Search results for " and immunity"

showing 10 items of 125 documents

Frequency of cytotoxic T lymphocyte precursors to herpes simplex virus type 1 as determined by limiting dilution analysis.

1983

The conditions for establishing a limiting dilution assay to measure cytotoxic T lymphocyte precursors (CTL-P) against herpes simplex virus type 1 (HSV-1) were determined. Analysis by Poisson statistics demonstrated that the estimated frequency of HSV-1-reactive cells in the spleens of normal mice was less than 1/250,000. In contrast, mice immunized previously with infectious HSV-1 demonstrated a CTL-P frequency between 1/3,500 and 1/15,670. The generation of a maximum cytotoxic T lymphocyte response required that mice be primed in vivo with infectious virus. Immunization with inactivated virus either failed to elicit detectable CTL-P frequencies or gave frequencies markedly less than thos…

Cytotoxicity ImmunologicT cellImmunologyPopulationchemical and pharmacologic phenomenaBiologymedicine.disease_causeMicrobiologyVirusMiceImmune systemAntigenmedicineCytotoxic T cellAnimalsAntigens LySimplexviruseducationCytotoxicityCells Culturededucation.field_of_studyVirologyInfectious Diseasesmedicine.anatomical_structureHerpes simplex virusImmunologic TechniquesMice Inbred CBAInterleukin-2ParasitologyImmunizationSpleenT-Lymphocytes CytotoxicViral Infections and ImmunityInfection and immunity
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Cyclin-dependent kinase inhibitor p21 controls adult neural stem cell expansion by regulating Sox2 gene expression.

2012

Summary In the adult brain, continual neurogenesis of olfactory neurons is sustained by the existence of neural stem cells (NSCs) in the subependymal niche. Elimination of the cyclin-dependent kinase inhibitor 1A (p21) leads to premature exhaustion of the subependymal NSC pool, suggesting a relationship between cell cycle control and long-term self-renewal, but the molecular mechanisms underlying NSC maintenance by p21 remain unexplored. Here we identify a function of p21 in the direct regulation of the expression of pluripotency factor Sox2, a key regulator of the specification and maintenance of neural progenitors. We observe that p21 directly binds a Sox2 enhancer and negatively regulate…

Cèl·lules mare neuralsCyclin-Dependent Kinase Inhibitor p21Chromatin ImmunoprecipitationImmunoblottingArticle03 medical and health sciencesMice0302 clinical medicineSOX2Neural Stem CellsCyclin-dependent kinaseNeurosphereSubependymal zoneGeneticsExpressió genèticaAnimalsProgenitor cellCells Cultured030304 developmental biology0303 health sciencesbiologyCell growthReverse Transcriptase Polymerase Chain ReactionSOXB1 Transcription FactorsNeurogenesisCell BiologyImmunohistochemistryNeural stem cellMice Mutant Strains3. Good healthAdult Stem Cellsnervous systemCancer researchbiology.proteinMolecular Medicinebiological phenomena cell phenomena and immunity030217 neurology & neurosurgeryProtein BindingCell stem cell
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CD95 death-inducing signaling complex formation and internalization occur in lipid rafts of type I and type II cells

2004

We investigated the membrane localization of CD95 in type I and type II cells, which differ in their ability to recruit and activate caspase-8. We found that CD95 was preferentially located in lipid rafts of type I cells, while it was present both in raft and non-raft plasma membrane sub-domains of type II cells. After stimulation, CD95 located in phospholipid-rich plasma membrane was recruited to lipid rafts in both types of cells. Similarly, CD95 cross-linking resulted in caspase-independent translocation of FADD/MORT1 and caspase-8 to the lipid rafts, which was prevented by a death domain-defective receptor. CD95 internalization was then rapid in type I and delayed in type II cells and s…

Death Domain Receptor Signaling Adaptor ProteinsEndosomeT-Lymphocytesmedia_common.quotation_subjectImmunologyApoptosisReceptors Tumor Necrosis FactorCell LineMembrane MicrodomainsSettore MED/04 - PATOLOGIA GENERALECell Line TumorReceptorsHumansImmunology and Allergyfas ReceptorFADDInternalizationLipid raftLipid raftsDeath domainmedia_commonTumorbiologyVesicleFas receptorEndocytosisCell biologyProtein TransportCholesterolCD95 death-inducing signaling complexCaspasesCD95biology.proteinlipids (amino acids peptides and proteins)biological phenomena cell phenomena and immunityCaspase-8Tumor Necrosis FactorCaspase-8; CD95; Lipid rafts; Apoptosis; Caspases; Cell Line Tumor; Cholesterol; Death Domain Receptor Signaling Adaptor Proteins; Humans; Membrane Microdomains; Protein Binding; Protein Transport; Receptors Tumor Necrosis Factor; T-Lymphocytes; fas Receptor; Endocytosis; Signal Transduction; Immunology and Allergy; ImmunologyProtein BindingSignal TransductionEuropean Journal of Immunology
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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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Nanog Regulates Primordial Germ Cell Migration Through Cxcr4b

