Search results for "Bone Marrow"

showing 10 items of 538 documents

Evidence against a key role for transforming growth factor-beta1 in cytomegalovirus-induced bone marrow aplasia.

1998

During immunodeficiency after sublethal haematoablative treatment, cytomegalovirus (CMV) infection interferes with haematopoietic reconstitution and can cause lethal bone marrow (BM) aplasia. The in vivo model of murine CMV infection has identified the BM stroma as the principal target site of CMV in the haematopoietic cord. The infected cell type is the reticular stromal cell which forms the stromal network and produces essential haemopoietins, such as stem-cell factor (SCF). The expression of SCF was found to be reduced in the infected stroma, but the stromal network was not disrupted and the number of infected stromal cells was too low to explain the functional deficiency. These facts ca…

Stromal cellmedicine.medical_treatmentCytomegalovirusGene ExpressionBone Marrow CellsBone Marrow AplasiaCD8-Positive T-LymphocytesKidneyVirus ReplicationMiceTransforming Growth Factor betaVirologymedicineAnimalsCytotoxic T cellBone Marrow DiseasesBone Marrow TransplantationMice Inbred BALB CbiologyTransforming growth factor betaVirologyHematopoiesisHaematopoiesisCytokinemedicine.anatomical_structureLiverCytomegalovirus Infectionsbiology.proteinFemaleImmunotherapyBone marrowStromal CellsTransforming growth factorJournal of General Virology
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Interferon-alpha (IFN-alpha) inhibits granulocyte-macrophage colony-stimulating factor (GM-CSF) expression at the post-transcriptional level in murin…

1995

Recently it has been shown that IFN-alpha inhibits expression of GM-CSF in adherent cells of human long-term bone marrow cultures (LTBMC) stimulated with interleukin-1 (IL-1), tumour necrosis factor-alpha (TNF-alpha) or endotoxin. The murine bone marrow stromal cell line +/+(-1).LDA11 was used to further define regulatory mechanisms of IFN-alpha inhibition on GM-CSF expression. This cell line originated from a murine Dexter type culture and exhibits a preadipocytic phenotype. As in human LTBMC, we could demonstrate a inhibitory effect of IFN-alpha co-incubation on GM-CSF activity in serum-free supernatants of +/+(-1).LDA11 stromal cell cultures stimulated with IL-1 or TNF-alpha or the combi…

Stromal cellmedicine.medical_treatmentDose-Response Relationship ImmunologicDown-RegulationBone Marrow CellsBiologyTransfectionCell LineMiceGene expressionmedicineAnimalsInterferon gammaNorthern blotRNA MessengerRNA Processing Post-TranscriptionalTumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating FactorHematologyMolecular biologyRecombinant Proteinsmedicine.anatomical_structureCytokineGranulocyte macrophage colony-stimulating factorCell cultureImmunologyInterferon Type IBone marrowStromal Cellsmedicine.drugInterleukin-1British journal of haematology
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Type-I interferons are potent inhibitors of interleukin-8 production in hematopoietic and bone marrow stromal cells

1993

Abstract nterleukin-8 (IL-8) is produced by many cell types upon stimulation with bacterial products or inflammation-associated cytokines such as tumor necrosis factor-alpha and IL-1. Interferons (IFNs) represent another group of cytokines that are induced by similar stimuli in inflammatory reactions. We show now that type-I IFNs are potent inhibitors of IL-8 expression in vitro and in vivo. A significant reduction of both secretion of IL-8 protein and accumulation of IL-8 mRNA in vitro was observed in several cell types comprising peripheral blood mononuclear cells (PBMNC) from healthy donors and from patients with chronic myelogenous leukemia (CML), the myelomonocytic cell line THP-1, and…

Stromal cellmedicine.medical_treatmentImmunologyCell BiologyHematologyBiologymedicine.diseaseBiochemistryPeripheral blood mononuclear cellHaematopoiesisLeukemiaCytokinemedicine.anatomical_structureInterferonImmunologymedicineCancer researchBone marrowChronic myelogenous leukemiamedicine.drugBlood
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Synergistic activation of dendritic cells by combined Toll-like receptor ligation induces superior CTL responses in vivo.

