Search results for "Knockout"

showing 10 items of 806 documents

Smad7 in T cells drives T helper 1 responses in multiple sclerosis and experimental autoimmune encephalomyelitis

2010

Autoreactive CD4+ T lymphocytes play a vital role in the pathogenesis of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis. Since the discovery of T helper 17 cells, there is an ongoing debate whether T helper 1, T helper 17 or both subtypes of T lymphocytes are important for the initiation of autoimmune neuroinflammation. We examined peripheral blood CD4+ cells from patients with active and stable relapsing-remitting multiple sclerosis, and used mice with conditional deletion or over-expression of the transforming growth factor-beta inhibitor Smad7, to delineate the role of Smad7 in T cell differentiation and autoimmune neuroinflammation. We found that Smad…

Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisT helper 1Regulatory T cellT cellMolecular Sequence DataMice TransgenicBiologySmad7 ProteinMiceInterleukin 21medicineAnimalsHumansCytotoxic T cellAmino Acid SequenceIL-2 receptorAntigen-presenting cellMice Knockoutintegumentary systemEAEimmune regulationCD28Original ArticlesTh1 CellsNatural killer T cellMice Inbred C57BLmedicine.anatomical_structureT cell responsesImmunologyNeurology (clinical)Brain
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Oligodendrocyte-specific FADD deletion protects mice from autoimmune-mediated demyelination.

2010

Abstract Apoptosis of oligodendrocytes (ODCs), the myelin-producing glial cells in the CNS, plays a central role in demyelinating diseases such as multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. To investigate the mechanism behind ODC apoptosis in EAE, we made use of conditional knockout mice lacking the adaptor protein FADD specifically in ODCs (FADDODC-KO). FADD mediates apoptosis by coupling death receptors with downstream caspase activation. In line with this, ODCs from FADDODC-KO mice were completely resistant to death receptor-induced apoptosis in vitro. In the EAE model, FADDODC-KO mice followed an ameliorated clinical di…

Encephalomyelitis Autoimmune ExperimentalMultiple Sclerosisgenetic structuresEncephalomyelitisFas-Associated Death Domain ProteinImmunologyApoptosisurologic and male genital diseasesMiceConditional gene knockoutDemyelinating diseasemedicineImmunology and AllergyAnimalsFADDLymphocytesMyelin SheathDeath domainInflammationMice KnockoutbiologyMultiple sclerosisMacrophagesfungiExperimental autoimmune encephalomyelitismedicine.diseaseOligodendrocyteOligodendrogliamedicine.anatomical_structureGene Expression RegulationSpinal CordCancer researchbiology.proteinbiological phenomena cell phenomena and immunityGene DeletionJournal of immunology (Baltimore, Md. : 1950)
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Dendritic Cells Ameliorate Autoimmunity in the CNS by Controlling the Homeostasis of PD-1 Receptor+ Regulatory T Cells

2012

SummaryMature dendritic cells (DCs) are established as unrivaled antigen-presenting cells (APCs) in the initiation of immune responses, whereas steady-state DCs induce peripheral T cell tolerance. Using various genetic approaches, we depleted CD11c+ DCs in mice and induced autoimmune CNS inflammation. Unexpectedly, mice lacking DCs developed aggravated disease compared to control mice. Furthermore, when we engineered DCs to present a CNS-associated autoantigen in an induced manner, we found robust tolerance that prevented disease, which coincided with an upregulation of the PD-1 receptor on antigen-specific T cells. Additionally, we showed that PD-1 was necessary for DC-mediated induction o…

Encephalomyelitis Autoimmune ExperimentalT cellProgrammed Cell Death 1 ReceptorImmunologyAntigen presentationCD11cAutoimmunity610 Medicine & healthchemical and pharmacologic phenomenaBiologymedicine.disease_causeAutoantigensT-Lymphocytes RegulatoryB7-H1 AntigenAutoimmunityImmune toleranceMiceImmune systemDownregulation and upregulationImmune TolerancemedicineAnimalsImmunology and AllergyReceptorMice KnockoutAntigen Presentation2403 Immunologyhemic and immune systemsDendritic Cells2725 Infectious DiseasesTh1 CellsCD11c AntigenMice Inbred C57BLInfectious Diseasesmedicine.anatomical_structure10032 Clinic for Oncology and HematologyImmunology2723 Immunology and AllergyTh17 CellsImmunity
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The protein tyrosine kinase Tec regulates a CD44highCD62L- Th17 subset.

