Search results for " immune system"

showing 10 items of 893 documents

Liver-primed memory T cells generated under noninflammatory conditions provide anti-infectious immunity.

2013

SummaryDevelopment of CD8+ T cell (CTL) immunity or tolerance is linked to the conditions during T cell priming. Dendritic cells (DCs) matured during inflammation generate effector/memory T cells, whereas immature DCs cause T cell deletion/anergy. We identify a third outcome of T cell priming in absence of inflammation enabled by cross-presenting liver sinusoidal endothelial cells. Such priming generated memory T cells that were spared from deletion by immature DCs. Similar to central memory T cells, liver-primed T cells differentiated into effector CTLs upon antigen re-encounter on matured DCs even after prolonged absence of antigen. Their reactivation required combinatorial signaling thro…

T cellReceptors Antigen T-CellPriming (immunology)chemical and pharmacologic phenomenaBiologyCD8-Positive T-LymphocytesLymphocyte ActivationGeneral Biochemistry Genetics and Molecular BiologyMiceCross-PrimingAntigenCD28 AntigensmedicineAnimalslcsh:QH301-705.5Innate immune systemGene Expression ProfilingT-cell receptorReceptors Interleukin-12CD28Endothelial Cellshemic and immune systemsDendritic CellsAcquired immune systemListeria monocytogenesImmunity InnateNeuropilin-1Mice Inbred C57BLmedicine.anatomical_structurelcsh:Biology (General)LiverImmunologyImmunologic MemoryCD8Cell reports
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Macrophages are dispensable for superantigen-mediated stimulation and anergy induction of peripheral T cells in vivo.

1994

Bacterial superantigens provoke T lymphocyte activation by cross-linking the variable part of the T cell receptor (TCR) beta-chain with MHC class II molecules on antigen-presenting cells. Although the molecular mechanisms of this interaction are well characterized, the in vivo accessory cell requirements for this stimulation of T lymphocytes by bacterial superantigens remain unknown. In the present study we have addressed the role of splenic macrophages in the activation of V beta 8+ peripheral T cells by staphylococcal enterotoxin B (SEB) in BALB/c mice. SEB-triggered clonal expansion and subsequent induction of unresponsiveness of both CD4+ and CD8+ T cells were investigated in naive anim…

T cellT-LymphocytesImmunologyAntigen-Presenting Cellschemical and pharmacologic phenomenaSpleenCell CommunicationEnterotoxinsMiceSuperantigenmedicineCytotoxic T cellAnimalsAntigen-presenting cellClonal AnergyMHC class IIMice Inbred BALB CSuperantigensbiologyMacrophagesT-cell receptorhemic and immune systemsFlow CytometryMolecular biologymedicine.anatomical_structureImmunologybiology.proteinInterleukin-2CD8Cell DivisionCellular immunology
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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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A Superantigen as Virulence Factor in an Acute Bacterial Infection

1994

This study addresses the role of a bacterial superantigen as a potential virulence factor during an acute systemic infection. BALB/c mice were intravenously infected with a recombinant Staphylococcus aureus strain capable of producing plasmid-encoded staphylococcal enterotoxin B (SEB) or with the SEB plasmid-deficient parental strain. Infection with SEB-producing bacteria resulted in an initial expansion and subsequent decrease of circulating V beta 8+ T lymphocytes. This numeric decrease was accompanied by a SEB-specific state of hyporesponsiveness of splenic T cells. In parallel with SEB-triggered unresponsiveness of a large proportion of T lymphocytes, a weakening of the overall T cell r…

T-LymphocytesT cellVirulencechemical and pharmacologic phenomenaEnterotoxinmedicine.disease_causeVirulence factorMicrobiologyEnterotoxinsMiceSuperantigenmedicineAnimalsImmunology and AllergyAntigens BacterialMice Inbred BALB CSuperantigensVirulencebiologyhemic and immune systemsT lymphocyteStaphylococcal Infectionsbiology.organism_classificationbiological factorsInfectious Diseasesmedicine.anatomical_structureOrgan SpecificityStaphylococcus aureusAcute DiseaseImmunologyBacteriaThe Journal of Infectious Diseases
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Host immune response to Cryptosporidium parvum infection

