Search results for "Th1"

showing 10 items of 238 documents

Vaccination with TAT-Antigen Fusion Protein Induces Protective, CD8+ T Cell-Mediated Immunity Against Leishmania Major

2010

In murine leishmaniasis, healing is mediated by IFN-γ-producing CD4 + and CD8 + T cells. Thus, an efficacious vaccine should induce Th1 and Tc1 cells. Dendritic cells (DCs) pulsed with exogenous proteins primarily induce strong CD4-dependent immunity; induction of CD8 responses has proven to be difficult. We evaluated the immunogenicity of fusion proteins comprising the protein transduction domain of HIV-1 TAT and the Leishmania antigen LACK ( Leishmania homolog of receptors for activated C kinase), as TAT-fusion proteins facilitate major histocompatibility complex class I-dependent antigen presentation. In vitro , TAT–LACK-pulsed DCs induced stronger proliferation of Leishmania -specific C…

Protozoan VaccinesAntigen presentationProtozoan ProteinsLeishmaniasis CutaneousAntigens ProtozoanDermatologyCD8-Positive T-LymphocytesBiologyMajor histocompatibility complexBiochemistryArticleMiceAntigenAnimalsCytotoxic T cellLeishmania majorMolecular BiologyLeishmania majorImmunogenicityDendritic CellsCell BiologyTh1 Cellsbiology.organism_classificationInterleukin-12Fusion proteinMice Mutant StrainsCell biologyMice Inbred C57BLImmunologybiology.proteintat Gene Products Human Immunodeficiency VirusViral Fusion ProteinsCD8Journal of Investigative Dermatology
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Divergent effects of biolistic gene transfer in a mouse model of allergic airway inflammation.

2007

Particle-mediated epidermal delivery (PMED) of allergen genes efficiently prevents systemic sensitization and suppresses specific immunoglobulin E synthesis. We investigated in a mouse model of allergic airway disease the effect of PMED on the elicitation of local inflammatory reactions in the lung. BALB/c mice were biolistically transfected with plasmids encoding beta-galactosidase (betaGal) as model allergen under control of the DC-targeting fascin promoter and the ubiquitously active cytomegalovirus promoter, respectively. Mice were challenged intranasally with betaGal-protein with or without intermediate sensitization with betaGal adsorbed to aluminiumhydroxide. Subsequently, local cyto…

Pulmonary and Respiratory Medicinemedicine.medical_treatmentClinical BiochemistryCytomegalovirusBiologymedicine.disease_causeDNA vaccinationInterferon-gammaMiceAllergenTh2 CellsmedicineRespiratory HypersensitivityAnimalsHumansPromoter Regions GeneticMolecular BiologyLungSensitizationCells CulturedInflammationMice Inbred BALB Cmedicine.diagnostic_testMicrofilament ProteinsGene Transfer TechniquesCell BiologyTransfectionDendritic Cellsrespiratory systemImmunoglobulin ETh1 Cellsmedicine.diseasebeta-Galactosidaserespiratory tract diseasesCellular infiltrationDisease Models Animalmedicine.anatomical_structureBronchoalveolar lavageCytokineNeutrophil InfiltrationImmunologyAntibody FormationFemaleEpidermisCarrier ProteinsBronchoalveolar Lavage FluidCD8T-Lymphocytes CytotoxicAmerican journal of respiratory cell and molecular biology
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Cyclic AMP-induced Chromatin Changes Support the NFATc-mediated Recruitment of GATA-3 to the Interleukin 5 Promoter

2008

Elevated intracellular cyclic AMP levels, which suppress the proliferation of naive T cells and type 1 T helper (Th1) cells are a property of T helper 2 (Th2) cells and regulatory T cells. While cyclic AMP signals interfere with the IL-2 promoter induction, they support the induction of Th2-type genes, in particular of il-5 gene. We show here that cyclic AMP signals support the generation of three inducible DNase I hypersensitive chromatin sites over the il-5 locus, including its promoter region. In addition, cyclic AMP signals enhance histone H3 acetylation at the IL-5 promoter and the concerted binding of GATA-3 and NFATc to the promoter. This is facilitated by direct protein-protein inte…

Quantitative Trait LociGATA3 Transcription FactorBiologyBiochemistryCell LineHistonesMiceTh2 CellsCyclic AMPTranscriptional regulationAnimalsHumansTranscription Chromatin and EpigeneticsPromoter Regions GeneticHistone H3 acetylationMolecular BiologyInterleukin 5Cell ProliferationMice Inbred BALB CNFATC Transcription FactorsEffectorLymphokineAcetylationZinc FingersPromoterCell BiologyDNA-binding domainTh1 CellsChromatin Assembly and DisassemblyMolecular biologyChromatinProtein Structure TertiaryChromatinGene Expression RegulationInterleukin-2Interleukin-5Signal TransductionJournal of Biological Chemistry
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Specific Regulation of T Helper Cell 1–mediated Murine Colitis by CEACAM1