2010

Abstract The generation of Th17 cells has to be tightly controlled during an immune response. In this study, we report an increase in a CD44highCD62L− Th17 subset in mice deficient for the protein tyrosine kinase Tec. CD44highCD62L− Tec−/− CD4+ T cells produced enhanced IL-17 upon activation, showed increased expression levels of IL-23R and RORγt, and IL-23–mediated expansion of Tec−/− CD4+ T cells led to an increased production of IL-17. Tec−/− mice immunized with heat-killed Streptococcus pneumoniae displayed increased IL-17 expression levels in the lung postinfection with S. pneumoniae, and this correlated with enhanced pneumococcal clearance and reduced lung inflammation compared with T…

Encephalomyelitis Autoimmune ExperimentalTECeducationImmunologyImmunoblottingInflammationEnzyme-Linked Immunosorbent AssayCell SeparationBiologyMiceImmune systemIn vivoRAR-related orphan receptor gammaT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsCell LineageL-SelectinMice KnockoutReverse Transcriptase Polymerase Chain ReactionCD44Interleukin-17hemic and immune systemsCell DifferentiationPneumoniaT-Lymphocytes Helper-InducerProtein-Tyrosine KinasesFlow CytometryMolecular biologyHyaluronan ReceptorsCancer researchbiology.proteinCytokinesmedicine.symptomSignal transductiontissuesTyrosine kinaseSignal TransductionJournal of immunology (Baltimore, Md. : 1950)
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Pre- and postsynaptic type-1 cannabinoid receptors control the alterations of glutamate transmission in experimental autoimmune encephalomyelitis

2013

Type-1 cannabinoid receptors (CB1R) are important regulators of the neurodegenerative damage in multiple sclerosis (MS) and in experimental autoimmune encephalomyelitis (EAE). In GABAergic striatal neurons, CB1R stimulation exerts protective effects by limiting inflammation-induced potentiation of glutamate-mediated spontaneous excitatory postsynaptic currents (sEPSCs). Here we show that CB1R located on GABAergic or on glutamatergic neurons are differentially involved in the pre- and postsynaptic alterations of sEPSCs caused by EAE in the striatum. After induction of EAE, mice selectively lacking CB1R on GABAergic neurons (GABA-CB1R-KO) showed exacerbated alterations of sEPSC duration in GA…

Encephalomyelitis Autoimmune ExperimentalTime FactorsPostsynaptic CurrentPresynaptic TerminalsExcitotoxicityGlutamic AcidIn Vitro TechniquesBiologyMedium spiny neuronmedicine.disease_causeSynaptic TransmissionMiceCellular and Molecular NeuroscienceGlutamatergicReceptor Cannabinoid CB1Postsynaptic potentialmedicineAnimalsgamma-Aminobutyric AcidMice KnockoutNeuronsPharmacologyExperimental autoimmune encephalomyelitisGlutamate receptorExcitatory Postsynaptic Potentialsmedicine.diseaseCorpus StriatumMice Inbred C57BLnervous systemDisease ProgressionExcitatory postsynaptic potentialFemaleSettore MED/26 - NeurologiaNeuroscience
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IL-6 controls Th17 immunity in vivo by inhibiting the conversion of conventional T cells into Foxp3+regulatory T cells

2008

The conditions leading to the induction of adaptive Foxp3+regulatory T cells (T-regs) from peripheral T cells in vivo are incompletely understood. Here, we show that unresponsiveness of T cells to IL-6 by T cell-selective deletion of gp130 or immunization of wild-type mice with antigen in incomplete Freund's adjuvant (IFA), which fails to induce IL-6, promotes the conversion of peripheral CD4+T cells into adaptive Foxp3+T-regs. Thus, both T cell-conditional gp130 knockout (KO) mice immunized with MOG35-55 in complete Freund's adjuvant (CFA) and wild-type mice immunized with MOG35-55 in IFA develop overwhelming antigen-specific T-reg responses and are protected from experimental autoimmune e…

Encephalomyelitis Autoimmune Experimentalmedicine.medical_treatmentchemical and pharmacologic phenomenaInflammationBiologyT-Lymphocytes RegulatoryMiceInterleukin 21Antigenimmune system diseasesmedicineAnimalsCytotoxic T cellIL-2 receptorMice KnockoutMultidisciplinaryInterleukin-6Experimental autoimmune encephalomyelitisFOXP3Forkhead Transcription Factorshemic and immune systemsT-Lymphocytes Helper-InducerBiological Sciencesmedicine.diseaseCytokineImmunologymedicine.symptomProceedings of the National Academy of Sciences
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Neuromuscular junction disassembly and muscle fatigue in mice lacking neurotrophin-4

2001

Neurotrophin-4 (NT-4) is produced by slow muscle fibers in an activity-dependent manner and promotes growth and remodeling of adult motorneuron innervation. However, both muscle fibers and motor neurons express NT-4 receptors, suggesting bidirectional NT-4 signaling at the neuromuscular junction. Mice lacking NT-4 displayed enlarged and fragmented neuromuscular junctions with disassembled postsynaptic acetylcholine receptor (AChR) clusters, reduced AChR binding, and acetylcholinesterase activity. Electromyographic responses, posttetanic potentiation, and action potential amplitude were also significantly reduced in muscle fibers from NT-4 knock-out mice. Slow-twitch soleus muscles from thes…

End-plate potentialNeuromuscular JunctionElectromyographyBiologyNeuromuscular junctionCellular and Molecular NeuroscienceMicePostsynaptic potentialmedicineAnimalsReceptors CholinergicNerve Growth FactorsMuscle SkeletalMolecular BiologyAcetylcholine receptorMice KnockoutMotor Neuronsmedicine.diagnostic_testMuscle fatigueElectromyographyAge FactorsLong-term potentiationneuromuscular junction; neurotrophin-4; synaptic transmissionCell Biologymedicine.anatomical_structureMuscle Fibers Slow-TwitchMuscle FatigueAcetylcholinesteraseTetanic stimulationNeuroscienceMuscle Contraction
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Lymphatic endothelial progenitors bud from the cardinal vein and intersomitic vessels in mammalian embryos.