2010

Species of the genus Cryptosporidium are protozoan parasites (Apicomplexa) that cause gastroenteritis in animals and humans. Of these Cryptosporidium parvum and Cryptosporidium hominis are the major causative agents of human cryptosporidiosis. Whereas infection is self-limiting in the immunocompetent hosts, immunocompromised individuals develop a chronic, life-threatening disease. As specific therapeutic or preventive interventions are not yet available, better understanding of the immune response to the parasite is required. This minireview briefly summarizes the factors involved in the innate and acquired immune response in this pathogen-host interaction with an emphasis on more recent da…

T-Lymphocytesanimal diseasesAIDS-Related Opportunistic InfectionsImmunologyAntibodies ProtozoanCryptosporidiosisAdaptive ImmunityBiologyNitric OxideImmunocompromised HostMiceImmune systemIntestinal mucosaImmunityparasitic diseasesAnimalsHumansIntestinal MucosaCryptosporidium parvumB-LymphocytesPhagocytesAIDS-Related Opportunistic InfectionsComplement System ProteinsDendritic CellsGeneral MedicineAcquired immune systembiology.organism_classificationVirologyImmunity InnateKiller Cells NaturalDisease Models AnimalInfectious DiseasesCryptosporidium parvumImmunologyCytokinesParasitologyImmunocompetenceImmunocompetenceCryptosporidium hominisExperimental Parasitology
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Different Efficiency of Heat Shock Proteins (HSP) to Activate Human Monocytes and Dendritic Cells: Superiority of HSP60

2002

Abstract One essential immunoregulatory function of heat shock protein (HSP) is activation of the innate immune system. We investigated the activation of human monocytes and monocyte-derived dendritic cells (DC) by recombinant human HSP60, human inducible HSP72, and preparations of human gp96 and HSP70 under stringent conditions, in the absence of serum and with highly purified monocytes. HSP60 induced human DC maturation and activated human DC to secrete proinflammatory cytokines. HSP72 induced DC maturation to a lesser extent, but activated human monocytes and immature DC as efficiently as HSP60 to release proinflammatory cytokines. The independence of the effects of HSP60 and HSP72 from …

T-Lymphocytesmedicine.medical_treatmentImmunologyHSP72 Heat-Shock ProteinsPeptide bindingBiologyLymphocyte ActivationMonocytesProinflammatory cytokineAntigens NeoplasmHeat shock proteinmedicineHumansImmunology and AllergyHSP70 Heat-Shock ProteinsSecretionHeat-Shock ProteinsInnate immune systemCell DifferentiationChaperonin 60Dendritic CellsMolecular biologyCoculture TechniquesRecombinant ProteinsHsp70CytokineCytokinesHSP60Inflammation MediatorsSignal TransductionThe Journal of Immunology
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Shared determinants between virus-infected and trinitrophenyl-conjugated H-2-identical target cells detected in cell-mediated lympholysis

1976

Infection of H-2-identical mice with either lymphocytic choriomeningitis (LCM) virus, vaccinia virus, or paramyxo (Sendai) virus resulted in the generation of specifically sensitized cytotoxic T lymphocytes (CTL). CTL generated in vitro against 2,4,6-trinitrophenyl (TNP)-conjugated syngeneic stimulator cells were specifically cytotoxic for TNP-conjugated H-2K (D) region identical targets. Both LCM and vaccinia-induced CTL, however, were found to be strongly cytotoxic towards TNP-conjugated, H-2K(D) region-identical target cells. In contrast, Sendai virus-induced CTL did not lyse TNP-conjugated, syngeneic target cells. Inhibition experiments using cold targets suggested that shared antigenic…

T-LymphocytesvirusesImmunologyMice Inbred StrainsVaccinia viruschemical and pharmacologic phenomenaCross ReactionsBiologyLymphocytic choriomeningitisVirusEpitopeEpitopesMicechemistry.chemical_compoundAntigenHistocompatibility AntigensmedicineAnimalsLymphocytic choriomeningitis virusImmunology and AllergyCytotoxic T cellCells CulturedNitrobenzeneshemic and immune systemsCytotoxicity Tests Immunologicmedicine.diseaseVirologyIn vitroParainfluenza Virus 1 HumanCold TemperatureCTL*chemistryTrinitrobenzenesVacciniaEuropean Journal of Immunology
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