2021
WEE1 inhibition induces anti-tumor immunity by activating ERV and the dsRNA pathway
Guo E, Xiao R, Wu Y, Lu F, Liu C, Yang B, Li X, Fu Y, Wang Z, Li Y, Huang Y, Li F, Wu X, You L, Qin T, Lu Y, Huang X, Ma D, Mills G, Sun C, Chen G. WEE1 inhibition induces anti-tumor immunity by activating ERV and the dsRNA pathway. Journal Of Experimental Medicine 2021, 219: e20210789. PMID: 34825915, PMCID: PMC8628262, DOI: 10.1084/jem.20210789.Peer-Reviewed Original ResearchMeSH KeywordsA549 CellsAnimalsAntineoplastic Combined Chemotherapy ProtocolsCD8-Positive T-LymphocytesCell Cycle ProteinsCell Line, TumorEndogenous RetrovirusesEnzyme InhibitorsFemaleGene Expression Regulation, NeoplasticHCT116 CellsHumansImmune Checkpoint InhibitorsMice, Inbred BALB CMice, Inbred C57BLMice, Inbred NODMice, SCIDNeoplasms, ExperimentalProtein-Tyrosine KinasesPyrazolesPyrimidinonesRNA, Double-StrandedSignal TransductionTumor BurdenConceptsImmune checkpoint blockadeAnti-tumor immunityEndogenous retroviral elementsWEE1 inhibitionCheckpoint blockadeCD8+ T cell-dependent mannerSensitivity to immune checkpoint blockadeResponse to immune checkpoint blockadeAnti-tumor T cellsCombination of WEE1 inhibitorT cell-dependent mannerPathway-targeted therapiesMultiple tumor modelsPopulation of patientsEmergence of resistanceDown-regulating FoxM1Viral defense pathwaysPD-L1Tumor regressionCombination therapyTargeted therapyCombination partnerT cellsPatient selectionWEE1 inhibitor
2015
Mature T cell responses are controlled by microRNA-142
Sun Y, Oravecz-Wilson K, Mathewson N, Wang Y, McEachin R, Liu C, Toubai T, Wu J, Rossi C, Braun T, Saunders T, Reddy P. Mature T cell responses are controlled by microRNA-142. Journal Of Clinical Investigation 2015, 125: 2825-2840. PMID: 26098216, PMCID: PMC4563679, DOI: 10.1172/jci78753.Peer-Reviewed Original ResearchConceptsCell cyclingE2F transcription factorsAtypical E2F transcription factorMature T cell responsesCell proliferationShort palindromic repeatsUpregulation of genesMiR-142T cell developmentTranscription factorsBioinformatics analysisTarget genesPalindromic repeatsMolecular approachesMolecular mechanismsCell developmentMolecular processesMicroRNA-142Targeted deletionWT T cellsGenesE2F8E2F7Multiple murine modelsT cell proliferation
2014
A Small-Molecule c-Rel Inhibitor Reduces Alloactivation of T Cells without Compromising Antitumor Activity
Shono Y, Tuckett A, Ouk S, Liou H, Altan-Bonnet G, Tsai J, Oyler J, Smith O, West M, Singer N, Doubrovina E, Pankov D, Undhad C, Murphy G, Lezcano C, Liu C, O'Reilly R, van den Brink M, Zakrzewski J. A Small-Molecule c-Rel Inhibitor Reduces Alloactivation of T Cells without Compromising Antitumor Activity. Cancer Discovery 2014, 4: 578-591. PMID: 24550032, PMCID: PMC4011979, DOI: 10.1158/2159-8290.cd-13-0585.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsFemaleGene Expression RegulationGraft vs Host DiseaseGraft vs Tumor EffectHematopoietic Stem Cell TransplantationHumansLymphocyte ActivationMiceMice, Inbred BALB CMice, Inbred C57BLProto-Oncogene Proteins c-relReceptors, Antigen, T-CellSmall Molecule LibrariesT-LymphocytesTransplantation, HomologousConceptsT cellsC-Rel activityAllogeneic hematopoietic stem cell transplantationHematopoietic stem cell transplantationEffector T cellsRegulatory T cellsIL-2 levelsStem cell transplantationAntigen-specific cytotoxicityC-Rel-deficient T cellsC-RelHuman T cellsT cell receptor activationGut homingGVT activityImmunomodulatory therapyInhibitor administrationCell transplantationTumor activityImmune systemReceptor activationPharmaceutical inhibitionSmall molecule-based inhibitionAlloactivationBroad suppression
