Search results for "g factor"

showing 10 items of 514 documents

Dendritic Cells Lose Ability to Present Protein Antigen after Stimulating Antigen-Specific T Cell Responses, despite Upregulation of MHC Class II Exp…

2000

Abstract Immature dendritic cells (DC) take up, process and present protein antigens; mature DC are specialized for stimulating primary T cell responses with increased expression of MHC class II and co-stimulatory molecules, but are incapable of processing and presenting soluble protein. The current study examined whether maturation of DC is triggered by T cell recognition of antigens presented by immature DC. Human DC derived from CD34+ progenitor cells by culture with granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-6 (IL-6) in serum-free medium could prime naive CD4+ T cells to keyhole limpet hemocyanin (KLH) and ovalbumin (OVA). The cultured DC retained the abil…

CD4-Positive T-LymphocytesTime FactorsOvalbuminT cellImmunologyCD1Bone Marrow CellsCell CommunicationCulture Media Serum-FreeInterferon-gammaInterleukin 21medicineHumansImmunology and AllergyCytotoxic T cellIL-2 receptorCD40 AntigensAntigen-presenting cellCells CulturedAntigen PresentationMHC class IIbiologyInterleukin-6Tumor Necrosis Factor-alphaHistocompatibility Antigens Class IIGranulocyte-Macrophage Colony-Stimulating FactorCell DifferentiationDendritic CellsHematologyIntercellular Adhesion Molecule-1Natural killer T cellMolecular biologyCoculture Techniquesmedicine.anatomical_structureHemocyaninsB7-1 Antigenbiology.proteinImmunobiology
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The DNA damage-induced decrease of Bcl-2 is secondary to the activation of apoptotic effector caspases.

2003

Apoptosis induced by DNA-damaging agents or radiation mainly proceeds through death receptor-independent caspase activation. The release of mitochondrial apoptogenic proteins, such as cytochrome c, into the cytoplasm leading to Apaf1-dependent activation of caspase-9 is a key event in this pathway. The permeability of the mitochondrial outer membrane is regulated by the various pro- and antiapoptotic Bcl-2 family proteins, and it is thought that DNA damage triggers apoptosis through the downregulation of antiapoptotic Bcl-2. Using murine embryonic fibroblasts (MEF) deficient and proficient in Apaf1, we show that DNA-damaging agents and radiation lead to a decline in Bcl-2 protein only in wt…

Cancer ResearchDNA damageCell TransplantationUltraviolet RaysTransplantation HeterologousApoptosisMice SCIDAdenocarcinomamedicine.disease_causeAdenoviridaeAmino Acid Chloromethyl KetonesMiceDownregulation and upregulationGeneticsmedicineTumor Cells CulturedAnimalsHumansAPAF1Enzyme InhibitorsMolecular BiologyCaspaseEtoposidebiologyDose-Response Relationship DrugCytochrome cProteinsDose-Response Relationship RadiationFibroblastsMolecular biologyCaspase InhibitorsCell biologyEnzyme ActivationPancreatic NeoplasmsApoptotic Protease-Activating Factor 1Proto-Oncogene Proteins c-bcl-2ApoptosisCytoplasmCaspasesbiology.proteinDactinomycinCarcinogenesisGene DeletionDNA DamageOncogene
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Recommendations from the iSBTc-SITC/FDA/NCI Workshop on Immunotherapy Biomarkers

2011

Abstract Purpose: To facilitate development of innovative immunotherapy approaches, especially for treatment concepts exploiting the potential benefits of personalized therapy, there is a need to develop and validate tools to identify patients who can benefit from immunotherapy. Despite substantial effort, we do not yet know which parameters of antitumor immunity to measure and which assays are optimal for those measurements. Experimental Design: The iSBTc-SITC (International Society for Biological Therapy of Cancer-Society for Immunotherapy of Cancer), FDA (Food and Drug Administration), and NCI (National Cancer Institute) partnered to address these issues for immunotherapy of cancer. Here…

Cancer ResearchPathologymedicine.medical_specialtyHealth Planning Guidelinesmedicine.medical_treatmentConsensus Development Conferences as TopicStandardized testImmune monitoringt-cell immunity cytokine flow-cytometry cancer vaccine consortium colony-stimulating factor b elispot assay phase-ii trial dendritic cells clinical-trials hiv vaccine harmonization guidelinesMedical OncologyArticleFood and drug administrationNeoplasmsmedicineBiomarkers TumorHumansMedical physicsPersonalized therapySocieties MedicalAntitumor immunitybusiness.industryQuality assessmentUnited States Food and Drug AdministrationCancerInternational AgenciesImmunotherapymedicine.diseaseNational Cancer Institute (U.S.)United StatesOncologyPractice Guidelines as TopicImmunotherapybusiness
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Hsp72 controls bortezomib-induced HepG2 cell death via interaction with pro-apoptotic factors.

