2025
A Phase I, First-in-Human, Dose-Escalation, Expansion Trial of Cytokine-Encoding Synthetic mRNA Mixture Alone or with Cemiplimab in Advanced Solid Tumors
Bechter O, Loquai C, Champiat S, Baurain J, Grob J, Utikal J, Rottey S, Berrocal A, Hassel J, Arance A, Sanmamed M, Boers-Sonderen M, Gastman B, Gebhardt C, Delafontaine B, Sahin U, Türeci Ö, Brueck P, Abbadessa G, Marpadga R, Lee H, Yang Y, Buday B, Di Genova G, Wang H, Xia B, Lee J, Lebbe C. A Phase I, First-in-Human, Dose-Escalation, Expansion Trial of Cytokine-Encoding Synthetic mRNA Mixture Alone or with Cemiplimab in Advanced Solid Tumors. Clinical Cancer Research 2025, 31: 2358-2369. PMID: 40152791, PMCID: PMC12163594, DOI: 10.1158/1078-0432.ccr-24-1983.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntibodies, Monoclonal, HumanizedAntineoplastic Combined Chemotherapy ProtocolsCytokinesFemaleGranulocyte-Macrophage Colony-Stimulating FactorHumansInterferon alpha-2Interleukin-12Interleukin-15MaleMaximum Tolerated DoseMiddle AgedNeoplasmsRNA, MessengerTreatment OutcomeConceptsAdvanced solid tumorsMaximum administered doseSolid tumorsCombination therapyEscalation phaseTreated with anti-PD-1 therapyTreated with anticancer therapyAnti-PD-1 therapyTreatment-related adverse eventsDose level 8Predefined dose levelsInjection-site painFirst-in-humanPlasma cytokine concentrationsDose escalationAntitumor responsePartial responseIntratumoral administrationExpansion trialIL-15IFN-gCemiplimabAdverse eventsCytokine concentrationsDose levels
2023
Assay optimization for the objective quantification of human multilineage colony-forming units
Thompson E, Carlino M, Scanlon V, Grimes H, Krause D. Assay optimization for the objective quantification of human multilineage colony-forming units. Experimental Hematology 2023, 124: 36-44.e3. PMID: 37271449, PMCID: PMC10527702, DOI: 10.1016/j.exphem.2023.05.007.Peer-Reviewed Original ResearchMeSH KeywordsCells, CulturedColony-Forming Units AssayGranulocyte-Macrophage Colony-Stimulating FactorHematopoietic Stem CellsHumansInterleukin-3Reproducibility of ResultsConceptsFluorescence-activated cell sortingLineage potentialCommon myeloid progenitorsHigh-throughput microscopyMultilineage colony-forming unitsProportion of coloniesSpecific growth factorsCFU assayColony-forming unit assaysMultipotent progenitorsProgenitor populationsLineage outputSitu immunofluorescenceMegakaryocytic lineageMK cellsMegakaryocytic cellsCell typesMyeloid progenitorsProgenitor cellsCell morphologyCell sortingUnit assaysIL-3Colony typesCulture conditions
2022
Human neutrophil development and functionality are enabled in a humanized mouse model
Zheng Y, Sefik E, Astle J, Karatepe K, Öz HH, Solis AG, Jackson R, Luo HR, Bruscia EM, Halene S, Shan L, Flavell RA. Human neutrophil development and functionality are enabled in a humanized mouse model. Proceedings Of The National Academy Of Sciences Of The United States Of America 2022, 119: e2121077119. PMID: 36269862, PMCID: PMC9618085, DOI: 10.1073/pnas.2121077119.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCytokinesGranulocyte Colony-Stimulating FactorGranulocyte-Macrophage Colony-Stimulating FactorHumansMiceNeutrophilsReceptors, Granulocyte Colony-Stimulating FactorConceptsHumanized mouse modelMouse modelHuman immune systemHuman neutrophilsImmune systemFunctional human immune systemGranulocyte colony-stimulating factorUnique mouse modelColony-stimulating factorHuman G-CSFMISTRG miceG-CSF receptor geneBacterial burdenInfectious challengeG-CSFNeutrophilsMiceNeutrophil developmentReceptor geneDiseaseArginase-1 Is Required for Macrophage-Mediated Renal Tubule Regeneration