2013
Pharmacologic inhibition of PKCα and PKCθ prevents GVHD while preserving GVL activity in mice
Haarberg K, Li J, Heinrichs J, Wang D, Liu C, Bronk C, Kaosaard K, Owyang A, Holland S, Masuda E, Tso K, Blazar B, Anasetti C, Beg A, Yu X. Pharmacologic inhibition of PKCα and PKCθ prevents GVHD while preserving GVL activity in mice. Blood 2013, 122: 2500-2511. PMID: 23908466, PMCID: PMC3790515, DOI: 10.1182/blood-2012-12-471938.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell SeparationDisease Models, AnimalEnzyme InhibitorsFlow CytometryGraft vs Host DiseaseGraft vs Leukemia EffectHematopoietic Stem Cell TransplantationIsoenzymesLeukemiaLymphocyte ActivationLymphomaMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutProtein Kinase CProtein Kinase C-alphaProtein Kinase C-thetaT-LymphocytesConceptsHematopoietic cell transplantationDonor T cell proliferationAllogeneic hematopoietic cell transplantationT cell proliferationGVL activityGVL effectCytokine productionT cellsPharmacologic inhibitionChemokine/cytokine productionT-cell cytotoxicDonor T cellsPreclinical murine modelsPotential therapeutic targetT cell activationGVHD inductionGVHD preventionPrevents GVHDHost diseaseLeukemia effectSevere graftTherapeutic optionsCell transplantationEffective therapyPharmacologic approachesPLZF Confers Effector Functions to Donor T Cells That Preserve Graft-versus-Tumor Effects while Attenuating GVHD
Ghosh A, Holland A, Dogan Y, Yim N, Rao U, Young L, West M, Singer N, Lee H, Na I, Tsai J, Jenq R, Penack O, Hanash A, Lezcano C, Murphy G, Liu C, Sadelain M, Sauer M, Sant'Angelo D, van den Brink M. PLZF Confers Effector Functions to Donor T Cells That Preserve Graft-versus-Tumor Effects while Attenuating GVHD. Cancer Research 2013, 73: 4687-4696. PMID: 23733752, PMCID: PMC3732814, DOI: 10.1158/0008-5472.can-12-4699.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsBone Marrow TransplantationFlow CytometryGraft vs Host DiseaseGraft vs Tumor EffectKruppel-Like Transcription FactorsLymphocyte ActivationLymphocyte Culture Test, MixedMiceMice, Inbred BALB CMice, Inbred C57BLNeoplasms, ExperimentalPromyelocytic Leukemia Zinc Finger ProteinT-LymphocytesTransplantation, HomologousConceptsDonor T cellsT cellsPromyelocytic leukemia zinc fingerGVT effectInvariant natural killer T (iNKT) cellsAlloreactive donor T cellsAllogeneic bone marrow transplantationNatural killer T cellsTranscription factor promyelocytic leukemia zinc fingerKiller T cellsAlloreactive T cellsBone marrow transplantationConventional T cellsOverall improved outcomesLess GVHDLower GVHDPreserves graftTumor effectImproved survivalMarrow transplantationCytokine responsesImproved outcomesTumor relapseEffector functionsGVHDc‐Rel is an essential transcription factor for the development of acute graft‐versus‐host disease in mice
