Search results for "ACTIVATION"

showing 10 items of 2079 documents

H-2(d) mice born to and reared by HBeAg-transgenic mothers do not develop T cell tolerance toward the hepatitis B virus core gene products.

2000

The function of the secretory core gene product (HBeAg) of the human hepatitis B virus (HBV) is unknown. It has been proposed that this protein may be passed from the mother to her offspring at the perinatal stage where it might induce immune tolerance. In a previous study we have shown that the murine placenta presents an efficient barrier for the HBe protein and that H-2(b) mice born to HBeAg-positive transgenic mothers do not develop tolerance of specific cytotoxic T cells. In the present work we demonstrate that transgenic mice expressing high serum levels of HBeAg secrete only small amounts of this protein into their milk and excrete minute amounts of the viral gene product in their ur…

Cytotoxicity ImmunologicMaleHepatitis B virusT cellvirusesT-LymphocytesMothersMice TransgenicBiologymedicine.disease_causeLymphocyte ActivationImmune toleranceMiceImmune systemVirologymedicineImmune ToleranceCytotoxic T cellAnimalsHepatitis B e AntigensHepatitis B AntibodiesHepatitis B virusMice Inbred BALB CH-2 Antigensvirus diseasesT-Lymphocytes Helper-InducerHepatitis Bmedicine.diseaseHepatitis BVirologydigestive system diseasesPeptide Fragmentsmedicine.anatomical_structureMilkHBeAgAnimals NewbornImmunologyFemaleCD8T-Lymphocytes CytotoxicVirology
researchProduct

P-selectin glycoprotein ligand-1 as a potential target for humoral immunotherapy of multiple myeloma.

2008

Monoclonal antibodies (mAbs), successfully adopted in the treatment of several haematological malignancies, have proved almost ineffective in multiple myeloma (MM), because of the lack of an appropriate antigen for targeting and killing MM cells. Here, we demonstrate that PSGL1, the major ligand of P-Selectin, a marker of plasmacytic differentiation expressed at high levels on normal and neoplastic plasma cells, may represent a novel target for mAb-mediated MM immunotherapy. The primary effectors of mAb-induced cell-death, complement-mediated lysis (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC), were investigated using U266B1 and LP1 cell-lines as models. Along with immunolo…

Cytotoxicity ImmunologicMembrane Glycoproteinsmieloma multiplo; ab therapy; PSGL-1ab therapyAntibody-Dependent Cell CytotoxicityDrug Evaluation PreclinicalAntibodies MonoclonalBone Marrow CellsSettore MED/08 - Anatomia Patologicamultiple myelomaDrug Delivery SystemsCell Line TumorHumanscomplementimmunotherapymieloma multiploPSGL-1ADCCComplement Activationmonoclonal antibodie
researchProduct

An Ovalbumin Peptide-Specific Cytotoxic T Cell Clone with Antigen Self-Presentation Capacity Uses Two Distinct Mechanisms to Kill Target Cells

1993

Abstract Cloned 10BK.1 T cells with specificity for the ovalbumin peptide OVA257-264 are representative of a novel cell type within the CD8 + subset of T cells. In the presence and in the absence of added antigen presenting cells these T cells react toward antigen (Ag) by proliferation and lymphokine production. These data suggest self-presentation of the Ag by 10BK.1 cells. Here we present evidence that 10BK.1 cells exhibit cytotoxic activity that involves two different cytotoxic effector mechanisms. (i) One mechanism is fast killing activity, apparent within 4 hr. Constitutive mouse T cell-specific proteinase-1 (MTSP-1) activity, constitutive expression of MTSP-1 RNA, increased by Ag chal…

Cytotoxicity ImmunologicPore Forming Cytotoxic ProteinsOvalbuminImmunologyAntigen presentationAntigen-Presenting CellsBiologyCytoplasmic GranulesLymphocyte ActivationGranzymesCell LineMiceInterleukin 21AntigenAnimalsCytotoxic T cellIL-2 receptorAntigen-presenting cellLymphotoxin-alphaMembrane GlycoproteinsCD40PerforinTumor Necrosis Factor-alphaSerine EndopeptidasesDegranulationMolecular biologyClone Cellsbiology.proteinInterleukin-2T-Lymphocytes CytotoxicCellular Immunology
researchProduct

Precursor frequency can compensate for lower TCR expression in T cell competition during priming in vivo.