2010

Abstract Gonadal development in vertebrates depends on the early determination of primordial germ cells (PGCs) and their correct migration to the sites where the gonads develop. Several genes have been implicated in PGC specification and migration in vertebrates. Additionally, some of the genes associated with pluripotency, such as Oct4 and Nanog, are expressed in PGCs and gonads, suggesting a role for these genes in maintaining pluripotency of the germ lineage, which may be considered the only cell type that perpetually maintains stemness properties. Here, we report that medaka Nanog (Ol-Nanog) is expressed in the developing PGCs. Depletion of Ol-Nanog protein causes aberrant migration of …

Fish ProteinsHomeobox protein NANOGChromatin ImmunoprecipitationReceptors CXCR4endocrine systemCell typeGenotypeOryziasBiologyNanogCxcr4bOpen Reading FramesCell MovementAnimalsPromoter Regions Genetic3' Untranslated RegionsGeneIn Situ Hybridizationreproductive and urinary physiologyHomeodomain ProteinsRegulation of gene expressionMessenger RNABinding SitesReverse Transcriptase Polymerase Chain Reactionurogenital systemThree prime untranslated regionPGCGene Expression Regulation DevelopmentalCell BiologyImmunohistochemistryPhenotypeMolecular biologyChemokine CXCL12MedakaGerm CellsPhenotypeGene Knockdown Techniquesembryonic structuresMolecular Medicinebiological phenomena cell phenomena and immunityChromatin immunoprecipitationDevelopmental BiologyStem Cells
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Nanog Regulates Proliferation During Early Fish Development

2009

Abstract Nanog is involved in controlling pluripotency and differentiation of stem cells in vitro. However, its function in vivo has been studied only in mouse embryos and various reports suggest that Nanog may not be required for the regulation of differentiation. To better understand endogenous Nanog function, more animal models should be introduced to complement the murine model. Here, we have identified the homolog of the mammalian Nanog gene in teleost fish and describe the endogenous expression of Ol-Nanog mRNA and protein during medaka (Oryzias latipes) embryonic development and in the adult gonads. Using medaka fish as a vertebrate model to study Nanog function, we demonstrate that …

Fish ProteinsHomeobox protein NANOGOryziasRex1ProliferationOryziasBiologyNanogPolymerase Chain ReactionGene expressionAnimalsRNA MessengerGonadsTranscription factorIn Situ Hybridizationreproductive and urinary physiologyCell ProliferationHomeodomain ProteinsRegulation of gene expressionCell CycleEmbryogenesisGene Expression Regulation DevelopmentalCell Biologybiology.organism_classificationImmunohistochemistryMolecular biologyMedakaDifferentiationembryonic structuresMolecular Medicinebiological phenomena cell phenomena and immunityStem cellDevelopmental BiologyStem Cells
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Preemptive CD8 T-Cell Immunotherapy of Acute Cytomegalovirus Infection Prevents Lethal Disease, Limits the Burden of Latent Viral Genomes, and Reduce…

1998

ABSTRACT In the immunocompetent host, primary cytomegalovirus (CMV) infection is resolved by the immune response without causing overt disease. The viral genome, however, is not cleared but is maintained in a latent state that entails a risk of virus recurrence and consequent organ disease. By using murine CMV as a model, we have shown previously that multiple organs harbor latent CMV and that reactivation occurs with an incidence that is determined by the viral DNA load in the respective organ (M. J. Reddehase, M. Balthesen, M. Rapp, S. Jonjic, I. Pavic, and U. H. Koszinowski. J. Exp. Med. 179:185–193, 1994). This predicts that a therapeutic intervention capable of limiting the load of lat…

Genes Viralmedicine.medical_treatmentImmunologyViral Pathogenesis and ImmunityGenome ViralCD8-Positive T-LymphocytesBiologymedicine.disease_causeMicrobiologyVirusMiceImmune systemRecurrenceRisk FactorsVirologyVirus latencymedicineAnimalsHumansCytotoxic T cellLungCells CulturedBone Marrow TransplantationMice Inbred BALB CCytomegalovirusImmunotherapyViral Loadmedicine.diseaseVirologyVirus LatencyDisease Models AnimalInsect ScienceAcute DiseaseCytomegalovirus InfectionsDNA ViralImmunologyFemaleImmunotherapyViral loadCD8Journal of Virology
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Disrupting immune regulation incurs transient costs in male reproductive function.