Shin NS, Marlier A, Xu L, Doilicho N, Linberg D, Guo J, Cantley LG. Arginase-1 Is Required for Macrophage-Mediated Renal Tubule Regeneration. Journal Of The American Society Of Nephrology 2022, 33: 1077-1086. PMID: 35577558, PMCID: PMC9161787, DOI: 10.1681/asn.2021121548.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArginaseGranulocyte-Macrophage Colony-Stimulating FactorMacrophagesMiceMice, Inbred C57BLRegenerationReperfusion InjuryConceptsIschemia-reperfusion injuryTubular cell proliferationArginase-1Contralateral nephrectomyRenal repairFl/Littermate controlsTubular cellsReceptor 1GM-CSFRenal tubular cell proliferationRenal tubule regenerationMacrophage scavenger receptor 1Mannose receptor 1Cell proliferative responsesCell proliferationScavenger receptor 1Coculture of macrophagesDead cell debrisKidney injuryKidney repairRenal responseProinflammatory activationTubule regenerationMouse survivalThe feasibility of using an autologous GM-CSF-secreting breast cancer vaccine to induce immunity in patients with stage II–III and metastatic breast cancers
Anderson KS, Erick TK, Chen M, Daley H, Campbell M, Colson Y, Mihm M, Zakka LR, Hopper M, Barry W, Winer EP, Dranoff G, Overmoyer B. The feasibility of using an autologous GM-CSF-secreting breast cancer vaccine to induce immunity in patients with stage II–III and metastatic breast cancers. Breast Cancer Research And Treatment 2022, 194: 65-78. PMID: 35482127, PMCID: PMC9046531, DOI: 10.1007/s10549-022-06562-y.Peer-Reviewed Original ResearchMeSH KeywordsBreast NeoplasmsCancer VaccinesFeasibility StudiesFemaleGenetic VectorsGranulocyte-Macrophage Colony-Stimulating FactorHumansConceptsBreast cancer vaccinesAutologous GM-CSFBreast cancerMetastatic diseaseGM-CSFStage IICancer vaccinesTumor cellsEvidence of diseaseStart of vaccinationInjection site reactionsMetastatic breast cancerUpper respiratory symptomsImmune cell infiltrationRole of vaccinationReplication-defective adenoviral vectorEvaluable patientsMethodsTumor cellsStable diseaseWeekly vaccinationsJoint painProgressive diseaseRespiratory symptomsFifth injectionTRIAL REGISTRATIONMultiomic characterization of pancreatic cancer-associated macrophage polarization reveals deregulated metabolic programs driven by the GM-CSF–PI3K pathway
Boyer S, Lee H, Steele N, Zhang L, Sajjakulnukit P, Andren A, Ward M, Singh R, Basrur V, Zhang Y, Nesvizhskii A, di Magliano M, Halbrook C, Lyssiotis C. Multiomic characterization of pancreatic cancer-associated macrophage polarization reveals deregulated metabolic programs driven by the GM-CSF–PI3K pathway. ELife 2022, 11: e73796. PMID: 35156921, PMCID: PMC8843093, DOI: 10.7554/elife.73796.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Line, TumorCell Transformation, NeoplasticGene Expression ProfilingGranulocyte-Macrophage Colony-Stimulating FactorHumansMetabolic Networks and PathwaysMetabolomicsMiceMice, Inbred C57BLPancreatic NeoplasmsProteomicsSignal TransductionTranscription FactorsTumor-Associated MacrophagesConceptsTumor-educated macrophagesSingle-cell RNA sequencing datasetsCancer cellsMultiomics characterizationRNA sequencing datasetsTumor-associated macrophagesPI3K-Akt pathwayPI3K pathwayMetabolic programsSequencing datasetsGene expressionMetabolic crosstalkFunction of TAMsCell typesK pathwayGM-CSFGranulocyte-macrophage colony-stimulating factorTumor promotingModel systemEpithelial cellsPathwayColony-stimulating factorMetabolic signaturesMutant KRASMalignant epithelial cells