2007

The proteasome inhibitor bortezomib is an efficacious inducer of apoptosis in the hepatoma HepG2 cell line. This study shows that bortezomib increased in these cells the level of the survival factor Hsp72 in a time- and dose-dependent manner. In a first phase of treatment, Hsp72 rapidly increased so that at 24 h of incubation with 50 nM bortezomib its level was approximately five-fold higher than the control. In this phase Hsp72 seemed to play a role in preventing HepG2 cell death, since it interacted with and sequestered the pro-apoptotic factors p53, AIF, Bax and Apaf-1. During a second day of treatment, although the nuclear levels of Hsp72, p53 and AIF increased, the interaction of Hsp72…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularTime FactorsCellBlotting WesternApoptosisHSP72 Heat-Shock ProteinsAmino Acid Chloromethyl KetonesBortezomibCell Line TumormedicineHumansImmunoprecipitationProtease Inhibitorscardiovascular diseasesCaspasebcl-2-Associated X ProteinOncogenebiologyBortezomibReverse Transcriptase Polymerase Chain ReactionLiver NeoplasmsApoptosis Inducing Factorproteasome inhibitor hepatocarcinoma apoptosisGeneral MedicineCell cycleBoronic Acidsmedicine.anatomical_structureApoptotic Protease-Activating Factor 1OncologyApoptosisPyrazinesProteasome inhibitorCancer researchbiology.proteinTumor Suppressor Protein p53Apoptosis Regulatory Proteinsmedicine.drugProtein Binding
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Regulation of CD1d expression by murine tumor cells: escape from immunosurveillance or alternate target molecules?

2002

alpha beta+ TCR T cells recognize peptide fragments displayed by MHC-class I or -class II molecules. Recently, additional mechanisms of antigen recognition by T cells have been identified, including CD1-mediated presentation of nonpeptide antigens. Only a limited number of CD1 antigens is retained in the mouse, i.e., the group II CD1 antigens, which are split into CD1D1 and CD1d2. Several T cell subsets have been shown to interact with murine CD1 antigens, including NK cells or "natural T cells" with the invariant V alpha 14 J alpha 281 TCR chain. Even if TAP defects may prevent classical endogenous antigen presentation in tumor cell lines, antigen presentation via CD1 is still functional. …

Cancer ResearchT cellAntigen presentationCD1chemical and pharmacologic phenomenaBiologyNatural killer cellAntigens CD1Immunoenzyme TechniquesInterferon-gammaMiceNK-92Monitoring ImmunologicmedicineCytotoxic T cellAnimalsRNA MessengerAntigen-presenting cellCells CulturedDNA PrimersMice Inbred BALB CReverse Transcriptase Polymerase Chain ReactionAntibodies MonoclonalGranulocyte-Macrophage Colony-Stimulating Factorhemic and immune systemsNeoplasms ExperimentalCytotoxicity Tests ImmunologicFlow CytometryCell biologyGene Expression Regulation NeoplasticKiller Cells NaturalMice Inbred C57BLmedicine.anatomical_structureOncologyCD1DImmunologybiology.proteinCytokinesAntigens CD1dInternational journal of cancer
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CD83+ human dendritic cells transfected with tumor peptide cDNA by electroporation induce specific T-cell responses: A potential tool for gene immuno…

2000

Dendritic cells (DC) are the most potent immunostimulatory cells, with the capacity to induce primary T-cell responses. Functional autologous DC can be generated from fetal calf serum-free peripheral blood mononuclear cells in the presence of interleukin-4 and granulocyte-macrophage colony-stimulating factor and are stimulated with a defined cytokine cocktail for terminal maturation. We were able to establish a nonviral transfection protocol for these DC by electroporation. Using enhanced green fluorescent protein as a reporter gene, we achieved transfection efficiencies of up to 10%. FACScan analyses revealed a stable phenotype, and the expression of major histocompatibility complex class …

Cancer Researchanimal structuresDNA Complementaryvirusesmedicine.medical_treatmentT cellT-LymphocytesGreen Fluorescent ProteinsImmunoglobulinsTransfectionGreen fluorescent proteinAntigens CDGenes ReportermedicineHumansMolecular BiologyCells CulturedReporter geneMembrane GlycoproteinsChemistryElectroporationfungiGranulocyte-Macrophage Colony-Stimulating FactorImmunotherapyTransfectionDendritic CellsGenetic TherapyFlow CytometryMolecular biologyRecombinant ProteinsLuminescent ProteinsCytokinemedicine.anatomical_structureElectroporationembryonic structuresMolecular MedicineImmunotherapyInterleukin-4Clone (B-cell biology)Cancer gene therapy
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53 LUSPATERCEPT INCREASES HEMOGLOBIN AND REDUCES TRANSFUSION BURDEN IN PATIENTS WITH LOW OR INTERMEDIATE-1 RISK MYELODYSPLASTIC SYNDROMES (MDS): PREL…