2006

Toll-like receptors (TLRs) are able to interact with pathogen-derived products and their signals induce the coordinated activation of innate and adaptive immune mechanisms. Dendritic cells (DCs) play a central role in these events. As the different TLRs are able to trigger MyD88/TRIF-dependent and -independent signaling pathways, we wondered if the simultaneous activation of these signaling cascades would synergize with respect to DC activation and induce superior cytotoxic T-lymphocyte (CTL) activity in vivo. We observed that indeed the combined activation of MyD88-dependent and -independent signaling induced by TLR7 and TLR3 ligands provoked a more rapid and more sustained bone marrow–der…

T-LymphocytesImmunologyBone Marrow CellsBiologyLigandsBiochemistryT-Lymphocytes RegulatoryMiceCytotoxic T cellAnimalsAntigen-presenting cellAdaptor Proteins Signal TransducingCD86Toll-like receptorCD40Membrane GlycoproteinsToll-Like ReceptorsImmunityhemic and immune systemsCell BiologyHematologyDendritic cellDendritic CellsAcquired immune systemCell biologyToll-Like Receptor 3Mice Inbred C57BLCTL*Toll-Like Receptor 7ImmunologyMyeloid Differentiation Factor 88biology.proteinSignal TransductionT-Lymphocytes CytotoxicBlood
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Dendritic cell aggresome-like-induced structure formation and delayed antigen presentation coincide in influenza virus-infected dendritic cells.

2005

Abstract Influenza virus infection induces maturation of murine dendritic cells (DCs), which is most important for the initiation of an immune response. However, in contrast to EL-4 and MC57 cells, DCs present viral CTL epitopes with a delay of up to 10 h. This delay in Ag presentation coincides with the up-regulation of MHC class I molecules as well as costimulatory molecules on the cell surface and the accumulation of newly synthesized ubiquitinated proteins in large cytosolic structures, called DC aggresome-like-induced structures (DALIS). These structures were observed previously after LPS-induced maturation of DCs, and it was speculated that they play a role in the regulation of MHC cl…

Time FactorsImmunologyAntigen presentationCellAntigen-Presenting CellsEpitopes T-Lymphocytechemical and pharmacologic phenomenaBone Marrow CellsVirusCell LineMiceImmune systemCell Line TumorMHC class ImedicineImmunology and AllergyAnimalsHumansReceptors ImmunologicCells CulturedAntigen PresentationMice Inbred C3HbiologyUbiquitinViral Core ProteinsRNA-Binding ProteinsCell DifferentiationDendritic cellDendritic CellsNucleocapsid ProteinsVirologyToll-Like Receptor 2Cell biologyNucleoproteinMice Inbred C57BLToll-Like Receptor 4Aggresomemedicine.anatomical_structureNucleoproteinsInfluenza A virusbiology.proteinCytoplasmic StructuresT-Lymphocytes CytotoxicJournal of immunology (Baltimore, Md. : 1950)
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The aryl hydrocarbon receptor modulates acute and late mast cell responses.

2012

Abstract The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor whose activity is modulated by xenobiotics as well as physiological ligands. These compounds may modulate inflammatory responses and contribute to the rising prevalence of allergic diseases observed in industrialized countries. Mast cells (MCs), located within tissues at the boundary of the external environment, represent a potential target of AhR ligands. In this study, we report that murine and human MCs constitutively express AhR, and its activation by the high-affinity ligand 6-formylindolo[3,2-b]carbazole (FICZ) determines a boost in degranulation. On the contrary, repeated exposure to FICZ inhibits…

Time FactorsInbred C57BLLigandsCell DegranulationPathogenesischemistry.chemical_compoundMiceAnaphylaxiReceptorsMast CellImmunology and AllergyMast CellsReceptorMice KnockoutbiologyInterleukin-17DegranulationMast cellUp-RegulationImmunology Mast Cell Aryl Receptormedicine.anatomical_structureAryl HydrocarbonBone Marrow Celldeficiency/metabolism/physiologyIgEmedicine.symptomimmunology/metabolism/pathologyHistamineHumanReceptorTime FactorKnockoutImmunologyDown-RegulationLigandInflammationBone Marrow CellsSettore MED/08 - Anatomia PatologicaCell LinebiosynthesiAnaphylaxis; immunology/metabolism/pathology Animals Bone Marrow Cells; immunology/metabolism/pathology Cell Degranulation; genetics/immunology Cell Line Down-Regulation; genetics/immunology Humans Interleukin-17; biosynthesis Interleukin-6; biosynthesis Ligands Mast Cells; immunology/metabolism/pathology Mice Mice; Inbred C57BL Mice; Knockout Receptors; Aryl Hydrocarbon; deficiency/metabolism/physiology Receptors; IgE; physiology Time Factors Up-Regulation; genetics/immunologymedicineAnimalsHumansTranscription factorAnaphylaxisAnimalInterleukin-6Receptors IgEAryl hydrocarbon receptorgenetics/immunologyMice Inbred C57BLMAST CELL; ARYL HYDROCARBON RECEPTORchemistryReceptors Aryl HydrocarbonImmunologyphysiologybiology.proteinbiosynthesisJournal of immunology (Baltimore, Md. : 1950)
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Characterization of lymphokine-mediated activation of macrophages for antigen presentation: studies with long-term cultured bone marrow-derived macro…