Yu Y, Wang D, Kaosaard K, Liu C, Fu J, Haarberg K, Anasetti C, Beg A, Yu X. c‐Rel is an essential transcription factor for the development of acute graft‐versus‐host disease in mice. European Journal Of Immunology 2013, 43: 2327-2337. PMID: 23716202, PMCID: PMC3940138, DOI: 10.1002/eji.201243282.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Marrow TransplantationCell DifferentiationCell ProliferationForkhead Transcription FactorsGraft vs Host DiseaseImmune ToleranceLymphocyte ActivationMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutProto-Oncogene Proteins c-relTh1 CellsTh17 CellsT-Lymphocytes, RegulatoryTransplantation, HomologousConceptsT cellsAcute GVHDHost diseaseAllogeneic bone marrow transplantationAllogeneic hematopoietic cell transplantationC-RelGVHD target organsHematopoietic cell transplantationRegulatory T cellsBone marrow transplantationAcute graftLeukemia responseTransplant toleranceAllogeneic recipientsMarrow transplantationMinor histocompatibilityCell transplantationTh1 cellsLymphoid organsMurine modelTarget organsTherapeutic interventionsNF-κB familyGraftPotential targetPhosphatidylinositol 3-Kinase–Independent Signaling Pathways Contribute to ICOS-Mediated T Cell Costimulation in Acute Graft-Versus-Host Disease in Mice
Li J, Heinrichs J, Leconte J, Haarberg K, Semple K, Liu C, Gigoux M, Kornete M, Piccirillo C, Suh W, Yu X. Phosphatidylinositol 3-Kinase–Independent Signaling Pathways Contribute to ICOS-Mediated T Cell Costimulation in Acute Graft-Versus-Host Disease in Mice. The Journal Of Immunology 2013, 191: 200-207. PMID: 23729441, PMCID: PMC4318500, DOI: 10.4049/jimmunol.1203485.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsDisease Models, AnimalGene Knock-In TechniquesGraft vs Host DiseaseInducible T-Cell Co-Stimulator ProteinLymphocyte ActivationMiceMice, 129 StrainMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicPhosphatidylinositol 3-KinaseSignal TransductionT-Lymphocyte SubsetsConceptsCD8 T cellsCD4 T cellsT cellsHost diseaseWild-type CD8 T cellsCD8 T cell compartmentAllogeneic bone marrow transplantationAcute Graft-VersusPathogenic potentialTotal T cellsAlloreactive T cellsBone marrow transplantationT cell compartmentWild-type T cellsIntracellular calcium mobilizationVivo pathogenic potentialT cell costimulationT cell activationKnockout T cellsAcute graftAcute GVHDGraft-VersusSevere GVHDGVHD modelMarrow transplantationEpigenetic Upregulation of HGF and c-Met Drives Metastasis in Hepatocellular Carcinoma
Ogunwobi O, Puszyk W, Dong H, Liu C. Epigenetic Upregulation of HGF and c-Met Drives Metastasis in Hepatocellular Carcinoma. PLOS ONE 2013, 8: e63765. PMID: 23723997, PMCID: PMC3665785, DOI: 10.1371/journal.pone.0063765.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceCarcinogenesisCarcinoma, HepatocellularCell Line, TumorDNA MethylationEpigenesis, GeneticEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHepatocyte Growth FactorHumansLiver NeoplasmsMesodermMiceMice, Inbred BALB CModels, BiologicalMolecular Sequence DataNeoplastic Cells, CirculatingPromoter Regions, GeneticProto-Oncogene Proteins c-metUp-RegulationConceptsEpithelial-mesenchymal transitionHepatocyte growth factorExpression of HGFHepatocellular carcinomaC-MetHematogenous disseminationTumor cellsRole of HGFOrthotopic syngeneic modelsMetastatic hepatocellular carcinomaMouse HCC modelC-Met expressionUpregulation of HGFPrimary tumor cellsPromoter demethylationNovel non-invasive approachPotential clinical applicationsPeripheral bloodSyngeneic modelHCC managementDrives metastasisEpigenetic upregulationHCC modelTumor progressionMetastatic potentialAdoptively transferred TRAIL+ T cells suppress GVHD and augment antitumor activity