2015

Introduction. ACE-536, a recombinant fusion protein containing modified activin receptor type IIB and IgG Fc, is being developed for the treatment of anemias due to ineffective erythropoiesis, such as myelodysplastic syndromes (MDS). Patients with MDS often have elevated levels of erythropoietin (EPO) and may be non-responsive or refractory to erythropoiesis-stimulating agents (ESAs). MDS patients have also been shown to have increased serum GDF11 levels (Suragani R et al., Nature Medicine 2014) and increased Smad 2/3 signaling in the bone marrow (Zhou L et al., Blood 2008). ACE-536 binds to ligands in the TGF-s superfamily, including GDF11, inhibits Smad 2/3 signaling, and promotes late-st…

Cancer Researchmedicine.medical_specialtybusiness.industryAnemiaMyelodysplastic syndromesPhases of clinical researchDecitabineHematologymedicine.diseaseGastroenterologyGranulocyte colony-stimulating factorOncologyErythropoietinInternal medicinemedicineAbsolute neutrophil countbusinessIntensive care medicineLenalidomidemedicine.drugLeukemia Research
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Comparative antitumor effect among GM-CSF, IL-12 and GM-CSF+IL-12 genetically modified tumor cell vaccines.

2013

Genetically modified cells have been shown to be one of the most effective cancer vaccine strategies. An evaluation is made of the efficacy of both preventive and therapeutic antitumor vaccines against murine melanoma, using C57BL/6 mice and irradiated B16 tumor cells expressing granulocyte and macrophage colony-stimulating factor (GM-CSF), interleukin-12 (IL-12) or both. Tumor was transplanted by the injection of wild-type B16 cells. Tumor growth and survival were measured to evaluate the efficacy of vaccination. Specific humoral response and immunoglobulin G (IgG) switch were evaluated measuring total IgG and IgG1 and IgG2a subtypes against tumor membrane proteins of B16 cells. In prevent…

Cancer Researchmedicine.medical_treatmentMelanoma ExperimentalBiologyTransfectionCancer VaccinesImmunotherapy AdoptiveImmunoglobulin GMicemedicineMacrophageAnimalsMolecular BiologyMicroscopy ConfocalMelanomaGranulocyte-Macrophage Colony-Stimulating FactorImmunotherapymedicine.diseaseInterleukin-12Survival AnalysisGenetically modified organismVaccinationMice Inbred C57BLImmunologyInterleukin 12biology.proteinMolecular MedicineCancer vaccineCancer gene therapy
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mRNA-induction and cytokine release during in vitro exposure of human nasal respiratory epithelia to methyl methacrylate

2007

Abstract Background Methyl methacrylate (MMA) has been reported to cause histopathological changes in rodent nasal epithelium after inhalation challenges. Data in humans are lacking. Methods In this in vitro design 22 primary cell cultures taken from inferior turbinate tissue of healthy individuals were exposed to MMA concentrations of 50 ppm (German MAK-value) and 200 ppm. mRNA expression and cytokine release of inflammatory mediators were quantified after 4 h and after 24 h. Controls were exposed to synthetic air. Q-PCR analysis was performed for TNF-α, IL-1β, IL-6, IL-8, MCP-1, GMCSF, Cox-1 and Cox-2. ELISA assays were performed from culture supernatants for TNF-α, IL-1β, IL-6, IL-8, MCP…

Cell Survivalmedicine.medical_treatmentCell Culture TechniquesEnzyme-Linked Immunosorbent AssayInflammationMethylmethacrylateBiologyToxicologyAndrologyDownregulation and upregulationmedicineHumansRNA MessengerRespiratory systemCells CulturedChemokine CCL2Dose-Response Relationship DrugReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaInterleukinsGranulocyte-Macrophage Colony-Stimulating FactorAntimutagenic AgentsEpithelial CellsGeneral MedicineEpitheliumIn vitroNasal MucosaDose–response relationshipCytokinemedicine.anatomical_structureGene Expression RegulationCyclooxygenase 2Cell cultureImmunologyCyclooxygenase 1Cytokinesmedicine.symptomToxicology Letters
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Laser capture microdissection and genetic analysis of carbon-labeled Kupffer cells.

2009

AIM: To develop a method of labeling and micro-dissecting mouse Kupffer cells within an extraordinarily short period of time using laser capture microdissection (LCM). METHODS: Tissues are complex structures comprised of a heterogeneous population of interconnected cells. LCM offers a method of isolating a single cell type from specific regions of a tissue section. LCM is an essential approach used in conjunction with molecular analysis to study the functional interaction of cells in their native tissue environment. The process of labeling and acquiring cells by LCM prior to mRNA isolation can be elaborate, thereby subjecting the RNA to considerable degradation. Kupffer cell labeling is ach…

Cell typeKupffer CellsCellPopulationReceptor Macrophage Colony-Stimulating FactorAsialoglycoprotein ReceptorBiologyMicemedicineAnimalsRNA MessengerReceptors ImmunologiceducationMicrodissectionLaser capture microdissectionOligonucleotide Array Sequence Analysiseducation.field_of_studyMicroarray analysis techniquesGene Expression ProfilingLasersKupffer cellGastroenterologyGeneral MedicineOriginal ArticlesMolecular biologyCarbonGene expression profilingMice Inbred C57BLmedicine.anatomical_structureFemaleMicrodissectionWorld journal of gastroenterology
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