Search results for "MICE"

showing 10 items of 6027 documents

Enhanced dendritic cell maturation by TNF-alpha or cytidine-phosphate-guanosine DNA drives T cell activation in vitro and therapeutic anti-tumor immu…

2000

Abstract Dendritic cells (DC) manipulated ex vivo can induce tumor immunity in experimental murine tumor models. To improve DC-based tumor vaccination, we studied whether DC maturation affects the T cell-activating potential in vitro and the induction of tumor immunity in vivo. Maturation of murine bone marrow-derived DC was induced by GM-CSF plus IL-4 alone or by further addition of TNF-α or a cytidine-phosphate-guanosine (CpG)-containing oligonucleotide (ODN-1826), which mimics the immunostimulatory effect of bacterial DNA. Flow cytometric analysis of costimulatory molecules and MHC class II showed that DC maturation was stimulated most by ODN-1826, whereas TNF-α had an intermediate effec…

T cellT-LymphocytesImmunologyAntineoplastic AgentsCell CommunicationBiologyLymphocyte ActivationImmunotherapy AdoptiveMiceImmune systemAdjuvants ImmunologicIn vivomedicineTumor Cells CulturedImmunology and AllergyAnimalsInterleukin 4Cells CulturedMice Inbred BALB CTumor Necrosis Factor-alphaCell DifferentiationDendritic cellDendritic CellsMolecular biologyInterleukin-12Coculture TechniquesGrowth InhibitorsMice Inbred C57BLmedicine.anatomical_structureOligodeoxyribonucleotidesColonic NeoplasmsInterleukin 12Cancer researchTumor necrosis factor alphaCpG IslandsFemaleInterleukin-4Ex vivoNeoplasm TransplantationJournal of immunology (Baltimore, Md. : 1950)
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Intrahepatic myeloid-cell aggregates enable local proliferation of CD8+T cells and successful immunotherapy against chronic viral liver infection

2013

Chronic infection is difficult to overcome because of exhaustion or depletion of cytotoxic effector CD8(+) T cells (cytotoxic T lymphoytes (CTLs)). Here we report that signaling via Toll-like receptors (TLRs) induced intrahepatic aggregates of myeloid cells that enabled the population expansion of CTLs (iMATEs: 'intrahepatic myeloid-cell aggregates for T cell population expansion') without causing immunopathology. In the liver, CTL proliferation was restricted to iMATEs that were composed of inflammatory monocyte-derived CD11b(+) cells. Signaling via tumor-necrosis factor (TNF) caused iMATE formation that facilitated costimulation dependent on the receptor OX40 for expansion of the CTL popu…

T cellmedicine.medical_treatmentImmunologyPopulationGreen Fluorescent ProteinsMice TransgenicBiologyCD8-Positive T-LymphocytesLymphocytic ChoriomeningitisMicemedicineImmunology and AllergyCytotoxic T cellAnimalsLymphocytic choriomeningitis virusMyeloid CellseducationCell ProliferationMice Knockouteducation.field_of_studyLiver infectionCD11b AntigenMicroscopy ConfocalLiver DiseasesImmunotherapyReceptors OX40Flow CytometryMice Inbred C57BLCTL*Chronic infectionmedicine.anatomical_structureAnimals NewbornLiverToll-Like Receptor 9ImmunologyChronic DiseaseHost-Pathogen InteractionsImmunotherapyCD8Signal TransductionT-Lymphocytes CytotoxicNature Immunology
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Efficient homologous prime-boost strategies for T cell vaccination based on virus-like particles.

2005

Induction of high frequencies of specific T cells by vaccination requires prime-boost regimens. To reach optimal immune responses, it is necessary to use different vectors for priming and boosting as e.g. DNA vaccination followed by boosting with a recombinant viral vector. Here, we show that vaccines based on virus-like particles (VLP) displaying peptide epitopes are equally effective to induce CTL responses if used in a homologous or heterologous prime-boost setting. Strikingly, high frequencies (>20% of CD8(+) cells) of protective CTL could be induced and maintained by weekly injection of VLP. Thus, the use of VLP may avoid the requirement for complicated heterologous prime-boost regi…

T cellvirusesT-LymphocytesImmunologyT-cell vaccinationPriming (immunology)HeterologousEpitopes T-LymphocyteVaccinia virusBiologycomplex mixturesEpitopeViral vectorDNA vaccinationMicemedicineVaccines DNAVacciniaImmunology and AllergyAnimalsVaccinationVirionViral VaccinesVirologyHepatitis B Core AntigensCTL*medicine.anatomical_structureImmunologyCpG IslandsFemale
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An innate cell-mediated, murine ulcerative colitis-like syndrome in the absence of nuclear factor of activated T cells.