2021
Autocrine GMCSF Signaling Contributes to Growth of HER2+ Breast Leptomeningeal CarcinomatosisGMCSF Contributes to Breast Leptomeningeal Carcinomatosis
Ansari K, Bhan A, Saotome M, Tyagi A, De Kumar B, Chen C, Takaku M, Jandial R. Autocrine GMCSF Signaling Contributes to Growth of HER2+ Breast Leptomeningeal CarcinomatosisGMCSF Contributes to Breast Leptomeningeal Carcinomatosis. Cancer Research 2021, 81: 4723-4735. PMID: 34247146, PMCID: PMC8986153, DOI: 10.1158/0008-5472.can-21-0259.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutocrine CommunicationBreast NeoplasmsCell Line, TumorCell ProliferationCell SurvivalDisease Models, AnimalGene ExpressionGranulocyte-Macrophage Colony-Stimulating FactorHumansMeningeal CarcinomatosisMiceOncogene ProteinsProtein Kinase InhibitorsReceptor, ErbB-2Signal TransductionXenograft Model Antitumor AssaysConceptsOligodendrocyte progenitor cellsLeptomeningeal carcinomatosisLC growthPan-Aurora kinase inhibitorKinase inhibitorsSuppression of HER2Growth of HER2Central nervous system cell typesProliferation of HER2Nervous system cell typesBreast cancer cellsPrimary HER2Targetable axisOminous complicationIntrathecal deliveryMolecular mechanismsTreatment optionsDire prognosisSpinal cordBreast cancerHER2LC developmentLeptomeningesLC/MS-MSCarcinomatosis
2020
Albumin fusion with granulocyte-macrophage colony-stimulating factor acts as an immunotherapy against chronic tuberculosis
Chuang YM, He L, Pinn ML, Tsai YC, Cheng MA, Farmer E, Karakousis PC, Hung CF. Albumin fusion with granulocyte-macrophage colony-stimulating factor acts as an immunotherapy against chronic tuberculosis. Cellular & Molecular Immunology 2020, 18: 2393-2401. PMID: 32382128, PMCID: PMC8484439, DOI: 10.1038/s41423-020-0439-2.Peer-Reviewed Original ResearchMeSH KeywordsAlbuminsAnimalsGranulocyte-Macrophage Colony-Stimulating FactorImmunotherapyMiceMycobacterium tuberculosisTuberculosisConceptsTuberculosis infectionChronic tuberculosis infectionPotent immune responsesGM-CSFLymph nodesDendritic cellsImmune responseChronic Mycobacterium tuberculosis infectionHigher IL-1β levelsAlbumin fusionLung bacillary burdenTB treatment regimensDendritic cell populationsDrug-resistant TBIL-1β levelsGM-CSF administrationMycobacterium tuberculosis infectionNaive T cellsIL-1β releaseBacillary burdenChronic tuberculosisNovel immunotherapiesTreatment regimensVaccination platformSubcutaneous administration
2019
Tubular GM-CSF Promotes Late MCP-1/CCR2-Mediated Fibrosis and Inflammation after Ischemia/Reperfusion Injury
