Search results for "Colony-Stimulating Factor"

showing 4 items of 174 documents

Granulocyte-macrophage colony-stimulating factor (CSF) and multilineage CSF recruit human monocytes to express granulocyte CSF

1989

Abstract We assessed the capacity of recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF) and multilineage (Multi)-CSF to induce release of granulocyte-CSF (G-CSF) by highly purified peripheral blood monocyte (Mo) preparations. Our results reveal that GM-CSF and Multi-CSF, either alone or in a synergistic concert, activate Mo to transcribe G-CSF messenger (m) RNA and release biologically active G- CSF protein into their culture supernatants. G-CSF had no regulatory effect on Mo expression of cytoplasmic G-CSF mRNA levels and G-CSF protein secretion by itself. These differential actions of CSFs provide further insight into self-regulatory mechanisms within the growth f…

medicine.medical_treatmentImmunologyGranulocyteBiologyBiochemistryMonocyteslaw.inventionColony-Stimulating FactorslawmedicineHumansRNA MessengerGrowth SubstancesCells CulturedCSF albuminCell-Free SystemGrowth factorGranulocyte-Macrophage Colony-Stimulating FactorRNABiological activityCell BiologyHematologyMolecular biologyRecombinant ProteinsDrug CombinationsGranulocyte macrophage colony-stimulating factorSecretory proteinmedicine.anatomical_structureImmunologyRecombinant DNAGranulocytesmedicine.drugBlood
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A MiR-142-3p/EGR2 Feedback Circuitry In Human CSF-1 Driven Differentiation of Monocytes Into Macrophages

2011

Abstract Abstract 2366 Colony-stimulating factor-1 (CSF-1 or M-CSF) triggers the differentiation of human peripheral blood monocytes into macrophages through and integrated cytokine/transcription factors circuitry. Using microarray profiling to explore the role of microRNAs (miRNAs) in this molecular circuitry, we identified the down-regulation of miR-142-3p in human macrophages obtained from CSF-1-treated monocytes. We show that miR-142-3p is a repressor of the transcription factor EGR2 (Early Growth Response 2) through direct 3'UTR interactions. Interestingly, EGR2 binds the promoter of the pre-miR-142-3p gene to negatively regulate its expression, identifying a self-regulatory feedback l…

medicine.medical_treatmentImmunologyRepressorChronic myelomonocytic leukemiaCell BiologyHematologyBiologyColony-stimulating factormedicine.diseaseBiochemistryCell biologyCytokinemicroRNAmedicineGeneTranscription factorProto-oncogene tyrosine-protein kinase SrcBlood
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Antitumor Cell-Complex Vaccines Employing Genetically Modified Tumor Cells and Fibroblasts

2014

The present study evaluates the immune response mediated by vaccination with cell complexes composed of irradiated B16 tumor cells and mouse fibroblasts genetically modified to produce GM-CSF. The animals were vaccinated with free B16 cells or cell complexes. We employed two gene plasmid constructions: one high producer (pMok) and a low producer (p2F). Tumor transplant was performed by injection of B16 tumor cells. Plasma levels of total IgG and its subtypes were measured by ELISA. Tumor volumes were measured and survival curves were obtained. The study resulted in a cell complex vaccine able to stimulate the immune system to produce specific anti-tumor membrane proteins (TMP) IgG. In the g…

non-viralHealth Toxicology and MutagenesisGenetic enhancementCellMelanoma Experimentallcsh:MedicineBiologyToxicologyArticleImmunoglobulin GMicePlasmidImmune systemCell Line TumormedicineAnimalsCells Culturedlcsh:RGranulocyte-Macrophage Colony-Stimulating FactorMembrane ProteinsTransfectionFibroblastsMolecular biologygene therapycell complexesTumor BurdenGenetically modified organismGranulocyte macrophage colony-stimulating factormedicine.anatomical_structureImmunoglobulin Gbiology.proteincancer vaccinesbystander cellsmedicine.drugToxins
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Enhancement by TNF-alpha of reactivation and replication of latent herpes simplex virus from trigeminal ganglia of mice.

1995

The influence of tumor-necrosis-factor-alpha (TNF-alpha), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukine-1 (IL-1) and IL-3 on the in vitro reactivation frequency and replication rate of trigeminal ganglia of mice latently infected with herpes simplex virus (HSV) strain KOS was studied. It could be demonstrated that TNF-alpha and possibility GM-CSF, but not IL-1 and IL-3, enhanced the reactivation frequency and replication of HSV. Interferon alpha/beta (IFN alpha/beta) prevented reactivation and replication.

virusesmedicine.medical_treatmentHerpesvirus 1 HumanBiologymedicine.disease_causeVirus ReplicationVirusHerpesviridaeMiceInterferonVirologyAlphaherpesvirinaeChlorocebus aethiopsmedicineAnimalsHumansVero CellsMice Inbred BALB CTumor Necrosis Factor-alphaGranulocyte-Macrophage Colony-Stimulating FactorInterferon-alphaGeneral MedicineInterferon-betabiology.organism_classificationVirologyIn vitroVirus LatencyCytokineHerpes simplex virusViral replicationTrigeminal GanglionInterleukin-3Virus Activationmedicine.drugInterleukin-1Archives of virology
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