Ghosh A, Dogan Y, Moroz M, Holland A, Yim N, Rao U, Young L, Tannenbaum D, Masih D, Velardi E, Tsai J, Jenq R, Penack O, Hanash A, Smith O, Piersanti K, Lezcano C, Murphy G, Liu C, Palomba M, Sauer M, Sadelain M, Ponomarev V, van den Brink M. Adoptively transferred TRAIL+ T cells suppress GVHD and augment antitumor activity. Journal Of Clinical Investigation 2013, 123: 2654-2662. PMID: 23676461, PMCID: PMC3668849, DOI: 10.1172/jci66301.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsAntigen-Presenting CellsCell Line, TumorCytotoxicity, ImmunologicGraft RejectionGraft vs Host DiseaseHEK293 CellsHumansImmunotherapy, AdoptiveLeukemia, Lymphocytic, Chronic, B-CellMiceMice, Inbred BALB CMice, Inbred C57BLNeoplasm TransplantationT-LymphocytesTNF-Related Apoptosis-Inducing LigandConceptsGVT responseT cellsAllo-HSCTAllogeneic hematopoietic stem cell transplantationHematopoietic stem cell transplantationCellular therapyAbsence of GVHDDR5-dependent mannerDonor T cellsAlloreactive T cellsStem cell transplantationChronic lymphocytic leukemia cellsPrecursor T cellsThird-party donorsLymphocytic leukemia cellsApoptosis-inducing ligandGVT activityHost diseaseCell transplantationCurative potentialTumor responseGVHDCertain malignanciesMouse modelHuman leukemia cell linesHost-derived CD8+ dendritic cells are required for induction of optimal graft-versus-tumor responses after experimental allogeneic bone marrow transplantation
Toubai T, Sun Y, Luker G, Liu J, Luker K, Tawara I, Evers R, Liu C, Mathewson N, Malter C, Nieves E, Choi S, Murphy K, Reddy P. Host-derived CD8+ dendritic cells are required for induction of optimal graft-versus-tumor responses after experimental allogeneic bone marrow transplantation. Blood 2013, 121: 4231-4241. PMID: 23520337, PMCID: PMC3656455, DOI: 10.1182/blood-2012-05-432872.Peer-Reviewed Original ResearchConceptsAntigen-presenting cellsTumor-specific antigensGVT responseAllo-HCTAPC subsetsDendritic cellsExperimental allogeneic bone marrow transplantationHost-derived antigen-presenting cellsAllogeneic bone marrow transplantationAllogeneic hematopoietic cell transplantationAlloantigen-specific responsesHost-derived CD8Donor T cellsHematopoietic cell transplantationBone marrow transplantationRelevant murine modelStimulation of TLR3Host diseaseTumor effectMarrow transplantationCell transplantationTumor responseSerious toxicityT cellsOptimal graftLong-Term In Vivo Imaging of Multiple Organs at the Single Cell Level
Chen B, Jiao Y, Zhang P, Sun A, Pitt G, Deoliveira D, Drago N, Ye T, Liu C, Chao N. Long-Term In Vivo Imaging of Multiple Organs at the Single Cell Level. PLOS ONE 2013, 8: e52087. PMID: 23300962, PMCID: PMC3534688, DOI: 10.1371/journal.pone.0052087.Peer-Reviewed Original Research
2012
Interleukin-22 Protects Intestinal Stem Cells from Immune-Mediated Tissue Damage and Regulates Sensitivity to Graft versus Host Disease
Hanash A, Dudakov J, Hua G, O’Connor M, Young L, Singer N, West M, Jenq R, Holland A, Kappel L, Ghosh A, Tsai J, Rao U, Yim N, Smith O, Velardi E, Hawryluk E, Murphy G, Liu C, Fouser L, Kolesnick R, Blazar B, van den Brink M. Interleukin-22 Protects Intestinal Stem Cells from Immune-Mediated Tissue Damage and Regulates Sensitivity to Graft versus Host Disease. Immunity 2012, 37: 339-350. PMID: 22921121, PMCID: PMC3477611, DOI: 10.1016/j.immuni.2012.05.028.Peer-Reviewed Original ResearchConceptsIL-23-responsive innate lymphoid cellsIntestinal IL-22IL-22Intestinal stem cellsTissue damageHost diseaseTransplant recipientsIL-22 deficiencyInflammatory intestinal damageDonor immune systemInnate lymphoid cellsBone marrow transplantIL-22 receptorStem cellsILC frequenciesPretransplant conditioningIntestinal damageMarrow transplantCrypt apoptosisLymphoid cellsImmune systemGVHDTissue sensitivityProtective factorsEpithelial integrityLBH589 Enhances T Cell Activation In Vivo and Accelerates Graft-versus-Host Disease in Mice
