Search results for "INTERFERON-GAMMA"

showing 10 items of 352 documents

IL-23-mediated mononuclear phagocyte crosstalk protects mice from Citrobacter rodentium-induced colon immunopathology.

2014

Gut homeostasis and mucosal immune defense rely on the differential contributions of dendritic cells (DC) and macrophages. Here we show that colonic CX3CR1+ mononuclear phagocytes are critical inducers of the innate response to Citrobacter rodentium infection. Specifically, the absence of IL-23 expression in macrophages or CD11b+ DC results in the impairment of IL-22 production and in acute lethality. Highlighting immunopathology as a death cause, infected animals are rescued by the neutralization of IL-12 or IFNγ. Moreover, mice are also protected when the CD103+ CD11b− DC compartment is rendered deficient for IL-12 production. We show that IL-12 production by colonic CD103+ CD11b− DC is r…

ChemokineColonCX3C Chemokine Receptor 1General Physics and Astronomychemical and pharmacologic phenomenaMice TransgenicInterleukin-23General Biochemistry Genetics and Molecular BiologyMonocytesArticleMicrobiologyInterferon-gammaMiceIntestinal mucosaAntigens CDImmunopathologyCitrobacter rodentiummedicineAnimalsHomeostasisInterferon gammaIntestinal MucosaImmunity MucosalMultidisciplinaryCD11b AntigenbiologyInterleukinsMacrophagesEnterobacteriaceae InfectionsGeneral ChemistryMononuclear phagocyte systemDendritic CellsInterleukin-12Survival AnalysisImmunity InnateIntegrin alpha MGene Expression RegulationImmunologyInterleukin 12biology.proteinCitrobacter rodentiumTh17 CellsReceptors ChemokineIntegrin alpha Chainsmedicine.drugSignal TransductionNature communications
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Influenza A virus infection inhibits the efficient recruitment of Th2 cells into the airways and the development of airway eosinophilia.

2003

Abstract Most infections with respiratory viruses induce Th1 responses characterized by the generation of Th1 and CD8+ T cells secreting IFN-γ, which in turn have been shown to inhibit the development of Th2 cells. Therefore, it could be expected that respiratory viral infections mediate protection against asthma. However, the opposite seems to be true, because viral infections are often associated with the exacerbation of asthma. For this reason, we investigated what effect an influenza A (flu) virus infection has on the development of asthma. We found that flu infection 1, 3, 6, or 9 wk before allergen airway challenge resulted in a strong suppression of allergen-induced airway eosinophil…

ChemokineEpitopes T-LymphocyteImmunoglobulin Emedicine.disease_causeMiceCell MovementInfluenza A virusImmunology and AllergyEosinophiliaChemokine CCL5LungCells CulturedChemokine CCL2Mice KnockoutMice Inbred BALB Cbiologymedicine.diagnostic_testrespiratory systemUp-Regulationmedicine.anatomical_structureInfluenza A virusChemokines CCGoblet CellsNippostrongylusmedicine.symptomBronchial HyperreactivityChemokine CCL11OvalbuminImmunologyDown-RegulationMice TransgenicCCL5VirusInterferon-gammaTh2 CellsOrthomyxoviridae InfectionsLymphopeniamedicineAnimalsLymphocyte CountPulmonary EosinophiliaStrongylida InfectionsGoblet cellMetaplasiaAllergensPeptide Fragmentsrespiratory tract diseasesMice Inbred C57BLBronchoalveolar lavageImmunologyCell Migration Inhibitionbiology.proteinInterleukin-5Journal of immunology (Baltimore, Md. : 1950)
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The fungal lactone oxacyclododecindione is a potential new therapeutic substance in the treatment of lupus-associated kidney disease.

2013

Recently oxacyclododecindione (Oxa), a macrocyclic lactone isolated from the imperfect fungus Exserohilum rostratum, has been described as a potent transcription inhibitor of inducible proinflammatory and profibrotic genes in cell culture models. As kidney disease in systemic lupus erythematosus is characterized by aberrant expression of inflammatory mediators and infiltration of immune cells, we investigated the effect of Oxa in MRL-Fas(lpr) mice, a model of systemic lupus erythematosus. These mice develop a spontaneous T-cell and macrophage-dependent autoimmune disease including severe glomerulonephritis that shares features with human lupus. Comparable to the results of in vitro models, …

ChemokineMice Inbred MRL lprMacrocyclic CompoundsAnti-Inflammatory AgentsProtein Array AnalysisGene ExpressionInflammationChemokine CXCL9Proinflammatory cytokineInterferon-gammaMiceImmune systemmedicineAnimalsCalgranulin ARNA MessengerChemokine CCL4Chemokine CCL5Chemokine CCL2Autoimmune diseaseSystemic lupus erythematosusbiologyInterleukin-6Tumor Necrosis Factor-alphaGlomerulonephritismedicine.diseaseLupus NephritisChemokine CXCL12Disease Models AnimalNephrologyImmunologybiology.proteinCytokinesFemaleOsteopontinmedicine.symptomKidney diseaseKidney international
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Role of the chemokine decoy receptor D6 in balancing inflammation, immune activation, and antimicrobial resistance in Mycobacterium tuberculosis infe…