2004

Carcinoembryonic antigen-related cellular adhesion molecule 1 (CEACAM1) is a cell surface molecule that has been proposed to negatively regulate T cell function. We have shown that CEACAM1 is associated with specific regulation of T helper cell (Th)1 pathways, T-bet–mediated Th1 cytokine signaling, and Th1-mediated immunopathology in vivo. Mice treated with anti–mouse CEACAM1-specific monoclonal antibody (mAb) CC1 during the effector phase exhibited a reduced severity of trinitrobenzene sulfonic acid colitis in association with decreased interferon (IFN)-γ production. Although oxazolone colitis has been reported as Th2 mediated, mice treated with the CC1 mAb or a CEACAM1-Fc chimeric protein…

Recombinant Fusion Proteinsmedicine.medical_treatmentT cellImmunologyBiologyArticleOxazoloneInterferon-gammaMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAntigeninflammatory bowel diseaseInterferonmedicineAnimalsImmunology and AllergyColitisCell adhesionCEACAM1030304 developmental biologyInflammationMice KnockoutMice Inbred BALB C0303 health sciencesT cell immunityOxazoloneAntibodies MonoclonalT-Lymphocytes Helper-InducerT helper cellTh1 CellsColitismedicine.diseaseMolecular biologyCarcinoembryonic AntigenImmunoglobulin Fc Fragments3. Good healthMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureCytokinechemistry030220 oncology & carcinogenesisFemaleTh1 cytokineInterleukin-1hapten-induced colitismedicine.drugJournal of Experimental Medicine
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B subunits of cholera toxin and thermolabile enterotoxin of Escherichia coli have similar adjuvant effect as whole molecules on rotavirus 2/6-VLP spe…

2015

The purpose of this study was to evaluate the adjuvant effect of the B subunits of cholera toxin (CT) and the thermolabile enterotoxin of Escherichia coli (LT) by the intrarectal route of immunization and compare them to the whole molecules CT and LT-R192G, a non toxic mutant of LT, using 2/6-VLP as an antigen, in mice. All molecules induced similar antigen specific antibody titers in serum and feces, whereas different T cell profiles were observed. CTB and LTB, conversely to CT and LT-R192G, did not induce detectable production of IL-2 by antigen specific T cells. Moreover, CTB, conversely to LT-R192G, CT and LTB, did not induce antigen specific CD4+CD25+Foxp3- and Foxp3+ T cells, thus sho…

RotavirusCholera Toxin[SDV]Life Sciences [q-bio]T cellmedicine.medical_treatmentBacterial ToxinsEnterotoxinBiologymedicine.disease_causeAntibodies ViralMicrobiologyAntibodiesMicrobiologyB subunitEnterotoxinsFecesMiceAntigenAdjuvants ImmunologicImmunologicAdministration RectalmedicineAnimalsViralAdjuvantsIL-2 receptorVaccines Virus-Like ParticleThermolabileB cellVaccinesIntrarectalEscherichia coli ProteinsCholera toxinRotavirus VaccinesLT-R192G3. Good healthVirus-Like ParticleInfectious Diseasesmedicine.anatomical_structureAdministrationAntibody FormationInterleukin-2Th17 CellsImmunizationRectalAdjuvantImmunologic MemoryMicrobial pathogenesis
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Role of myeloïd derived suppressive cells (MDSC) and Th17 lymphocytes in chemotherapy and immunotherapy efficacy

2017

Actual oncology is still facing resistance and rapid progression of cancer. Intrinsic resistance mechanisms developed by tumor cells determine chemotherapy and immunotherapy efficacy. It is now recognized that the host immune response status is in part implicated in the therapeutic outcome of patients. The aim of our research team is to characterize this response and to study the impact of therapies in order to identify the mechanisms associated with future exhaust of the tumor. In this context, we have shown that chemotherapy (5-FU, oxaliplatin, anti-VEGF: FOLFOX-bevacizumab) in some patients causes a drop in devices gMDSC (granulocytic myeloid derived suppressive cells) that is associated…

SIRT1[SDV.IMM] Life Sciences [q-bio]/ImmunologyImmunothérapieMDSCChemotherapyTh17ImmunotherapyChimiothérapieCancer
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MiR-29b antagonizes the pro-inflammatory tumor-promoting activity of multiple myeloma-educated dendritic cells

2017

Dendritic cells (DCs) have a key role in regulating tumor immunity, tumor cell growth and drug resistance. We hypothesized that multiple myeloma (MM) cells might recruit and reprogram DCs to a tumor-permissive phenotype by changes within their microRNA (miRNA) network. By analyzing six different miRNA-profiling data sets, miR-29b was identified as the only miRNA upregulated in normal mature DCs and significantly downregulated in tumor-associated DCs. This finding was validated in primary DCs co-cultured in vitro with MM cell lines and in primary bone marrow DCs from MM patients. In DCs co-cultured with MM cells, enforced expression of miR-29b counteracted pro-inflammatory pathways, includin…