2004

Abstract Background & Aims: Nuclear factor of activated T cells transcription factors plays a central role in immunity by regulating the expression of multiple cytokines and other regulatory molecules, many of which have been heavily implicated in the pathogenesis of inflammatory bowel disease. However, few studies have directly investigated the nuclear factor of activated T cells proteins in inflammatory bowel disease. We describe here a specific role for nuclear factor of activated T cells c2 in the pathogenesis of murine inflammatory bowel disease. Methods: Mice deficient for nuclear factor of activated T cells c2, recombinase activating gene-2, or both and transgenic or nontransgenic fo…

T-LymphocytesBiologyInterleukin 21MicemedicineImmune ToleranceCytotoxic T cellAnimalsIL-2 receptorB-LymphocytesImmunity CellularMice Inbred BALB CHepatologyNFATC Transcription FactorsZAP70Innate lymphoid cellGastroenterologyNuclear ProteinsT helper cellRectal ProlapseNatural killer T cellAcquired immune systemMice Mutant StrainsDNA-Binding ProteinsMice Inbred C57BLmedicine.anatomical_structureImmunologyCancer researchColitis UlcerativeTranscription FactorsGastroenterology
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CD4+CD25+ regulatory T cells suppress mast cell degranulation and allergic responses through OX40-OX40L interaction.

2008

T regulatory (Treg) cells play a role in the suppression of immune responses, thus serving to induce tolerance and control autoimmunity. Here, we explored whether Treg cells influence the immediate hypersensitivity response of mast cells (MCs). Treg cells directly inhibited the FcεRI-dependent MC degranulation through cell-cell contact involving OX40-OX40L interactions between Treg cells and MCs, respectively. When activated in the presence of Treg cells, MCs showed increased cyclic adenosine monophosphate (cAMP) concentrations and reduced Ca2+ influx, independently of phospholipase C (PLC)-γ2 or Ca2+ release from intracellular stores. Antagonism of cAMP in MCs reversed the inhibitory effec…

T-LymphocytesCELLIMMUNO; Animals; Calcium; Cell Line Tumor; Gene Knockdown Techniques; Histamine Release; Humans; Hypersensitivity; Mast Cells; Membrane Glycoproteins; Mice; Mice Inbred BALB C; Mice Inbred C57BL; Phospholipase C gamma; Receptors OX40; T-Lymphocytes Regulatory; Tumor Necrosis Factors; Cell Degranulation; Immunology and Allergy; Infectious Diseases; ImmunologyInbred C57BLmedicine.disease_causeHistamine ReleaseT-Lymphocytes RegulatoryCell DegranulationAutoimmunityMicechemistry.chemical_compoundReceptorsImmunology and AllergyOX40Mast CellsInbred BALB CMice Inbred BALB CTumorMembrane GlycoproteinsDegranulationhemic and immune systemsRegulatoryhumanitiesCell biologyTregInfectious DiseasesGene Knockdown TechniquesTumor Necrosis FactorsMembrane GlycoproteinMast cell; Treg; OX40-OX40L interactionIntracellularHumanCell DegranulationImmunologyInfectious Diseasechemical and pharmacologic phenomenaBiologybehavioral disciplines and activitiesArticleCell LineMast cellImmune systemCell Line TumorHypersensitivitymedicineAnimalsHumansCyclic adenosine monophosphatePhospholipase CAnimalPhospholipase C gammaReceptors OX40Mice Inbred C57BLchemistryCELLIMMUNOCell cultureGene Knockdown TechniqueImmunologyOX40-OX40L interactionCalciumTumor Necrosis Factor
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Unexpected Modulation of Recall B and T Cell Responses after Immunization with Rotavirus-like Particles in the Presence of LT-R192G

2010

LT-R192G, a mutant of the thermolabile enterotoxin of E. coli, is a potent adjuvant of immunization. Immune responses are generally analyzed at the end of protocols including at least 2 administrations, but rarely after a prime. To investigate this point, we compared B and T cell responses in mice after one and two intrarectal immunizations with 2/6 rotavirus-like particles (2/6-VLP) and LT-R192G. After a boost, we found, an unexpected lower B cell expansion measured by flow cytometry, despite a secondary antibody response. We then analyzed CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs) and CD4(+)CD25(+)Foxp3(-) helper T cells after in vitro (re)stimulation of mesenteric lymph node cells …