2008

D6 is a decoy and scavenger receptor for inflammatory CC chemokines. D6-deficient mice were rapidly killed by intranasal administration of low doses of Mycobacterium tuberculosis. The death of D6(-/-) mice was associated with a dramatic local and systemic inflammatory response with levels of M. tuberculosis colony-forming units similar to control D6-proficient mice. D6-deficient mice showed an increased numbers of mononuclear cells (macrophages, dendritic cells, and CD4 and CD8 T lymphocytes) infiltrating inflamed tissues and lymph nodes, as well as abnormal increased concentrations of CC chemokines (CCL2, CCL3, CCL4, and CCL5) and proinflammatory cytokines (tumor necrosis factor alpha, int…

Chemokinedecoy receptor inflammation Mycobacterium tuberculosis infectionmedicine.medical_treatmentInterleukin-1betaImmunologyMice TransgenicInflammationReceptors CCR10BiologyModels BiologicalArticleCCL5Proinflammatory cytokineInterferon-gammaMiceImmune systemAnti-Infective AgentsDrug Resistance BacterialmedicineAnimalsImmunology and AllergyInterferon gammaInflammationTumor Necrosis Factor-alphaArticlesMycobacterium tuberculosisPhenotypeCytokineImmune SystemImmunologybiology.proteinTumor necrosis factor alphaLymph Nodesmedicine.symptommedicine.drug
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Toll-like receptor 2 is dispensable for acquired host immune resistance to Candida albicans in a murine model of disseminated candidiasis

2004

Previous work by our group showed that Toll-like receptor 2 (TLR2) is essential for activation of innate immunity, playing a major role in the response of macrophages to Candida albicans, triggering cytokine and chemokine expression, and therefore TLR2 -/- mice are more susceptible to systemic primary candidiasis. In this work, we used a murine model of systemic C. albicans infection, in which resistance to reinfection with virulent wild-type cells is induced by prior exposure of mice to a low-virulence agerminative strain of C. albicans (primary sublethal infection), to study the influence of TLR2 gene deletion on (i) the ability to develop an acquired resistance upon vaccination; (ii) the…

Chemokinemedicine.medical_treatmentImmunologyReceptors Cell SurfaceMicrobiologyMicrobiologyInterferon-gammaMiceCandida albicansmedicineAnimalsCandida albicansAntibodies FungalMice KnockoutToll-like receptorMembrane GlycoproteinsInnate immune systembiologyTumor Necrosis Factor-alphaToll-Like ReceptorsCandidiasisbiology.organism_classificationDisseminated CandidiasisInterleukin-12Immunity InnateToll-Like Receptor 2Corpus albicansMice Inbred C57BLTLR2Infectious DiseasesCytokineImmunoglobulin GImmunologybiology.proteinCytokinesMicrobes and Infection
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Study of conformational effects of recombinant interferon gamma adsorbed on a non-porous reversed-phase silica support.

1995

Abstract Reversed-phase chromatography is a powerful method for separating recombinant interferon γ and one of its analogues differing only by a single amino acid residue. Structural differences of the proteins explain this separation ability as demonstrated from adsorption studies on a non-porous reversed-phase support. To reveal the structural differences occurring in the adsorbed state, two different and independent methods were employed. The variation of the retention with the slope of the linear gradient gave information about the molecular contact area of the protein with the support. For different experimental conditions, these data were correlated with the adsorbent capacities measu…

ChromatographyRecombinant interferonChemistryProtein ConformationTemperatureGeneral ChemistrySilicon DioxideRecombinant Proteinslaw.inventionResidue (chemistry)Interferon-gammaAdsorptionlawPhase (matter)Recombinant DNAmedicineHumansInterferon gammaAdsorptionContact areaPorosityChromatography High Pressure Liquidmedicine.drugJournal of chromatography. B, Biomedical applications
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“Cysteinyl leukotriene-1 receptor activation in a human bronchial epithelial cell line leads to signal transducer and activator of transcription 1-me…

2008

Abstract We studied the effect of leukotriene D(4) (LTD(4)) on a human bronchial epithelial cell line (16HBE) overexpressing the cysteinyl leukotriene (CysLT) (1) receptor (HBECysLT(1)R), looking at the associated signal transduction mechanisms as well as at effects on inflammatory cell adhesion. The results obtained showed that LTD(4) increases the phosphorylation of extracellular signal-regulated protein kinase (ERK) 1/2 and of the signal transducer and activator of transcription 1 (STAT-1) in serine 727 (STAT-1Ser727), resulting in increased eosinophil adhesion to HBECysLT(1)R, associated with enhanced surface expression of intercellular adhesion molecule (ICAM) 1. Pretreatment with a Cy…