2006

The factors controlling clonal dominance of cytotoxic T lymphocyte (CTL) responses are currently not well understood. To study the functional impact of the strength of the interaction of a T cell with an antigen-presenting cell in this context, we established a new mouse model comprised of two T cell receptor (TCR)-transgenic strains expressing the identical TCR in differing amounts, hence providing two CTL clones with different avidities but identical specificity and affinity. Utilizing this new model, we show that upon antigen challenge higher-avidity CTL expand at the expense of moderate-avidity CTL in vivo if present in equal numbers. Beyond this, moderate-avidity T cells can also contr…

Cytotoxicity ImmunologicT cellImmunologyReceptors Antigen T-CellPriming (immunology)chemical and pharmacologic phenomenaMice TransgenicStreptamerImmunodominanceBiologyLymphocyte ActivationMiceAntigenmedicineImmunology and AllergyCytotoxic T cellAnimalsAntigen PresentationStem CellsT-cell receptorhemic and immune systemsFlow CytometryAdoptive TransferCell biologyMice Inbred C57BLCTL*medicine.anatomical_structureImmunologyT-Lymphocytes CytotoxicEuropean journal of immunology
researchProduct

Cyclosporin A mediates immunosuppression of primary cytotoxic T cell responses by impairing the release of interleukin 1 and interleukin 2

1981

The site of action of the immunosuppressive drug cyclosporin A in in vitro cytotoxic allograft responses has been localized. General cytotoxic effects of the drug on proliferating T cells became apparent at concentrations of 500-1000 ng/ml, while selective effects were observed at concentrations of 10-100 ng/ml. The selective effects included a blockade of interleukin 2 release from activated T helper cells on the one hand and inhibition of interleukin 1 release from splenic adherent cells on the other. While cyclosporin A did not interfere with the intracellular events required for the activation and subsequent clonal expansion of alloreactive T cells, the lack of interleukin 1 and interle…

Cytotoxicity ImmunologicT-LymphocytesImmunologyCyclosporinsPharmacologyBiologyLymphocyte ActivationMiceInterleukin 21Cyclosporin aAnimalsImmunology and AllergyInterleukin 5Interleukin 4Interleukin 3Mice Inbred BALB CProteinsInterleukinInterleukin 33Protein BiosynthesisMice Inbred CBAInterleukin 12Interleukin-2Lymphocyte Culture Test MixedImmunosuppressive AgentsInterleukin-1European Journal of Immunology
researchProduct

RNA Transfer by Electroporation into Mature Dendritic Cells Leading to Reactivation of Effector-Memory Cytotoxic T Lymphocytes: A Quantitative Analys…

2005

Previous studies have analyzed transfer of RNA-encoded tumor-associated antigens (TAAs) into immature dendritic cells (DCs) because of their exceptional ability to internalize antigens. Concerns have been raised regarding the use of immature DCs in clinical studies because of their capacity to tolerize T cells. Therefore, we focused on optimizing RNA transfer into mature DCs using the method of electroporation and obtained high protein expression in 90% of mature DCs. Particular emphasis was placed on quantifying RNA transfer. Reconstitution of peptide-MHC (pMHC) ligands on RNA-pulsed DCs was measured with the help of effector-memory cytotoxic T lymphocytes (CTLs) specific for the melanoma-…

Cytotoxicity Immunologicchemical and pharmacologic phenomenaBiologyLymphocyte ActivationTransfectionEpitopeAntigenCell Line TumorDrug DiscoveryGeneticsHumansCytotoxic T cellMelanomaMolecular BiologyPharmacologyEffectorElectroporationRNAhemic and immune systemsDendritic CellsTransfectionMolecular biologyElectroporationPhenotypedendritic cells; RNA transfection; electroporation; effector-memory cytotoxic T lymphocytes; peptide-MHC ligands; tumor immunotherapy; melanoma; tyrosinase; CDK4; EGFPRNAMolecular MedicineImmunotherapyRNA transfectionT-Lymphocytes CytotoxicMolecular Therapy
researchProduct

Cytotoxicity of tumor antigen specific human T cells is unimpaired by arginine depletion.

2013

Tumor-growth is often associated with the expansion of myeloid derived suppressor cells that lead to local or systemic arginine depletion via the enzyme arginase. It is generally assumed that this arginine deficiency induces a global shut-down of T cell activation with ensuing tumor immune escape. While the impact of arginine depletion on polyclonal T cell proliferation and cytokine secretion is well documented, its influence on chemotaxis, cytotoxicity and antigen specific activation of human T cells has not been demonstrated so far. We show here that chemotaxis and early calcium signaling of human T cells are unimpaired in the absence of arginine. We then analyzed CD8(+) T cell activation…

Cytotoxicity Immunologiclcsh:MedicineCD8-Positive T-LymphocytesARGINASELymphocyte ActivationGranzymesInterleukin 21Cytotoxic T cellIL-2 receptorlcsh:ScienceCells CulturedMultidisciplinarybiologyT CellsChemotaxisVaccinationCOFILINCD28Natural killer T cellCANCERmedicine.anatomical_structureMedicineScience & Technology - Other TopicsImmunotherapyResearch ArticleTumor ImmunologyEXPRESSIONINFILTRATING LYMPHOCYTESCARCINOMAGeneral Science & TechnologyT cellImmune CellsImmunologyArginineImmune SuppressionDENDRITIC CELLSImmunomodulationInterferon-gammaMART-1 AntigenMULTIPLE-MYELOMAMD MultidisciplinarymedicineImmune ToleranceHumansCalcium SignalingAntigen-presenting cellBiologyCell ProliferationCD40Science & TechnologyMULTIDISCIPLINARY SCIENCESPerforinlcsh:RImmunityImmunoregulationIN-VITROImmunologic SubspecialtiesMolecular biologybiology.proteinMYELOID SUPPRESSOR-CELLSClinical ImmunologyTumor Escapelcsh:QT-Lymphocytes CytotoxicPLoS ONE
researchProduct