2012

Abstract The lymphatic vasculature preserves tissue fluid balance by absorbing fluid and macromolecules and transporting them to the blood vessels for circulation. The stepwise process leading to the formation of the mammalian lymphatic vasculature starts by the expression of the gene Prox1 in a subpopulation of blood endothelial cells (BECs) on the cardinal vein (CV) at approximately E9.5. These Prox1-expressing lymphatic endothelial cells (LECs) will exit the CV to form lymph sacs, primitive structures from which the entire lymphatic network is derived. Until now, no conclusive information was available regarding the cellular processes by which these LEC progenitors exit the CV without co…

EndotheliumMesenchymegovernment.form_of_governmentRecombinant Fusion ProteinsImmunologyEmbryonic DevelopmentMice TransgenicBiologyBiochemistryMiceMicroscopy Electron TransmissionCell MovementVascular BiologymedicineAnimalsLymph sacsProgenitor cellEmbryonic Stem CellsHomeodomain ProteinsMice KnockoutBuddingMembrane GlycoproteinsCommon cardinal veinsTumor Suppressor ProteinsfungiCell BiologyHematologyAnatomyAdherens JunctionsCadherinsEmbryo MammalianCoronary VesselsCell biologyPlatelet Endothelial Cell Adhesion Molecule-1Lymphatic Endotheliummedicine.anatomical_structureLymphatic systemgovernmentsense organsEndothelium LymphaticBlood
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Crucial role of aspartic acid at position 265 in the CH2 domain for murine IgG2a and IgG2b Fc-associated effector functions.

2008

Abstract Replacement of aspartic acid by alanine at position 265 (D265A) in mouse IgG1 results in a complete loss of interaction between this isotype and low-affinity IgG Fc receptors (FcγRIIB and FcγRIII). However, it has not yet been defined whether the D265A substitution could exhibit similar effects on the interaction with two other FcγR (FcγRI and FcγRIV) and on the activation of complement. To address this question, 34-3C anti-RBC IgG2a and IgG2b switch variants bearing the D265A mutation were generated, and their effector functions and in vivo pathogenicity were compared with those of the respective wild-type Abs. The introduction of the D265A mutation almost completely abolished the…

ErythrocytesAspartic Acid/genetics/physiologyAntibodies Monoclonal/toxicityImmunologyMutantReceptors Fcddc:616.07Complement Activation/genetics/immunologyAlanine/geneticsMiceStructure-Activity RelationshipProtein structureImmunoglobulin G/chemistry/metabolismProtein Isoforms/chemistry/deficiency/genetics/physiologyAspartic acidImmunology and AllergyAnimalsProtein IsoformsErythrocytes/immunologyReceptorComplement ActivationAutoantibodiesAlanineMice KnockoutAspartic AcidMice Inbred BALB CAlaninebiologyAnemia Hemolytic Autoimmune/genetics/immunologyAntibodies MonoclonalReceptors Fc/chemistry/deficiency/genetics/physiologyFragment crystallizable regionIsotypeAmino Acid Substitution/genetics/physiologySialic Acids/geneticsProtein Structure TertiaryMice Inbred C57BLBiochemistryAmino Acid SubstitutionImmunoglobulin Gbiology.proteinSialic AcidsAutoantibodies/toxicityAnemia Hemolytic AutoimmuneAntibodyProtein Structure Tertiary/genetics/physiologyJournal of immunology (Baltimore, Md. : 1950)
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TALPID3/KIAA0586 regulates multiple aspects of neuromuscular patterning during gastrointestinal development in animal models and human

2021

ABSTRACTTALPID3/KIAA0586 is an evolutionary conserved protein, which plays an essential role in protein trafficking. Its role during gastrointestinal (GI) and enteric nervous system (ENS) development has not been studied previously. Here, we analysed chicken, mouse and human embryonic GI tissues with TALPID3 mutations. The GI tract of TALPID3 chicken embryos was shortened and malformed. Histologically, the gut smooth muscle was mispatterned and enteric neural crest cells were scattered throughout the gut wall. Analysis of the Hedgehog pathway and gut extracellular matrix provided causative reasons for these defects. Interestingly, chicken intra-species grafting experiments and a conditional…

Extracellular matrixMutationConditional gene knockoutmedicineNeural crestEnteric nervous systemEmbryoBiologymedicine.disease_causeEmbryonic stem cellHedgehog signaling pathwayCell biology
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