Xu L, Sharkey D, Cantley LG. Tubular GM-CSF Promotes Late MCP-1/CCR2-Mediated Fibrosis and Inflammation after Ischemia/Reperfusion Injury. Journal Of The American Society Of Nephrology 2019, 30: 1825-1840. PMID: 31315923, PMCID: PMC6779361, DOI: 10.1681/asn.2019010068.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedChemokine CCL2FibrosisGranulocyte-Macrophage Colony-Stimulating FactorInflammationKidneyKidney TubulesMacrophagesMiceReceptors, CCR2Reperfusion InjuryConceptsIschemia/reperfusion injuryWild-type miceTubular cellsTubular injuryReperfusion injuryImmune cellsKidney ischemia/reperfusion injuryUnilateral ischemia/reperfusion injuryMCP-1/CCR2Monocyte chemoattractant protein-1Initial kidney damageInjured tubular cellsKidney 14 daysKidney injury markersProgressive interstitial fibrosisProfibrotic growth factorsChemoattractant protein-1MCP-1 receptorGranulocyte-macrophage colony-stimulating factorRenal tubular cellsNumber of macrophagesTime of repairColony-stimulating factorCoculture of macrophagesMacrophages persistRipk3-induced inflammation by I-MDSCs promotes intestinal tumors
Jayakumar A, Bothwell ALM. Ripk3-induced inflammation by I-MDSCs promotes intestinal tumors. Cancer Research 2019, 79: canres.2153.2018. PMID: 30786994, PMCID: PMC7395226, DOI: 10.1158/0008-5472.can-18-2153.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsColorectal NeoplasmsGranulocyte-Macrophage Colony-Stimulating FactorHumansInflammationInterleukinsMiceMice, Inbred C57BLMyeloid-Derived Suppressor CellsReceptor-Interacting Protein Serine-Threonine KinasesConceptsReceptor-interacting protein kinase 3I-MDSCsIntestinal tumorsIntestinal tumor modelTumor modelColorectal cancerT cellsKey inflammatory mechanismsAntitumor T cellsTransplantable tumor modelsPotential therapeutic targetPossible therapeutic interventionsI-MDSCMDSC subsetsInflammatory mechanismsMDSC functionSuppressor cellsTumor sizeInflammatory cytokinesMC38 tumorsCytokine synthesisMonocytic markersTherapeutic targetTumorigenic factorsTherapeutic interventions
2018
Antigen-Specific CD8 Lytic Phenotype Induced by Sipuleucel-T in Hormone-Sensitive or Castration-Resistant Prostate Cancer and Association with Overall Survival
Antonarakis ES, Small EJ, Petrylak D, Quinn DI, Kibel AS, Chang NN, Dearstyne E, Harmon M, Campogan D, Haynes H, Vu T, Sheikh NA, Drake CG. Antigen-Specific CD8 Lytic Phenotype Induced by Sipuleucel-T in Hormone-Sensitive or Castration-Resistant Prostate Cancer and Association with Overall Survival. Clinical Cancer Research 2018, 24: 4662-4671. PMID: 29858218, PMCID: PMC6481607, DOI: 10.1158/1078-0432.ccr-18-0638.Peer-Reviewed Original ResearchMeSH KeywordsAcid PhosphataseCD8-Positive T-LymphocytesCell Line, TumorCell ProliferationClinical Trials as TopicGene Expression Regulation, NeoplasticGranulocyte-Macrophage Colony-Stimulating FactorHumansLysosomal-Associated Membrane Protein 1MaleNeoplasm MetastasisNeoplasms, Hormone-DependentProstatic Neoplasms, Castration-ResistantRecombinant Fusion ProteinsT-Lymphocytes, CytotoxicTissue ExtractsConceptsSipuleucel-T treatmentMetastatic castration-resistant prostate cancerProstatic acid phosphataseOverall survivalCTL activityWeek 26Immune responseWeek 6Peripheral cellular immune responsesCytotoxic T lymphocyte activityCastration-resistant prostate cancerEfficacy of sipuleucelImproved overall survivalMedian overall survivalT lymphocyte activityT cell responsesCellular immune responsesT cell proliferationClin Cancer ResHealthy volunteer samplesCD107a expressionLonger OSLymphocyte activityCytolytic responsesTertile analysis
2016
Differential Regulation of Macrophage Glucose Metabolism by Macrophage Colony-stimulating Factor and Granulocyte-Macrophage Colony-stimulating Factor: Implications for 18F FDG PET Imaging of Vessel Wall Inflammation.