Coordinated induction of drug transporters and phase I and II metabolism in human liver slices

2008

Although regulation of phase I drug metabolism in human liver is relatively well studied, the regulation of phase II enzymes and of drug transporters is incompletely characterized. Therefore, we used human liver slices to investigate the PXR, CAR and AhR-mediated induction of drug transporters and phase I and II metabolic enzymes. Precision-cut human liver slices were incubated for 5 or 24 h with prototypical inducers: phenobarbital (PB) (50 mu M) for CAR, beta-naphthoflavone (BNF) (25 mu M) for AhR, and rifampicin (RIF) (10 mu M) for PXR, and gene expression of the phase I enzymes CYP1A1, 1A2, 3A4, 3A5, 2136, 2A6, the phase II enzymes UGT1A1 and 1A6, and the transporters MRP2, MDR1, BSEP, …

DIFFERENTIAL REGULATIONQUANTITATIVE RT-PCRRAT-LIVERGene ExpressionPharmaceutical Sciencedrug transportersIn Vitro TechniquesPharmacologydigestive systemCytochrome P-450 Enzyme SystemUDP-GLUCURONOSYLTRANSFERASE 1A1Constitutive androstane receptorHumansSTELLATE CELL ACTIVATIONEnzyme inducerinductionliver slicesCONSTITUTIVE ANDROSTANE RECEPTORchemistry.chemical_classificationPregnane X receptorbiologyCYP3A4Multidrug resistance-associated protein 2TransporterPRIMARY HUMAN HEPATOCYTESMetabolic Detoxication Phase IIdrug metabolismEnzymeLiverPharmaceutical PreparationsBiochemistrychemistryEnzyme Inductionbiology.proteinMetabolic Detoxication Phase IPREGNANE-X-RECEPTORCarrier ProteinsPROTOTYPICAL INDUCERSDrug metabolismBILE-ACIDEuropean Journal of Pharmaceutical Sciences
researchProduct

EGFP Reporters for Direct and Sensitive Detection of Mutagenic Bypass of DNA Lesions

2020

The sustainment of replication and transcription of damaged DNA is essential for cell survival under genotoxic stress

DNA RepairTranscription GeneticDNA damageMutantGenetic VectorsGreen Fluorescent Proteinslcsh:QR1-502host cell reactivation (HCR)BiochemistryArticlelcsh:Microbiology03 medical and health scienceschemistry.chemical_compoundmutation assay0302 clinical medicinetranslesion synthesis (TLS)transcriptional mutagenesisTranscription (biology)Genes ReporterHumansCloning MolecularMolecular Biologyenhanced green fluorescent protein (EGFP)PolymeraseCells CulturedDNA damage tolerance030304 developmental biology0303 health sciencesbiologyDNA synthesisChemistryPoint mutationreporter assayRNACell biologyAmino Acid SubstitutionMutagenesis030220 oncology & carcinogenesisMutationbiology.proteinDNA damageDNAHeLa Cellsdamage bypassBiomolecules
researchProduct

Cockayne syndrome: varied requirement of transcription-coupled nucleotide excision repair for the removal of three structurally different adducts fro…

2014

Hereditary defects in the transcription-coupled nucleotide excision repair (TC-NER) pathway of damaged DNA cause severe neurodegenerative disease Cockayne syndrome (CS), however the origin and chemical nature of the underlying DNA damage had remained unknown. To find out, to which degree the structural properties of DNA lesions determine the extent of transcription arrest in human CS cells, we performed quantitative host cell reactivation analyses of expression vectors containing various synthetic adducts. We found that a single 3-(deoxyguanosin-N 2-yl)-2-acetylaminofluorene adduct (dG(N 2)-AAF) constitutes an unsurmountable obstacle to transcription in both CS-A and CS-B cells and is remov…

DNA RepairTranscription GeneticGenetic ToxicologyDNA damagelcsh:MedicineBiologyToxicologyHost-Cell ReactivationBiochemistryCockayne syndromeCell LineDNA Adductschemistry.chemical_compoundGenes ReporterTranscription (biology)Nucleic AcidsMolecular Cell BiologyGene expressionmedicineHumansGene SilencingCockayne SyndromePoly-ADP-Ribose Binding Proteinslcsh:ScienceFluorenesMultidisciplinaryBiology and life sciencesOligonucleotidelcsh:RDNA HelicasesDeoxyguanosineDNACell Biologymedicine.diseaseMolecular biologyDNA Repair EnzymesGene Expression RegulationchemistryBiochemistrylcsh:QDNAResearch ArticleNucleotide excision repairPLoS ONE
researchProduct