Search results for "t-lymphocytes"

showing 10 items of 1380 documents

Rotavirus-Specific Cytotoxic T Lymphocytes Recognize Overlapping Epitopes in the Amino-Terminal Region of the VP7 Glycoprotein

1999

Abstract Rotavirus-specific cytotoxic T lymphocytes (CTL) play an important role in the resolution of rotavirus infection. The outer capsid glycoprotein, VP7, elicits a class I MHC-restricted CTL response. Vaccinia virus recombinants expressing the VP7 genes from simian rotavirus SA11 (serotype G3) and from the RF strain of bovine rotavirus (serotype G6) were used to analyze the CTL activity to this antigen in BALB/c (H-2 d ) and C57BL/6 (H-2 b ) mice neonatally infected with homologous and heterologous rotaviruses. A vaccinia virus recombinant expressing the first amino-terminal 88 amino acids of VP7 was constructed and used to search for cross-reactive CTL against this region of the prote…

RotavirusRecombinant Fusion ProteinsvirusesGenetic VectorsEpitopes T-LymphocyteGene ExpressionVaccinia virusBiologymedicine.disease_causeVirusEpitopeMicechemistry.chemical_compoundCapsidfluids and secretionsAntigenVirologyRotavirusmedicineAnimalsCytotoxic T cellAntigens ViralGlycoproteinschemistry.chemical_classificationMice Inbred BALB CVaccines SyntheticVaccinationH-2 Antigensvirus diseasesViral VaccinesVirologyMolecular biologyMice Inbred C57BLCTL*Animals NewbornchemistryCapsid ProteinsCattleVacciniaPeptidesGlycoproteinT-Lymphocytes CytotoxicVirology
researchProduct

Different profile and distribution of antigen specific T cells induced by intranasal and intrarectal immunization with rotavirus 2/6-VLP with and wit…

2013

International audience; In this study, we compared both the profile and distribution of antigen specific primed T cells after intrarectal (IR) and intranasal (IN) immunization with rotavirus (RV) 2/6-VLP, alone or in the presence of LT-R192G, in order to highlight the differences between the two routes and the impact of the adjuvant. Adult BALB/c mice were immunized once with 2/6-VLP with or without adjuvant and the T cell response was analyzed in lymphoid tissues after in vitro restimulation with the antigen. IN, but not IR, immunization of mice with 2/6-VLP alone induced antigen-specific IL-10 and IL-17 secreting T cells. IL-10-, in contrast to IL-17-, secreting T cells did not migrate to…

Rotavirusmedicine.medical_treatmentT-Lymphocytes[SDV]Life Sciences [q-bio]Priming (immunology)DistributionPHENOTYPEPROTECTSEnterotoxins0302 clinical medicineCell MovementINFECTIONMesenteric lymph nodesHEAT-LABILE TOXINIMMUNE-RESPONSEIL-2 receptorAntigens Viral0303 health sciencesB-LymphocytesMice Inbred BALB CIntrarectalEscherichia coli ProteinsVaccinationFOXP3CHOLERA-TOXINLT-R192G3. Good healthInfectious Diseasesmedicine.anatomical_structureIntranasal030220 oncology & carcinogenesisMolecular MedicineFemaleAdjuvantLymphoid TissueT cellBacterial ToxinsSpleenBiologyMUCOSAL VACCINESRotavirus Infections03 medical and health sciencesCross-PrimingAntigenAdjuvants ImmunologicAdministration RectalVIRUS-LIKE PARTICLESmedicineAnimalsVaccines Virus-Like ParticleImmunity MucosalAdministration Intranasal030304 developmental biologyGeneral VeterinaryGeneral Immunology and MicrobiologyInterleukinsPublic Health Environmental and Occupational HealthRotavirus VaccinesT cellMICEImmunologyCHALLENGE
researchProduct

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
researchProduct

Generation of T Follicular Helper Cells Is Mediated by Interleukin-21 but Independent of T Helper 1, 2, or 17 Cell Lineages

2008

After activation, CD4(+) helper T (Th) cells differentiate into distinct effector subsets. Although chemokine (C-X-C motif) receptor 5-expressing T follicular helper (Tfh) cells are important in humoral immunity, their developmental regulation is unclear. Here we show that Tfh cells had a distinct gene expression profile and developed in vivo independently of the Th1 or Th2 cell lineages. Tfh cell generation was regulated by ICOS ligand (ICOSL) expressed on B cells and was dependent on interleukin-21 (IL-21), IL-6, and signal transducer and activator of transcription 3 (STAT3). However, unlike Th17 cells, differentiation of Tfh cells did not require transforming growth factor beta (TGF-beta…