Tavakoli S, Short JD, Downs K, Nguyen HN, Lai Y, Zhang W, Jerabek P, Goins B, Sadeghi MM, Asmis R. Differential Regulation of Macrophage Glucose Metabolism by Macrophage Colony-stimulating Factor and Granulocyte-Macrophage Colony-stimulating Factor: Implications for 18F FDG PET Imaging of Vessel Wall Inflammation. Radiology 2016, 283: 87-97. PMID: 27849433, PMCID: PMC5375627, DOI: 10.1148/radiol.2016160839.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationCells, CulturedFluorodeoxyglucose F18GlucoseGranulocyte-Macrophage Colony-Stimulating FactorInflammationMacrophage Colony-Stimulating FactorMacrophagesMicePositron-Emission TomographyRadiopharmaceuticalsConceptsM-CSFMurine atherosclerotic aortasStable isotope tracingActivation stateExtracellular acidification rateGM-CSFMitochondrial biogenesisMacrophage colony-stimulating factorGlycolytic enzymesGlucose fluxMurine peritoneal macrophagesDistinct activation statesGlycolytic pathwayGlucose transporterCritical glycolytic enzymeGlycolytic metabolismAcidification rateIsotope tracingIntermediary metabolitesGlucose uptakeImmunometabolic phenotypeMurine atherosclerotic plaquesCell culturesSimilar levelsOxidative metabolismIL-17 Promotes Neutrophil-Mediated Immunity by Activating Microvascular Pericytes and Not Endothelium
Liu R, Lauridsen HM, Amezquita RA, Pierce RW, Jane-Wit D, Fang C, Pellowe AS, Kirkiles-Smith NC, Gonzalez AL, Pober JS. IL-17 Promotes Neutrophil-Mediated Immunity by Activating Microvascular Pericytes and Not Endothelium. The Journal Of Immunology 2016, 197: 2400-2408. PMID: 27534549, PMCID: PMC5010945, DOI: 10.4049/jimmunol.1600138.Peer-Reviewed Original ResearchMeSH KeywordsCaspase 9Cells, CulturedCulture MediaCytokinesEndothelium, VascularGranulocyte Colony-Stimulating FactorGranulocyte-Macrophage Colony-Stimulating FactorHumansInterleukin-17Neutrophil InfiltrationNeutrophilsPericytesReceptors, Interleukin-17Sequence Analysis, RNATumor Necrosis Factor-alphaVenulesConceptsIL-17Endothelial cellsIL-17RAIL-17RC subunitsCultured human endothelial cellsInflammatory gene expressionMicrovascular endothelial cellsNeutrophil-mediated immunityNeutrophil infiltrationNeutrophilic inflammationHuman endothelial cellsAcute inflammationIL-1βNeutrophil functionProinflammatory cytokinesIL-8Proinflammatory moleculesIL-1αIL-17RCIL-1Human pericytesG-CSFMicrovascular pericytesNeutrophil productionNeutrophil survivalGranulocyte‐macrophage colony‐stimulating factor (GM‐CSF) is released by female mouse bladder urothelial cells and expressed by the urothelium as an early response to lipopolysaccharides (LPS)
Li Y, Lu M, Alvarez‐Lugo L, Chen G, Chai TC. Granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) is released by female mouse bladder urothelial cells and expressed by the urothelium as an early response to lipopolysaccharides (LPS). Neurourology And Urodynamics 2016, 36: 1020-1025. PMID: 27337494, DOI: 10.1002/nau.23057.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, IntravesicalAnimalsCells, CulturedFemaleGranulocyte-Macrophage Colony-Stimulating FactorLipopolysaccharidesMiceMice, Inbred C57BLModels, AnimalUrinary BladderUrotheliumConceptsBladder urotheliumCyclooxygenase-2GM-CSFCyclooxygenase-1GM-CSFRαBladder tissueMRNA expressionTumor necrosis factor αCOX-2 mRNA expressionVivo LPS exposureVascular endothelial growth factorNecrosis factor αDose-dependent releaseIncrease of VEGFGranulocyte-macrophage colony-stimulating factor (GM-CSF) signalingBladder urothelial cellsConcentrations of lipopolysaccharideGM-CSF mRNA expressionEndothelial growth factorGM-CSF antibodyMouse bladder urotheliumGM-CSF activityLPS exposurePain transductionSingle doseAutoreactive T Cells from Patients with Myasthenia Gravis Are Characterized by Elevated IL-17, IFN-γ, and GM-CSF and Diminished IL-10 Production