2014

9 pages; International audience; BACKGROUND: Immune protection against pathogenic organisms has been shown to incur costs. Previous studies investigating the cost of immunity have mostly focused on the metabolic requirements of immune maintenance and activation. In addition to these metabolic costs, the immune system can induce damage to the host if the immune response is mis-targeted or over-expressed. Given its non-specific nature, an over-expressed inflammatory response is often associated with substantial damage for the host. Here, we investigated the cost of an over-expressed inflammatory response in the reproductive function of male mice. METHODOLOGY/PRINCIPAL FINDINGS: We experimenta…

Genetics and Molecular Biology (all)0106 biological sciencesMalemedicine.medical_treatmentlcsh:MedicineBiochemistry01 natural sciencesMiceMonoclonalReceptorsTestis[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/Symbiosis[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyReceptors Interleukin-10Animals; Antibodies Monoclonal; Body Weight; Inflammation; Male; Mice; Organ Size; Receptors Interleukin-10; Reproduction; Spermatozoa; Testis; Immunomodulation; Medicine (all); Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)lcsh:ScienceReceptorImmune Response0303 health sciencesMultidisciplinaryReproductive functionMedicine (all)ReproductionAging and ImmunityAntibodies MonoclonalOrgan SizeSpermatozoaInterleukin-103. Good healthCytokineCytokines[SDV.IMM]Life Sciences [q-bio]/Immunologymedicine.symptomResearch ArticleInfertilityEvolutionary ImmunologyImmunologyInflammationBiology010603 evolutionary biologyImmune SuppressionAntibodiesImmunomodulation03 medical and health sciencesImmune systemImmunitymedicineAnimalsBiology030304 developmental biologyInflammationEvolutionary Biology[ SDE.BE ] Environmental Sciences/Biodiversity and Ecologylcsh:RBody WeightImmunityImmunoregulationmedicine.diseaseBlockadeAgricultural and Biological Sciences (all)Immune SystemImmunologyHumoral Immunitylcsh:Q[SDE.BE]Environmental Sciences/Biodiversity and Ecology[SDV.EE.IEO]Life Sciences [q-bio]/Ecology environment/Symbiosis
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RB1 in cancer: Different mechanisms of RB1 inactivation and alterations of pRb pathway in tumorigenesis

2013

Loss of RB1 gene is considered either a causal or an accelerating event in retinoblastoma. A variety of mechanisms inactivates RB1 gene, including intragenic mutations, loss of expression by methylation and chromosomal deletions, with effects which are species-and cell type-specific. RB1 deletion can even lead to aneuploidy thus greatly increasing cancer risk. The RB1gene is part of a larger gene family that includes RBL1 and RBL2, each of the three encoding structurally related proteins indicated as pRb, p107, and p130, respectively. The great interest in these genes and proteins springs from their ability to slow down neoplastic growth. pRb can associate with various proteins by which it …

GeneticsPhysiologyRetinoblastomaClinical BiochemistryCancerCell BiologyBiologymedicine.diseasemedicine.disease_causeE2F Transcription Factor Familyeye diseasesCell biologyRetinoblastoma-like protein 1medicineGene familyGene silencingbiological phenomena cell phenomena and immunityE2FCarcinogenesisJournal of Cellular Physiology
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CENPA overexpression promotes genome instability in pRb-depleted human cells

2009

Abstract Background Aneuploidy is a hallmark of most human cancers that arises as a consequence of chromosomal instability and it is frequently associated with centrosome amplification. Functional inactivation of the Retinoblastoma protein (pRb) has been indicated as a cause promoting chromosomal instability as well centrosome amplification. However, the underlying molecular mechanism still remains to be clarified. Results Here we show that pRb depletion both in wild type and p53 knockout HCT116 cells was associated with the presence of multipolar spindles, anaphase bridges, lagging chromosomes and micronuclei harbouring whole chromosomes. In addition aneuploidy caused by pRb acute loss was…

Genome instabilityCancer ResearchChromosomal Proteins Non-HistoneBlotting WesternBiologyAutoantigensRetinoblastoma Proteinlcsh:RC254-282Genomic InstabilityRNA interferenceChromosome instabilityCentromere Protein ACell Line TumorHumansRNA Processing Post-TranscriptionalDNA PrimersCENPABase SequenceReverse Transcriptase Polymerase Chain ReactionResearchRetinoblastoma proteincentromere protein aneuploidy pRBlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMolecular biologyCell biologySettore BIO/18 - GeneticaSpindle checkpointOncologyMicroscopy FluorescenceCentrosomebiology.proteinMolecular MedicineRNA Interferencebiological phenomena cell phenomena and immunityCentromere Protein AMolecular Cancer
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