STAT3 Transcription FactorAdoptive cell transferCellular differentiationCellImmunologyGene ExpressionLymphocyte ActivationCXCR5ArticleInducible T-Cell Co-Stimulator LigandMiceInterleukin 21T-Lymphocyte SubsetsTransforming Growth Factor betaFollicular phasemedicineAnimalsCytotoxic T cellImmunology and AllergyCell LineageMOLIMMUNOOligonucleotide Array Sequence AnalysisB-LymphocytesT follicular helper cell differentiationbiologyInterleukin-6Reverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingInterleukinsInterleukin-17ProteinsGerminal centerCell DifferentiationT-Lymphocytes Helper-InducerTransforming growth factor betaFlow CytometryGerminal CenterAdoptive TransferImmunohistochemistryMolecular biologyMice Mutant Strainsmedicine.anatomical_structureInfectious DiseasesT helper 1CELLIMMUNOImmunologybiology.proteinInterleukin 17Signal TransductionImmunity
researchProduct

Osteopontin shapes immunosuppression in the metastatic niche.

2014

Abstract The matricellular protein osteopontin (OPN, Spp-1) is widely associated with cancer aggressiveness when produced by tumor cells, but its impact is uncertain when produced by leukocytes in the context of the tumor stroma. In a broad study using Spp1−/− mice along with gene silencing in tumor cells, we obtained evidence of distinct and common activities of OPN when produced by tumor or host cells in a spontaneously metastatic model of breast cancer. Different cellular localization of OPN is associated with its distinct activities, being mainly secreted in tumor cells while intracellular in myeloid cells. OPN produced by tumor cells supported their survival in the blood stream, wherea…

STAT3 Transcription FactorCancer ResearchPathologymedicine.medical_specialtyLung NeoplasmsosteopontinCellContext (language use)Breast NeoplasmsT-Lymphocytes RegulatoryMonocytesMicestomatognathic systemCell Line TumormedicineImmune ToleranceAnimalsHumansMyeloid CellsOsteopontinNeoplasm MetastasisCellular localizationImmunosuppression TherapyMice Inbred BALB CMice Inbred C3HimmunosuppressionbiologyArginaseInterleukin-6Matricellular proteinCancerosteopontin; niche; immunosuppressionmedicine.diseaseMice Inbred C57BLnichemedicine.anatomical_structureOncologyTumor progressionCell culturebiology.proteinFemale
researchProduct

Cucurbitacin R Reduces the Inflammation and Bone Damage Associated with Adjuvant Arthritis in Lewis Rats by Suppression of Tumor Necrosis Factor-α in…

2006

The aim of this study was to investigate the effects of cucurbitacin R on an experimental model of adjuvant-induced arthritis in rats. The treatment of arthritic rats with cucurbitacin R (1 mg/kg p.o. daily) modified the evolution of the clinical symptoms, whereas the histopathology of paws demonstrated a reduction in the signs of arthritis. Compared with the control group, radiography of the tibiotarsal joints of cucurbitacin R-treated rats showed a decrease in joint damage and soft tissue swelling of the footpad. The in vivo study of the expression of proinflammatory enzymes (nitric-oxide synthase-2 and cyclooxygenase-2) with the aid of the Western blot technique, and that of tumor necros…

STAT3 Transcription FactorT-Lymphocytesmedicine.medical_treatmentAnti-Inflammatory AgentsArthritisInflammationPharmacologyDinoprostoneCell LineNitric oxideProinflammatory cytokineMicechemistry.chemical_compoundSuperoxidesIn vivomedicineAnimalsHumansPharmacologyPancreatic ElastaseTumor Necrosis Factor-alphaCucurbitacinbusiness.industryMacrophagesCucurbitacinsmedicine.diseaseArthritis ExperimentalTriterpenesRatschemistryRats Inbred LewImmunologyMolecular MedicineFemaleTumor necrosis factor alphamedicine.symptombusinessProstaglandin EJournal of Pharmacology and Experimental Therapeutics
researchProduct

Induction of tolerogenic lung CD4+ T cells by local treatment with a pSTAT-3 and pSTAT-5 inhibitor ameliorated experimental allergic asthma.

2010

Signal transducer and activator of transcription (STAT)-3 inhibitors play an important role in regulating immune responses. Galiellalactone (GL) is a fungal secondary metabolite known to interfere with the binding of phosphorylated signal transducer and activator of transcription (pSTAT)-3 as well of pSTAT-6 dimers to their target DNA in vitro. Intra nasal delivery of 50 μg GL into the lung of naive Balb/c mice induced FoxP3 expression locally and IL-10 production and IL-12p40 in RNA expression in the airways in vivo. In a murine model of allergic asthma, GL significantly suppressed the cardinal features of asthma, such as airway hyperresponsiveness, eosinophilia and mucus production, after…