T-LymphocytesHealth Toxicology and Mutagenesismedicine.medical_treatmentT cellBacterial ToxinsDose-Response Relationship Immunologiclcsh:Medicinechemical and pharmacologic phenomenaBiologyToxicologyArticleregulatory T cellsEnterotoxinsMiceInterleukin 21Immune systemB-1a lymphocyteAdjuvants ImmunologicAntigenmedicineAnimalsIL-2 receptorCD25B cellB-LymphocytesMice Inbred BALB CB lymphocytemucosal immunizationEscherichia coli Proteinslcsh:RRotavirus VaccinesVirionFOXP3LT-R192Ghemic and immune systemsrotavirusmedicine.anatomical_structureFoxp3ImmunologyFemaleImmunizationAdjuvantToxins
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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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NFATc1 affects mouse splenic B cell function by controlling the calcineurin–NFAT signaling network

2011

Mouse B cells lacking NFATc1 exhibit defective proliferation, survival, isotype class switching, cytokine production, and T cell help.

T-LymphocytesImmunologyNaive B cellB-cell receptorReceptors Antigen B-CellLymphocyte ActivationArticleMice03 medical and health sciences0302 clinical medicinemedicineAnimalsImmunology and AllergyB cell030304 developmental biologyB-Lymphocytes0303 health sciencesCD40NFATC Transcription Factorsintegumentary systembiologyCalcineurinCD22Germinal centerImmunoglobulin Class SwitchingMolecular biology3. Good healthB-1 cellCalcineurinmedicine.anatomical_structure030220 oncology & carcinogenesisCancer researchbiology.proteinCalciumSpleenSignal TransductionJournal of Experimental Medicine
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New therapies for sepsis: focus on the interleukin (IL)12 family member IL27

2007

Sepsis is a severe complication of abdominal infections such as peritonitis and is associated with high mortality. Unfortunately, the molecular mechanisms controlling the development of sepsis are still incompletely understood. Interestingly, the interleukin (IL) 12 family member IL27 seems to play a key role in sepsis. In a murine model of septic peritonitis induced by caecal ligation and puncture (CLP), IL27 levels were found to be strongly induced. Furthermore, mice deficient for the EBI3 subunit of IL27 were resistant to CLP-induced septic peritonitis as compared to wild-type controls. This effect could be suppressed by injection of recombinant IL27. Further studies demonstrated that IL…

T-LymphocytesImmunologyPeritonitisPeritonitisGeneral Biochemistry Genetics and Molecular BiologySepsisMiceRheumatologySepsismedicineAnimalsHumansImmunology and AllergyInterleukin 27business.industryInterleukin-17InterleukinCell DifferentiationEBI3medicine.diseaseBlockadeDisease Models AnimalImmunologyInterleukin 12ImmunotherapyInterleukin 17Reactive Oxygen SpeciesbusinessSupplementAnnals of the Rheumatic Diseases
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Primary in vivo T cell reactivity of NZB grafts in H-2 identical allogenic hosts.

1983

By means of the Simonson GVH-assay and the popliteal lymph node (PLN) assay, the T-cell reactivity of NZB mice against H-2 identical allogenic cells was investigated in vivo and compared to that of normal mice. None of the normal mice did react, but a highly significant NZB response could be demonstrated, which did not depend on differences in Mls antigens. These in vivo results extend previous findings of a T-cell hyperreactivity of NZB mice in primary in vitro reactions. They favour the possibility that the T-cell hyperreactivity might be relevant in vivo in facilitating autoimmune responses.

T-LymphocytesImmunologychemical and pharmacologic phenomenaAutoimmune responsesBiologySerologyAutoimmune DiseasesMinor Lymphocyte Stimulatory AntigensGraft vs Host ReactionMiceIn vivoImmunology and AllergyAnimalsLymphocytesMice Inbred BALB CMice Inbred NZBH-2 AntigensT cell reactivityHematologyOrgan SizeIn vitroTransplantationMice Inbred C57BLKineticsLiverMice Inbred DBALymphocyte TransfusionImmunologyPopliteal Lymph NodeSpleenImmunobiology
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