1984

In cultures of bone marrow (BM) supplemented with L cell-derived colony-stimulating factor a pure population of macrophages (M phi) differentiates, which can be further propagated with a doubling time of 3.8 days. "Young" BMM phi obtained on day 8 of culture were shown to act as antigen-presenting cells inducing the antigen-specific proliferation of the cloned T cell line ST2/K.9, whereas "old" M phi had lost this ability. However, at any time tested (up to 132 days) the presentation function of old BMM phi could be completely restored by pulsing the cells with lymphokines (LK). A duration of 11 hr for the LK-pulse was sufficient to trigger the M phi to exert an optimal presentation functio…

Time FactorsT cellT-LymphocytesImmunologyPopulationAntigen presentationAntigen-Presenting CellsBone Marrow CellsBiologyLymphocyte ActivationInterferon-gammaMiceImmune systemAntigenmedicineImmunology and AllergyDoubling timeAnimalseducationCells Culturededucation.field_of_studyLymphokinesLymphokineHematologyMacrophage ActivationMolecular biologymedicine.anatomical_structureImmunologyBone marrowImmunobiology
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The TH1 Lymphokine Interferon-γ is a Potent Upregulator of Dendritic Cells with Phagocytic Capacity in GM-CSF Supplemented Bone Marrow Cultures

1997

Myeloid dendritic cells (DC), macrophages and granulocytes are descendants of a hematopoietic progenitor cell that originates in the bone marrow1. Thus, bone marrow derived cells distributed in tissue culture in the presence of GM-CSF give rise to the three leukocyte populations which under various in vitro culture conditions proceed in differentiation and phenotypic maturation2–7.

Tissue culturemedicine.anatomical_structureMyeloidChemistryCellImmunologymedicineLymphokineDendritic cellBone marrowMolecular biologyPhenotypeIn vitro
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Immune Evasion Proteins Enhance Cytomegalovirus Latency in the Lungs

2009

ABSTRACT CD8 T cells control cytomegalovirus (CMV) infection in bone marrow transplantation recipients and persist in latently infected lungs as effector memory cells for continuous sensing of reactivated viral gene expression. Here we have addressed the question of whether viral immunoevasins, glycoproteins that specifically interfere with antigen presentation to CD8 T cells, have an impact on viral latency in the murine model. The data show that deletion of immunoevasin genes in murine CMV accelerates the clearance of productive infection during hematopoietic reconstitution and leads to a reduced latent viral genome load, reduced latency-associated viral transcription, and a lower inciden…

Transcription GeneticImmunologyAntigen presentationAntigen-Presenting CellsCytomegalovirusBone Marrow CellsGenome ViralCD8-Positive T-LymphocytesBiologymedicine.disease_causeMicrobiologyHerpesviridaeVirusMiceImmune systemRecurrenceVirologyVirus latencymedicineAnimalsCytotoxic T cellAntigen-presenting cellLungGlycoproteinsMice Inbred BALB Cmedicine.diseaseVirologyVirus LatencyInsect ScienceCytomegalovirus InfectionsImmunologyPathogenesis and ImmunityFemaleViral diseaseJournal of Virology
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CD8 T Cells Control Cytomegalovirus Latency by Epitope-Specific Sensing of Transcriptional Reactivation

2006

ABSTRACT During murine cytomegalovirus (mCMV) latency in the lungs, most of the viral genomes are transcriptionally silent at the major immediate-early locus, but rare and stochastic episodes of desilencing lead to the expression of IE1 transcripts. This low-frequency but perpetual expression is accompanied by an activation of lung-resident effector-memory CD8 T cells specific for the antigenic peptide 168-YPHFMPTNL-176, which is derivedfrom the IE1 protein. These molecular and immunological findings were combined in the “silencing/desilencing and immune sensing hypothesis” of cytomegalovirus latency and reactivation. This hypothesis proposes that IE1 gene expression proceeds to cell surfac…

Transcriptional ActivationMuromegalovirusvirusesImmunologyAntigen presentationCD8-Positive T-LymphocytesVirus ReplicationMajor histocompatibility complexModels BiologicalMicrobiologyEpitopeImmediate-Early ProteinsEpitopesImmunocompromised HostMiceAntigenVirologyMHC class IVirus latencymedicineAnimalsGene silencingCytotoxic T cellAmino Acid SequenceAntigens ViralLungBone Marrow TransplantationMice Inbred BALB CBase Sequencebiologyvirus diseasesHerpesviridae Infectionsbiochemical phenomena metabolism and nutritionmedicine.diseaseVirologyMolecular biologyVirus LatencyVirus-Cell InteractionsPhenotypeAmino Acid SubstitutionInsect ScienceDNA ViralMutagenesis Site-DirectedTrans-Activatorsbiology.proteinFemaleJournal of Virology
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