STAT3 Transcription Factormedicine.medical_treatmentImmunologyCD11cSuppressor of Cytokine Signaling ProteinsT-Lymphocytes RegulatoryLactonesMiceImmune systemIn vivomedicineSTAT5 Transcription FactorImmunology and AllergyAnimalsIndoleamine-Pyrrole 23-DioxygenaseAnti-Asthmatic AgentsLungAdministration IntranasalCells CulturedMice Inbred BALB CbiologyChemistryFOXP3General MedicineDendritic CellsT-Lymphocytes Helper-Inducerrespiratory systemAsthmaReceptors Interleukin-3CD11c Antigenrespiratory tract diseasesOvalbuminInterleukin 10CytokineSuppressor of Cytokine Signaling 3 ProteinImmunologySTAT proteinCancer researchbiology.proteinFemaleInterleukin-4T-Box Domain Proteins
researchProduct

Tristetraprolin regulation of interleukin-22 production

2015

AbstractInterleukin (IL)-22 is a STAT3-activating cytokine displaying characteristic AU-rich elements (ARE) in the 3′-untranslated region (3′-UTR) of its mRNA. This architecture suggests gene regulation by modulation of mRNA stability. Since related cytokines undergo post-transcriptional regulation by ARE-binding tristetraprolin (TTP), the role of this destabilizing protein in IL-22 production was investigated. Herein, we demonstrate that TTP-deficient mice display augmented serum IL-22. Likewise, IL-22 mRNA was enhanced in TTP-deficient splenocytes and isolated primary T cells. A pivotal role for TTP is underscored by an extended IL-22 mRNA half-life detectable in TTP-deficient T cells. Lu…

STAT3 Transcription Factormedicine.medical_treatmentT-LymphocytesTristetraprolinPrimary Cell CultureMAP Kinase Kinase 1BiologyJurkat cellsArticleInterleukin 22Jurkat CellsMiceTristetraprolinNitrilesmedicineButadienesAnimalsHumansRNA Messengerddc:610Regulation of gene expressionAU-rich elementAU Rich ElementsInflammationMultidisciplinaryInterleukinsHEK 293 cellsInterleukinCell biologyCytokineHEK293 CellsGene Expression RegulationImmunologyErratumScientific Reports
researchProduct

Novel Signal Transduction Pathways: Analysis of STAT-3 and Rac-1 Signaling in Inflammatory Bowel Disease

2006

Although the precise etiology of inflammatory bowel disease still remains unclear, considerable progress has been made in the identification of novel signal transduction pathways that elucidate the immunopathogenesis involved in the perpetuation of the inflammatory process. Augmented T cell resistance against apoptosis is regarded as a pivotal factor in the pathogenesis, as it impairs mucosal homeostasis and leads to unrestrained accumulation of activated T cells, which subsequently lead to the amplification of the inflammatory response. Therefore novel therapeutic strategies aim at restoring mucosal T cell susceptibility to apoptosis through targeting of signal transduction pathways that a…

STAT3 Transcription Factorrac1 GTP-Binding ProteinT-LymphocytesT cellApoptosisTherapeutic ProcedureAzathioprineBiologyInflammatory bowel diseaseGeneral Biochemistry Genetics and Molecular BiologystatPathogenesisHistory and Philosophy of ScienceAzathioprinemedicineHumansGeneral NeuroscienceInflammatory Bowel Diseasesmedicine.diseasemedicine.anatomical_structureApoptosisImmunologySignal transductionImmunosuppressive AgentsSignal Transductionmedicine.drugAnnals of the New York Academy of Sciences
researchProduct

Arginine deficiency leads to impaired cofilin dephosphorylation in activated human T lymphocytes

2012

The amino acid arginine is fundamentally involved in the regulation of the immune response during infection, inflammatory diseases and tumor growth. Arginine deficiency (e.g. due to the myeloid cell enzyme arginase) inhibits proliferation and effector functions of activated T lymphocytes. Here, we studied intracellular mechanisms mediating this suppression of human T lymphocytes. Our proteomic analysis revealed an impaired dephosphorylation of the actin-binding protein cofilin upon T-cell activation in the absence of arginine. We show that this correlates with alteration of actin polymerization and impaired accumulation of CD2 and CD3 in the evolving immunological synapse in T cell-antigen …

STIMULATIONEXPRESSIONHYPORESPONSIVENESSArginineCell SurvivalT-Lymphocytesmedicine.medical_treatmentCD3ImmunologyT cellsmacromolecular substancesMETABOLISMBiologyArginineLymphocyte ActivationDephosphorylationmedicineHumansImmunology and AllergyPhosphorylationCell ProliferationHUMAN GRANULOCYTE ARGINASEScience & TechnologySYNAPSE FORMATIONimmune regulationACTIN CYTOSKELETONGeneral MedicineT lymphocyteCofilincell activationTRANSLOCATIONCell biologyArginaseCytokineActin Depolymerizing Factors1107 ImmunologyCELL-ACTIVATIONLeukocytes Mononuclearbiology.proteinPhosphorylationIMMUNE-SYSTEMLife Sciences & BiomedicineInternational Immunology
researchProduct