Wang D, Iclozan C, Liu C, Xia C, Anasetti C, Yu X. LBH589 Enhances T Cell Activation In Vivo and Accelerates Graft-versus-Host Disease in Mice. Transplantation And Cellular Therapy 2012, 18: 1182-1190.e1. PMID: 22698484, PMCID: PMC3417119, DOI: 10.1016/j.bbmt.2012.06.002.Peer-Reviewed Original ResearchConceptsBone marrow transplantSuberoylanilide hydroxamic acidAllogeneic bone marrow transplantAllogeneic transplant modelElevated Th1 cytokinesPrevention of GVHDDonor T cellsT cell infiltrationHistone deacetylase inhibitorsT cell activationTumor cell growthCXCR3 expressionHost diseaseRecipient serumPan-HDACiTh1 cytokinesMarrow transplantProinflammatory cytokinesTransplant modelCell infiltrationInflammatory diseasesGVHDT cellsMouse modelDisease amelioration
2011
Induction of acute GVHD by sex-mismatched H-Y antigens in the absence of functional radiosensitive host hematopoietic–derived antigen-presenting cells
Toubai T, Tawara I, Sun Y, Liu C, Nieves E, Evers R, Friedman T, Korngold R, Reddy P. Induction of acute GVHD by sex-mismatched H-Y antigens in the absence of functional radiosensitive host hematopoietic–derived antigen-presenting cells. Blood 2011, 119: 3844-3853. PMID: 22101894, PMCID: PMC3335388, DOI: 10.1182/blood-2011-10-384057.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsAntigen-Presenting CellsBone Marrow TransplantationCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCells, CulturedDendritic CellsEndothelial CellsFemaleGraft vs Host DiseaseHematopoiesisHistocompatibilityH-Y AntigenIsoantigensMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, Mutant StrainsRadiation ToleranceThymectomyConceptsAcute GVHDT cellsAg presentationAlloreactive donor T cellsAllogeneic BM transplantationDonor T cellsMinor histocompatibility AgAntigen-presenting cellsGvH responseGVHD lethalityBM transplantationHistocompatibility AgClinical dataGVHDY antigenAPCY AgPresentationCellsTransplantationAbsenceInfusionAntigenRecipientsHost Basophils Are Dispensable for Induction of Donor T Helper 2 Cell Differentiation and Severity of Experimental Graft-versus-Host Disease
Tawara I, Nieves E, Liu C, Evers R, Toubai T, Sun Y, Alrubaie M, Reddy P. Host Basophils Are Dispensable for Induction of Donor T Helper 2 Cell Differentiation and Severity of Experimental Graft-versus-Host Disease. Transplantation And Cellular Therapy 2011, 17: 1747-1753. PMID: 21871863, PMCID: PMC3220796, DOI: 10.1016/j.bbmt.2011.08.013.Peer-Reviewed Original ResearchConceptsAntigen-presenting cellsAllogeneic bone marrow transplantationSeverity of GVHDBone marrow transplantationHost diseaseTh2 responsesMarrow transplantationDonor T cell proliferationDonor T-cell responsesInduction of graftT cell responsesT cell proliferationT helper 2 (Th2) cell differentiationTh2 polarizationLymphocyte responsesExperimental graftGVHDCell responsesBasophilsCell proliferationSeverityTransplantationGraftRecent dataDiseaseHepatocyte growth factor upregulation promotes carcinogenesis and epithelial-mesenchymal transition in hepatocellular carcinoma via Akt and COX-2 pathways