CyclopropanesMAPK/ERK pathwayIndolesBronchiAcetatesSulfidesBiologyCysteinyl leukotriene-1cysteinyl leukotrieneCell LineLeukotriene D4MaleimidesInterferon-gammaCell AdhesionHumansProtein kinase ACells CulturedProtein kinase CReceptors LeukotrienePharmacologyKinaseMEK inhibitorMembrane ProteinsEpithelial CellsIntercellular Adhesion Molecule-1Intercellular adhesion moleculeCell biologyEosinophilsSTAT1 Transcription FactorQuinolinesLeukotriene AntagonistsMolecular MedicinePhosphorylationMitogen-Activated Protein KinasesSignal transduction
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The efficient bovine insulin presentation capacity of bone marrow-derived macrophages activated by granulocyte-macrophage colony-stimulating factor c…

1993

Bone marrow-derived macrophages (BMM phi) were shown before to function as antigen-presenting cells. We show here, that the antigen presentation capacity of BMM phi depends on the nature of the antigen and is differently regulated by the lymphokines interferon-gamma (IFN-gamma) and granulocyte/macrophage-colony-stimulating factor (GM-CSF). When bovine insulin (BI) was employed as antigen, only BMM phi treated with GM-CSF (GM-CSF-M phi) were efficient presenters, but when presentation of the antigens ovalbumin and conalbumin was tested, IFN-gamma-pulsed BMM phi (IFN-gamma-M phi) proved superior to GM-CSF-M phi. The lack of efficient BI presentation function of IFN-gamma-M phi was only obviou…

CytoplasmImmunologyAntigen presentationAntigen-Presenting CellsBone Marrow CellsBiologyInterferon-gammachemistry.chemical_compoundAntigenmedicineAnimalsInsulinImmunology and AllergyCysteineSulfhydryl CompoundsAntigen-presenting cellAntigen processingMacrophagesLymphokineGranulocyte-Macrophage Colony-Stimulating FactorGlutathioneMacrophage ActivationGlutathioneCell biologyGranulocyte macrophage colony-stimulating factorBiochemistrychemistryCattleIntracellularmedicine.drugEuropean Journal of Immunology
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T cells engineered to express a T-cell receptor specific for glypican-3 to recognize and kill hepatoma cells in vitro and in mice

2015

Background & Aims Cancer therapies are being developed based on our ability to direct T cells against tumor antigens. Glypican-3 (GPC3) is expressed by 75% of all hepatocellular carcinomas (HCC), but not in healthy liver tissue or other organs. We aimed to generate T cells with GPC3-specific receptors that recognize HCC and used them to eliminate GPC3-expressing xenograft tumors grown from human HCC cells in mice. Methods We used mass spectrometry to obtain a comprehensive peptidome from GPC3-expressing hepatoma cells after immune-affinity purification of human leukocyte antigen (HLA)-A2 and bioinformatics to identify immunodominant peptides. To circumvent GPC3 tolerance resulting from feta…

Cytotoxicity ImmunologicCancer Immunotherapy ; Immune Response ; Liver Cancer ; Tumor-associated AntigensCarcinoma HepatocellularTime FactorsCell SurvivalMice SCIDCD8-Positive T-LymphocytesBiologyLymphocyte ActivationTransfectionImmunotherapy AdoptiveInterferon-gammaInterleukin 21GlypicansHLA-A2 AntigenAnimalsHumansCytotoxic T cellIL-2 receptorAntigen-presenting cellInterleukin 3HepatologyImmunodominant EpitopesZAP70Liver NeoplasmsGastroenterologyDendritic CellsHep G2 CellsNatural killer T cellXenograft Model Antitumor AssaysMolecular biologyCoculture TechniquesGenes T-Cell ReceptorInterleukin 12FemaleGenetic Engineering
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Cytotoxic T lymphocytes define multiple peptide isoforms derived from the melanoma-associated antigen MART-1/Melan-A

1999

Peptides derived from the melanoma-associated MART-1/Melan-A antigen are currently implemented in immunotherapy for inducing or augmenting T-cell responses directed against peptides expressed by autologous tumor cells in HLA-A2+ patients with melanoma. Here, we describe the specificity of the T-cell clone SK29-FFM1.1, which secretes GM-CSF in response to a panel of synthetic MART-1/Melan-A-derived peptides, including the naturally presented ILTVILGVL32–40, but exhibits cytotoxicity and IFN-γ secretion exclusively to the MART-1/Melan-A derived peptide AAGIGILTV27–35. In addition, cytotoxic T-lymphocyte (CTL) clone SK29-FFM1.1 recognizes 3 different naturally processed and presented peptides …

Cytotoxicity ImmunologicCancer ResearchCellular immunityReceptors Antigen T-Cell alpha-betaT-Lymphocytesmedicine.medical_treatmentBiologyTransfectionEpitopeInterferon-gammaMART-1 AntigenImmune systemAntigenAntigens NeoplasmHLA-A2 AntigenTumor Cells CulturedmedicineHumansProtein IsoformsCytotoxic T cellAmino Acid SequenceMelanomaneoplasmsintegumentary systemReverse Transcriptase Polymerase Chain ReactionImmunotherapyMolecular biologyRecombinant ProteinsClone CellsNeoplasm ProteinsCTL*OncologyImmunologyClone (B-cell biology)T-Lymphocytes CytotoxicInternational Journal of Cancer
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