Cao Y, Amezquita RA, Kleinstein SH, Stathopoulos P, Nowak RJ, O'Connor KC. Autoreactive T Cells from Patients with Myasthenia Gravis Are Characterized by Elevated IL-17, IFN-γ, and GM-CSF and Diminished IL-10 Production. The Journal Of Immunology 2016, 196: 2075-2084. PMID: 26826242, PMCID: PMC4761502, DOI: 10.4049/jimmunol.1501339.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAutoimmunityCD4-Positive T-LymphocytesCell SeparationCytokinesEnzyme-Linked Immunosorbent AssayFemaleGranulocyte-Macrophage Colony-Stimulating FactorHumansInterferon-gammaInterleukin-10Interleukin-17MaleMiddle AgedMyasthenia GravisPhenotypePolymerase Chain ReactionT-Lymphocyte SubsetsConceptsAutoreactive T cellsT cell compartmentHealthy control subjectsMyasthenia gravisT cellsMG patientsIL-17Control subjectsT cell librariesB cellsGM-CSFMemory T cell compartmentElevated IL-17Prototypical autoimmune diseaseIL-10 productionMemory T cellsCell compartmentIL-10 expressionB cell compartmentPathogenic phenotypeMG cohortPathogenic autoantibodiesAutoimmune responseClinical manifestationsProinflammatory phenotype
2015
Gatekeeper role of brain antigen‐presenting CD11c+ cells in neuroinflammation
Paterka M, Siffrin V, Voss JO, Werr J, Hoppmann N, Gollan R, Belikan P, Bruttger J, Birkenstock J, Jung S, Esplugues E, Yogev N, Flavell RA, Bopp T, Zipp F. Gatekeeper role of brain antigen‐presenting CD11c+ cells in neuroinflammation. The EMBO Journal 2015, 35: 89-101. PMID: 26612827, PMCID: PMC4718005, DOI: 10.15252/embj.201591488.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigen-Presenting CellsBrainCD11c AntigenCell MovementDendritic CellsEncephalomyelitis, Autoimmune, ExperimentalGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-17Mice, Inbred C57BLT-LymphocytesTh17 CellsConceptsPathogenic T cellsT cellsFrequent chronic inflammatory diseaseChronic inflammatory diseaseAntigen-presenting cellsInflammatory chemokines CCL5Autoimmune neuroinflammationPerivascular clustersTh17 cellsDendritic cellsMultiple sclerosisInflammatory diseasesChemokine CCL5Disease severityCNSGM-CSFExpression correlatesTwo-photon microscopyNeuroinflammationGatekeeper functionSurvivalCellsGatekeeper rolePotent typeImpaired enrichmentPersistent change in cardiac fibroblast physiology after transient ACE inhibition
D'Souza K, Biwer L, Madhavpeddi L, Ramaiah P, Shahid W, Hale T. Persistent change in cardiac fibroblast physiology after transient ACE inhibition. AJP Heart And Circulatory Physiology 2015, 309: h1346-h1353. PMID: 26371174, DOI: 10.1152/ajpheart.00615.2015.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin-Converting Enzyme InhibitorsAnimalsCardiomyopathiesCell ProliferationCells, CulturedChemokine CCL2Collagen Type IDisease Models, AnimalEnalaprilFibroblastsFibrosisGranulocyte-Macrophage Colony-Stimulating FactorHeart VentriclesHypertensionInflammation MediatorsMaleNG-Nitroarginine Methyl EsterNitric Oxide SynthasePhenotypeRats, Inbred SHRTime FactorsConceptsTransient ACE inhibitionACE inhibitionFibroblast physiologyArginine methyl ester treatmentCardiac fibroblastsAngiotensin-Converting Enzyme InhibitionPersistent changesMethyl ester treatmentChemoattractant protein-1Granulocyte macrophage-colony stimulating factorArginine methyl esterMacrophage-colony stimulating factorMacrophage-recruiting chemokinesCardiac fibroblast phenotypeRole of fibroblastsUntreated SHRHypertensive ratsNOS inhibitionWashout periodACE inhibitorsCardioprotective effectsChemokine releaseMyocardial injuryCardiac fibrosisNOS inhibitorBiologic Activity of Autologous, Granulocyte–Macrophage Colony-Stimulating Factor Secreting Alveolar Soft-Part Sarcoma and Clear Cell Sarcoma Vaccines