STAT3 Transcription Factor0301 basic medicineCancer Researchdendritic cellDown-RegulationInflammationMice SCIDBiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationBone MarrowCell Line Tumorhemic and lymphatic diseasesmicroRNAmedicineAnimalsHumanstumor immunologyMultiple myelomaCell ProliferationInflammationmicroRNA.Cell growthNF-kappa BDendritic CellsHematologySTAT3 Transcription Factormedicine.diseaseNFKB1Up-RegulationGene Expression Regulation Neoplasticmultiple myelomaMicroRNAs030104 developmental biologymedicine.anatomical_structureOncologyCancer researchOriginal ArticleFemaleBone marrowTh17medicine.symptom030215 immunology
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PKM2 promotes Th17 cell differentiation and autoimmune inflammation by fine-tuning STAT3 activation

2019

Th17 cells undergo metabolic reprogramming towards glycolysis to support their differentiation and pathogenicity. Damasceno et al. report that PKM2, a glycolytic enzyme, plays a nonmetabolic role in mediating Th17 cell differentiation and autoimmune neuroinflammation by fine-tuning STAT3 activation.

STAT3 Transcription Factor0301 basic medicineEncephalomyelitis Autoimmune ExperimentalCellular differentiationEncephalomyelitisPyruvate KinaseImmunologyFluorescent Antibody TechniqueAutoimmunityInflammationPKM2Real-Time Polymerase Chain ReactionArticleMice03 medical and health sciences0302 clinical medicineNeuroinflammationmedicineAnimalsImmunology and AllergySTAT3InflammationbiologyChemistryExperimental autoimmune encephalomyelitisCell Differentiationhemic and immune systemsFlow Cytometrymedicine.diseaseCell biologyMice Inbred C57BL030104 developmental biologyTumor progression030220 oncology & carcinogenesisbiology.proteinTh17 Cellsmedicine.symptomREAÇÃO EM CADEIA POR POLIMERASEPyruvate kinaseJournal of Experimental Medicine
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Protein kinase CK2 governs the molecular decision between encephalitogenic T H 17 cell and T reg cell development

2016

T helper 17 (TH17) cells represent a discrete TH cell subset instrumental in the immune response to extracellular bacteria and fungi. However, TH17 cells are considered to be detrimentally involved in autoimmune diseases like multiple sclerosis (MS). In contrast to TH17 cells, regulatory T (Treg) cells were shown to be pivotal in the maintenance of peripheral tolerance. Thus, the balance between Treg cells and TH17 cells determines the severity of a TH17 cell-driven disease and therefore is a promising target for treating autoimmune diseases. However, the molecular mechanisms controlling this balance are still unclear. Here, we report that pharmacological inhibition as well as genetic ablat…

STAT3 Transcription Factor0301 basic medicineEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisCellMice Transgenicchemical and pharmacologic phenomenaBiologySeverity of Illness IndexT-Lymphocytes RegulatoryMice03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsHumansIL-2 receptorPhosphorylationCasein Kinase IISTAT3MultidisciplinaryCell growthInterleukin-17Experimental autoimmune encephalomyelitisGranulocyte-Macrophage Colony-Stimulating FactorFOXP3Peripheral toleranceForkhead Transcription Factorshemic and immune systemsReceptors Interleukinmedicine.diseasePeptide FragmentsMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureGene Expression RegulationImmunologybiology.proteinCancer researchTh17 CellsMyelin-Oligodendrocyte GlycoproteinSignal Transduction030215 immunologyProceedings of the National Academy of Sciences
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Socs3 induction by PPARγ restrains cancer-promoting inflammation

2013

The presence of proinflammatory cytokines in the tumor microenvironment can support further growth of established cancers. Docosahexaenoic acid (DHA), a peroxisome proliferator-activated receptor-gamma (PPARγ) ligand, has been shown to suppress inflammation and limit tumor progression in vivo. Are the anticancer properties of DHA relying on its ability to prevent inflammation? If so, what are the molecular links between the anti-inflammatory properties of DHA and its anticancer effects? DHA is an n-3 polyinsaturated fatty acid mainly found in fish oil that was shown to contribute to inflammation resolution by preventing the release of proinflammatory mediators in vivo.1 DHA has also been as…

STAT3 Transcription FactorDocosahexaenoic AcidsCellular differentiationPeroxisome proliferator-activated receptorInflammationSuppressor of Cytokine Signaling ProteinsBiologyEditorials: Cell Cycle FeaturesProinflammatory cytokineMicemedicineAnimalsHumansPhosphorylationPromoter Regions GeneticMolecular BiologyCells Culturedchemistry.chemical_classificationInflammationTumor microenvironmentInterleukin-17TroglitazoneCell DifferentiationCell BiologyPPAR gammaCell Transformation NeoplasticchemistryGene Expression RegulationSuppressor of Cytokine Signaling 3 ProteinImmunologyCancer cellCancer researchTh17 CellsInterleukin 17medicine.symptomDevelopmental Biologymedicine.drugProtein BindingSignal TransductionCell Cycle
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