearch ArticlePrionsNeurogenesisScienceBiologyModels BiologicalCell Growth03 medical and health sciencesModel OrganismsDevelopmental NeuroscienceNeuroglial Developmentmental disordersDevelopmental biologymedicineAnimalsPrPC ProteinsBiology030304 developmental biologyCell ProliferationCell growthLineage markersMolecular DevelopmentOligodendrocytenervous system diseasesMice Inbred C57BLImmunologyOrganism Development030217 neurology & neurosurgeryDevelopmental BiologyNeuroscience
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Mice lacking Plexin-B3 display normal CNS morphology and behaviour

2009

Semaphorins and their receptors, plexins, have emerged as important regulators of a multitude of biological processes. Plexin-B3 has been shown to be selectively expressed in postnatal oligodendrocytes. In contrast to the well-characterized Plexin-A family and the Plexin-B family members Plexin-B1 and -B2, no data are available on the functional role of Plexin-B3 in the central nervous system in vivo. Here we have elucidated the functional significance of Plexin-B3 by generating and analyzing constitutive knock-out mice. Plexin-B3-deficient mice were found to be viable and fertile. A systematic histological analysis revealed no morphological defects in the brain or spinal cord of mutant ani…

Central Nervous Systemanimal structuresCentral nervous systemNerve Tissue ProteinsReceptors Cell SurfaceAnxietyMotor ActivityNeuropsychological TestsBiologyMiceCellular and Molecular NeuroscienceSemaphorinmedicineAnimalsReceptorMolecular BiologyCells CulturedMice KnockoutBehavior AnimalPlexinAge FactorsCell BiologySpinal cordMotor coordinationOligodendrogliamedicine.anatomical_structureSpinal Cordembryonic structuresbiology.proteinMotor learningNeuroscienceBiomarkersFunction (biology)Molecular and Cellular Neuroscience
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Kif3a interacts with Dynactin subunit p150 Glued to organize centriole subdistal appendages.

2013

Formation of cilia, microtubule-based structures that function in propulsion and sensation, requires Kif3a, a subunit of Kinesin II essential for intraflagellar transport (IFT). We have found that, Kif3a is also required to organize centrioles. In the absence of Kif3a, the subdistal appendages of centrioles are disorganized and lack p150(Glued) and Ninein. Consequently, microtubule anchoring, centriole cohesion and basal foot formation are abrogated by loss of Kif3a. Kif3a localizes to the mother centriole and interacts with the Dynactin subunit p150(Glued) . Depletion of p150(Glued) phenocopies the effects of loss of Kif3a, indicating that Kif3a recruitment of p150(Glued) is critical for s…

CentrioleKnockoutKinesinsBiologycentriole cohesionKif3aMedical and Health SciencesArticleGeneral Biochemistry Genetics and Molecular BiologyMiceMicrotubuleIntraflagellar transportInformation and Computing SciencesAnimalsHumansKIF3AMicrotubule anchoringMolecular BiologyCentriolesMice KnockoutGeneral Immunology and MicrobiologyGeneral NeuroscienceCiliumTumor Suppressor ProteinsNuclear ProteinsKinesinDynactin ComplexBiological SciencesCell biologyCytoskeletal ProteinscentrosomeCentrosomeHela CellsDynactinGeneric health relevanceMicrotubule-Associated Proteinsp150(Glued)HeLa Cellssubdistal appendageDevelopmental Biology
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The angiopoietin-Tie2 pathway regulates Purkinje cell dendritic morphogenesis in a cell-autonomous manner.

2021

Neuro-vascular communication is essential to synchronize central nervous system development. Here, we identify angiopoietin/Tie2 as a neuro-vascular signaling axis involved in regulating dendritic morphogenesis of Purkinje cells (PCs). We show that in the developing cerebellum Tie2 expression is not restricted to blood vessels, but it is also present in PCs. Its ligands angiopoietin-1 (Ang1) and angiopoietin-2 (Ang2) are expressed in neural cells and endothelial cells (ECs), respectively. PC-specific deletion of Tie2 results in reduced dendritic arborization, which is recapitulated in neural-specific Ang1-knockout and Ang2 full-knockout mice. Mechanistically, RNA sequencing reveals that Tie…

CerebellumalphaCytoskeleton organizationAngiogenesisPurkinje cellprotocadherinsMorphogenesisneural progenitor cellsMice Transgenicself-avoidanceBiologyModels BiologicalGeneral Biochemistry Genetics and Molecular BiologyAngiopoietinAngiopoietin-2Purkinje Cellsddc:570CerebellumexpressionGene expressionmedicineAngiopoietin-1MorphogenesisAnimalsmouseMice KnockoutIntegrasessubventricular zonedifferentiationDendritesmtorc2Angiopoietin receptorReceptor TIE-2Cell biologyMice Inbred C57BLmedicine.anatomical_structuremessenger-rnaGene Expression RegulationOrgan Specificityembryonic structurescardiovascular systembiology.proteinGene DeletionSignal TransductionCell reports
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