Goldberg J, Fisher D, Demetri G, Neuberg D, Allsop S, Fonseca C, Nakazaki Y, Nemer D, Raut C, George S, Morgan J, Wagner A, Freeman G, Ritz J, Lezcano C, Mihm M, Canning C, Hodi F, Dranoff G. Biologic Activity of Autologous, Granulocyte–Macrophage Colony-Stimulating Factor Secreting Alveolar Soft-Part Sarcoma and Clear Cell Sarcoma Vaccines. Clinical Cancer Research 2015, 21: 3178-3186. PMID: 25805798, PMCID: PMC4506240, DOI: 10.1158/1078-0432.ccr-14-2932.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultCancer VaccinesChildEnzyme-Linked Immunosorbent AssayFemaleGranulocyte-Macrophage Colony-Stimulating FactorHumansMaleMiddle AgedSarcoma, Alveolar Soft PartSarcoma, Clear CellSoft Tissue NeoplasmsYoung AdultConceptsAlveolar soft part sarcomaClear cell sarcomaGranulocyte-macrophage colony-stimulating factorColony-stimulating factorSoft part sarcomaTissue-type plasminogen activatorMicrophthalmia transcription factorGM-CSFReplication-defective adenoviral vector encoding GM-CSFSecrete granulocyte-macrophage colony-stimulating factorCCS patientsImmune-mediated tumor destructionT-cell-mediated delayed-type hypersensitivity reactionCD8(+) T cellsAdenoviral-mediated gene transferPhase I clinical trialDelayed-type hypersensitivity reactionAutologous tumor cellsPD-ligand 1Sarcoma cellsNo tumor regressionRare mesenchymal malignancySingle-cell suspensionsTumor regressionMetastatic tumors
2014
GM-CSF Promotes Macrophage Alternative Activation after Renal Ischemia/Reperfusion Injury
Huen SC, Huynh L, Marlier A, Lee Y, Moeckel GW, Cantley LG. GM-CSF Promotes Macrophage Alternative Activation after Renal Ischemia/Reperfusion Injury. Journal Of The American Society Of Nephrology 2014, 26: 1334-1345. PMID: 25388222, PMCID: PMC4446881, DOI: 10.1681/asn.2014060612.Peer-Reviewed Original ResearchMeSH KeywordsAcute Kidney InjuryAnalysis of VarianceAnimalsBlotting, WesternCell ProliferationCells, CulturedDisease Models, AnimalGene Expression RegulationGranulocyte-Macrophage Colony-Stimulating FactorImmunohistochemistryKidney Tubules, ProximalMacrophage ActivationMaleMiceMice, Inbred C57BLMultivariate AnalysisPhenotypeRandom AllocationReal-Time Polymerase Chain ReactionReperfusion InjurySignal TransductionUp-RegulationConceptsIschemia/reperfusion injuryMacrophage alternative activationBone marrow-derived macrophagesAlternative activationMarrow-derived macrophagesTubular cellsGM-CSFReperfusion injuryReparative phenotypeTubular proliferationKidney ischemia/reperfusion injuryRenal ischemia/reperfusion injuryMouse proximal tubule cellsInitial kidney damageRepair phaseProximal tubule cellsTubular factorsIschemic injuryKidney damageProinflammatory macrophagesRenal repairMacrophage activationTubule cellsPharmacologic inhibitionMacrophagesAssessment of Phagocytic Activity of Cultured Macrophages Using Fluorescence Microscopy and Flow Cytometry
Sharma L, Wu W, Dholakiya SL, Gorasiya S, Wu J, Sitapara R, Patel V, Wang M, Zur M, Reddy S, Siegelaub N, Bamba K, Barile FA, Mantell LL. Assessment of Phagocytic Activity of Cultured Macrophages Using Fluorescence Microscopy and Flow Cytometry. Methods In Molecular Biology 2014, 1172: 137-145. PMID: 24908301, DOI: 10.1007/978-1-4939-0928-5_12.ChaptersMeSH KeywordsAnimalsCell LineFlow CytometryFluorescein-5-isothiocyanateFluorescent DyesGene ExpressionGranulocyte-Macrophage Colony-Stimulating FactorHMGB1 ProteinInterleukin-1betaMacrophagesMiceMicroscopy, FluorescenceMicrospheresPhagocytosisTransforming Growth Factor beta1Tumor Necrosis Factor-alphaConceptsCultured macrophagesHigh mobility group box 1Individual cellsInnate immune systemFluorescence microscopyNumerous diseasesPhagocytic processFluorescence microscopePhagocytic functionPhagocytic activityCell debrisPhagocytosisFlow cytometryMobility group box 1PhagocytesGroup box 1GM-CSFMacrophagesImmune systemTGF-β1Different cytokinesFlow cytometerIL-1βEngulfmentHomeostasis
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply