Search results for "Knockout"

showing 10 items of 806 documents

IgG1 B cell receptor signaling is inhibited by CD22 and promotes the development of B cells whose survival is less dependent on Ig alpha/beta.

2007

We describe a mouse strain in which B cell development relies either on the expression of membrane-bound immunoglobulin (Ig) gamma1 or mu heavy chains. Progenitor cells expressing gamma1 chains from the beginning generate a peripheral B cell compartment of normal size with all subsets, but a partial block is seen at the pro- to pre-B cell transition. Accordingly, gamma1-driven B cell development is disfavored in competition with developing B cells expressing a wild-type (WT) IgH locus. However, the mutant B cells display a long half-life and accumulate in the mature B cell compartment, and even though partial truncation of the Ig alpha cytoplasmic tail compromises their development, it does…

Cell SurvivalCellular differentiationSialic Acid Binding Ig-like Lectin 2ImmunologyNaive B cellB-cell receptorImmunoglobulinsReceptors Antigen B-CellBiologyArticle03 medical and health sciencesMice0302 clinical medicinemedicineImmunology and AllergyAnimalsProgenitor cellMemory B cellB cell030304 developmental biologyCell ProliferationMice Knockout0303 health sciencesB-LymphocytesCell growthCD22Toll-Like ReceptorsCell DifferentiationArticlesMolecular biologyCell biologyMice Inbred C57BLmedicine.anatomical_structureImmunoglobulin GMutationCalciumDimerizationCD79 AntigensSpleen030215 immunologyProtein BindingSignal TransductionThe Journal of experimental medicine
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NKG2D induces Mcl-1 expression and mediates survival of CD8 memory T cell precursors via phosphatidylinositol 3-kinase.

2013

Abstract Memory formation of activated CD8 T cells is the result of a specific combination of signals that promote long-term survival and inhibit differentiation into effector cells. Much is known about initial cues that drive memory formation, but it is poorly understood which signals are essential during the intermediate stages before terminal differentiation. NKG2D is an activating coreceptor on Ag-experienced CD8 T cells that promotes effector cell functions. Its role in memory formation is currently unknown. In this study, we show that NKG2D controls formation of CD8 memory T cells by promoting survival of precursor cells. We demonstrate that NKG2D enhances IL-15–mediated PI3K signalin…

Cell SurvivalImmunologyCytomegalovirusBiologyCD8-Positive T-LymphocytesLymphocyte ActivationMiceMemory cellPrecursor cellmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorReceptors ImmunologicInterleukin-15Mice KnockoutPrecursor Cells T-LymphoidNK cells; NKG2D; CD8 T cellsEffectorCell DifferentiationNKG2DNKG2D; CD8 T cell memory; Mcl1; PI3KCell biologyMice Inbred C57BLmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2NK Cell Lectin-Like Receptor Subfamily KCytomegalovirus InfectionsMyeloid Cell Leukemia Sequence 1 ProteinPhosphatidylinositol 3-KinaseMemory T cellImmunologic MemoryCD8Signal TransductionJournal of immunology (Baltimore, Md. : 1950)
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An unconventional role for miRNA: let-7 activates Toll-like receptor 7 and causes neurodegeneration

2011

Activation of innate immune receptors by host-derived factors exacerbates CNS damage, but the identity of these factors remains elusive. We uncovered an unconventional role for the microRNA let-7, a highly abundant regulator of gene expression in the CNS, in which extracellular let-7 activates the RNA-sensing Toll-like receptor (TLR) 7 and induces neurodegeneration through neuronal TLR7. Cerebrospinal fluid (CSF) from individuals with Alzheimer’s disease contains increased amounts of let-7b, and extracellular introduction of let-7b into the CSF of wild-type mice by intrathecal injection resulted in neurodegeneration. Mice lacking TLR7 were resistant to this neurodegenerative effect, but thi…

Cell signalingApoptosisElectrophoretic Mobility Shift AssayBiologyReal-Time Polymerase Chain ReactionMiceAlzheimer DiseasemicroRNAExtracellularmedicineAnimalsHumansReceptorIn Situ HybridizationMice KnockoutNeuronsToll-like receptorMembrane GlycoproteinsMicroscopy ConfocalInnate immune systemGeneral NeuroscienceNeurodegenerationBrainvirus diseasesTLR7medicine.diseaseImmunohistochemistryMice Inbred C57BLMicroRNAsHEK293 CellsToll-Like Receptor 7Nerve DegenerationCancer researchSignal TransductionNature Neuroscience
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The translocation of signaling molecules in dark adapting mammalian rod photoreceptor cells is dependent on the cytoskeleton.

2008

In vertebrate rod photoreceptor cells, arrestin and the visual G-protein transducin move between the inner segment and outer segment in response to changes in light. This stimulus dependent translocation of signalling molecules is assumed to participate in long term light adaptation of photoreceptors. So far the cellular basis for the transport mechanisms underlying these intracellular movements remains largely elusive. Here we investigated the dependency of these movements on actin filaments and the microtubule cytoskeleton of photoreceptor cells. Co-cultures of mouse retina and retinal pigment epithelium were incubated with drugs stabilizing and destabilizing the cytoskeleton. The actin a…

Cell signalingCytochalasin Dgenetic structuresLightPaclitaxelPhalloidineDark AdaptationBiologyHeterocyclic Compounds 4 or More RingsMicrotubulesRetinaMiceStructural BiologyMicrotubuleRetinal Rod Photoreceptor CellsCytoskeletal drugsThiabendazolemedicineArrestinAnimalsTransducinCytoskeletonMicroscopy ImmunoelectronActinCytoskeletonVision OcularMice KnockoutRetinal pigment epitheliumArrestinHomozygoteCell BiologyDarknessRod Cell Outer Segmenteye diseasesActinsCell biologyMice Inbred C57BLActin CytoskeletonProtein Transportmedicine.anatomical_structureMicroscopy Fluorescencesense organsTransducinCell Migration AssaysSignal TransductionCell motility and the cytoskeleton
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Oligodendrocyte Precursor Cells Synthesize Neuromodulatory Factors

2015

NG2 protein-expressing oligodendrocyte progenitor cells (OPC) are a persisting and major glial cell population in the adult mammalian brain. Direct synaptic innervation of OPC by neurons throughout the brain together with their ability to sense neuronal network activity raises the question of additional physiological roles of OPC, supplementary to generating myelinating oligodendrocytes. In this study we investigated whether OPC express neuromodulatory factors, typically synthesized by other CNS cell types. Our results show that OPC express two well-characterized neuromodulatory proteins: Prostaglandin D2 synthase (PTGDS) and neuronal Pentraxin 2 (Nptx2/Narp). Expression levels of the enzym…

Cell typeCellular differentiationPopulationlcsh:MedicineNerve Tissue ProteinsBiologyCell LineMiceAnimalsHumansAntigenslcsh:ScienceeducationMice Knockouteducation.field_of_studyMultidisciplinarylcsh:RHEK 293 cellsProstaglandin D2 synthaseCell DifferentiationTransfectionCell sortingMolecular biologyLipocalinsCell biologyIntramolecular Oxidoreductasesstomatognathic diseasesAdult Stem CellsOligodendrogliaC-Reactive ProteinHEK293 Cellsnervous systembiology.proteinlcsh:QProteoglycansAdult stem cellResearch ArticlePLoS ONE
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Cre-mediated cell ablation contests mast cell contribution in models of antibody- and T cell-mediated autoimmunity.

2011

SummaryImmunological functions of mast cells remain poorly understood. Studies in Kit mutant mice suggest key roles for mast cells in certain antibody- and T cell-mediated autoimmune diseases. However, Kit mutations affect multiple cell types of both immune and nonimmune origin. Here, we show that targeted insertion of Cre-recombinase into the mast cell carboxypeptidase A3 locus deleted mast cells in connective and mucosal tissues by a genotoxic Trp53-dependent mechanism. Cre-mediated mast cell eradication (Cre-Master) mice had, with the exception of a lack of mast cells and reduced basophils, a normal immune system. Cre-Master mice were refractory to IgE-mediated anaphylaxis, and this defe…

Cell typeEncephalomyelitis Autoimmune ExperimentalCarboxypeptidases AT cellT-LymphocytesImmunologyAutoimmunityImmunoglobulin E03 medical and health sciencesMice0302 clinical medicineImmune systemTh2 CellsmedicineImmunology and AllergyAnimalsGenetic Predisposition to DiseaseMast CellsIntestinal MucosaInterleukin 5Anaphylaxis030304 developmental biologyAutoantibodiesMice Knockout0303 health sciencesStem Cell FactorbiologyIntegrasesGene Expression ProfilingImmunoglobulin EMast cellArthritis Experimental3. Good healthInterleukin 33Mice Inbred C57BLDisease Models Animalmedicine.anatomical_structureInfectious DiseasesImmunologyGene Targetingbiology.proteinAntibodyTumor Suppressor Protein p53030215 immunologyImmunity
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Mast Cell–deficient KitW-sh “Sash” Mutant Mice Display Aberrant Myelopoiesis Leading to the Accumulation of Splenocytes That Act as Myeloid-Derived S…

2013

Abstract Mast cell-deficient KitW-sh “sash” mice are widely used to investigate mast cell functions. However, mutations of c-Kit also affect additional cells of hematopoietic and nonimmune origin. In this study, we demonstrate that KitW-sh causes aberrant extramedullary myelopoiesis characterized by the expansion of immature lineage-negative cells, common myeloid progenitors, and granulocyte/macrophage progenitors in the spleen. A consistent feature shared by these cell types is the reduced expression of c-Kit. Populations expressing intermediate and high levels of Ly6G, a component of the myeloid differentiation Ag Gr-1, are also highly expanded in the spleen of sash mice. These cells are …

Cell typeMyeloidT cellImmunologyBiologyImmunophenotypingMice03 medical and health sciences0302 clinical medicineNeoplasmsmedicineAnimalsAntigens LyImmunology and AllergyMyeloid CellsMast CellsProgenitor cell030304 developmental biologyMice KnockoutMyelopoiesis0303 health sciencesCD11b AntigenMast cellAdoptive Transfer3. Good healthCell biologyProto-Oncogene Proteins c-kitHaematopoiesismedicine.anatomical_structureHematopoiesis ExtramedullaryMutationImmunologyMyeloid-derived Suppressor CellFemaleMyelopoiesisNeoplasm TransplantationSpleen030215 immunologyThe Journal of Immunology
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In Activated Murine Mast Cells, NFATc2 Is Critical for the Production of Autocrine IL-3, Thereby Promoting the Expression of IL-9

2019

Abstract IL-9 has lent its numerical designation to the Th9 subset of CD4+ Th cells, although it is also produced by additional cell types, including mast cells. It is a pleiotropic cytokine involved in allergic reactions, parasitic infections, autoimmune inflammation, and cancer immunity. In this article, we provide evidence that NFATc2 has contradictory functions in the expression of IL-9 in murine Th9 cells and bone marrow–derived mast cells (BMMC). The basis for this is our observation that the production of IL-9 in NFATc2-deficient Th9 cells is increased, whereas it is decreased in BMMC devoid of NFATc2. In addition, NFATc2 deficiency almost completely abrogates the expression of IL-3 …

Cell typeNFATC2medicine.medical_treatmentImmunologyCellAutocrine CommunicationMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationSTAT5 Transcription FactormedicineAnimalsImmunology and AllergyMast CellsAutocrine signallingCells CulturedSTAT5Feedback PhysiologicalMice KnockoutMice Inbred BALB CNFATC Transcription FactorsbiologyChemistryInterleukin-9T-Lymphocytes Helper-InducerUp-RegulationCell biologyMice Inbred C57BLAutocrine CommunicationCytokinemedicine.anatomical_structurebiology.proteinInterleukin-3030215 immunologyThe Journal of Immunology
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Mast cells control the expansion and differentiation of IL-10-competent B cells

2014

Abstract The discovery of B cell subsets with regulatory properties, dependent on IL-10 production, has expanded our view on the mechanisms that control inflammation. Regulatory B cells acquire the ability to produce IL-10 in a stepwise process: first, they become IL-10 competent, a poised state in which B cells are sensitive to trigger signals but do not actually express the Il-10 gene; then, when exposed to appropriate stimuli, they start producing IL-10. Even if the existence of IL-10–competent B cells is now well established, it is not yet known how different immune cell types cross talk with B cells and affect IL-10–competent B cell differentiation and expansion. Mast cells (MCs) contr…

Cell typeRegulatory B cellsCellular differentiationImmunologyCD40 LigandB-Lymphocyte SubsetsRegulatory B cellsB-cellBiologyExosomesLymphocyte ActivationImmunophenotypingMast cellMiceImmunophenotypingImmune systemmedicineImmunology and AllergyAnimalsMast CellsB cell differentiationCD40 AntigensB cellmast cell; IL-10; B-cellMice KnockoutCD40Cell DifferentiationCell biologyInterleukin-10Gastrointestinal TractInterleukin 10medicine.anatomical_structurePhenotypeMast cell; Regulatory B cells; IL-10; B cell differentiationImmunologyIL-10biology.proteinFemaleJournal of immunology (Baltimore, Md.
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The transcription factor Interferon Regulatory Factor 4 is required for the generation of protective effector CD8 + T cells

2013

Robust cytotoxic CD8 + T-cell response is important for immunity to intracellular pathogens. Here, we show that the transcription factor IFN Regulatory Factor 4 (IRF4) is crucial for the protective CD8 + T-cell response to the intracellular bacterium Listeria monocytogenes . IRF4-deficient ( Irf4 −/− ) mice could not clear L. monocytogenes infection and generated decreased numbers of L. monocytogenes -specific CD8 + T cells with impaired effector phenotype and function. Transfer of wild-type CD8 + T cells into Irf4 −/− mice improved bacterial clearance, suggesting an intrinsic defect of CD8 + T cells in Irf4 −/− mice. Following transfer into wild-type recipients, Irf4 −/− CD8 + T cells bec…

Cellular differentiationGene ExpressionEomesoderminBiologyMiceInterleukin 21AnimalsCytotoxic T cellListeriosisIL-2 receptorAntigen-presenting cellSTAT4Cell ProliferationMice KnockoutMultidisciplinaryCell DifferentiationBiological SciencesListeria monocytogenesMolecular biologyMice Inbred C57BLHost-Pathogen InteractionsInterferon Regulatory FactorsImmunologyPositive Regulatory Domain I-Binding Factor 1CD8T-Lymphocytes CytotoxicTranscription FactorsProceedings of the National Academy of Sciences
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