Ogunwobi O, Liu C. Hepatocyte growth factor upregulation promotes carcinogenesis and epithelial-mesenchymal transition in hepatocellular carcinoma via Akt and COX-2 pathways. Clinical & Experimental Metastasis 2011, 28: 721-731. PMID: 21744257, PMCID: PMC3732749, DOI: 10.1007/s10585-011-9404-x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCadherinsCarcinoma, HepatocellularCell AdhesionCell DifferentiationCell Line, TumorCell MovementCell ProliferationCyclooxygenase 2Enzyme-Linked Immunosorbent AssayEpithelial-Mesenchymal TransitionExtracellular Signal-Regulated MAP KinasesHepatocyte Growth FactorLiver Neoplasms, ExperimentalMiceMice, Inbred BALB CNeoplasm InvasivenessPhosphorylationProto-Oncogene Proteins c-aktReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSignal TransductionUp-RegulationVimentinConceptsEpithelial-mesenchymal transitionHepatocyte growth factorCyclooxygenase-2Hepatocellular carcinomaBNL cellsMarkers of EMTDevelopment of HCCAdvanced hepatocellular carcinomaCOX-2 pathwayMetastatic hepatocellular carcinomaUpregulation of HGFMesenchymal characteristicsGrowth factor upregulationE-cadherinCharacteristic epithelial morphologyCancer mortalitySubsequent metastasisEMT markersImportant causeMigratory capacityHCC cellsBNL CLCancer progressionCollagen 1Growth factorAbrogation of donor T-cell IL-21 signaling leads to tissue-specific modulation of immunity and separation of GVHD from GVL
Hanash A, Kappel L, Yim N, Nejat R, Goldberg G, Smith O, Rao U, Dykstra L, Na I, Holland A, Dudakov J, Liu C, Murphy G, Leonard W, Heller G, van den Brink M. Abrogation of donor T-cell IL-21 signaling leads to tissue-specific modulation of immunity and separation of GVHD from GVL. Blood 2011, 118: 446-455. PMID: 21596854, PMCID: PMC3138694, DOI: 10.1182/blood-2010-07-294785.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsGene Knockdown TechniquesGraft vs Host DiseaseGraft vs Leukemia EffectHumansImmunity, InnateInterleukin-21 Receptor alpha SubunitInterleukinsLymphocytes, Tumor-InfiltratingMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred DBAMice, KnockoutOrgan SpecificitySignal TransductionTissue DonorsT-LymphocytesTransplantation ImmunologyConceptsSeparation of GVHDDonor T cellsKO T cellsIL-21T cellsTissue-specific modulationGastrointestinal GVHDCytokine productionWild-type donor T cellsDonor regulatory T cellsTh cell cytokine productionPeripheral T cell functionMesenteric lymph nodesRegulatory T cellsTh cell functionIL-21 signalingInflammatory cytokine productionBM transplantation modelT cell functionLymphoma responseLymph nodesProinflammatory cytokinesTransplantation outcomesTransplantation modelGVHDPretransplant CSF-1 therapy expands recipient macrophages and ameliorates GVHD after allogeneic hematopoietic cell transplantation
Hashimoto D, Chow A, Greter M, Saenger Y, Kwan W, Leboeuf M, Ginhoux F, Ochando J, Kunisaki Y, van Rooijen N, Liu C, Teshima T, Heeger P, Stanley E, Frenette P, Merad M. Pretransplant CSF-1 therapy expands recipient macrophages and ameliorates GVHD after allogeneic hematopoietic cell transplantation. Journal Of Experimental Medicine 2011, 208: 1069-1082. PMID: 21536742, PMCID: PMC3092347, DOI: 10.1084/jem.20101709.Peer-Reviewed Original ResearchConceptsDonor allogeneic T cellsDonor T cell expansionAllogeneic hematopoietic cell transplantationAllogeneic T cellsHematopoietic cell transplantationAllo-HCTT cell expansionT cellsAcute GVHDCell transplantationHost macrophagesHost antigen-presenting cellsMacrophage poolPotential prophylactic therapyAlloreactive T cellsAntigen-presenting cellsAcute graftGVHD morbidityGVHD mortalityHost DCsHost diseaseProphylactic therapyRecipient miceGVHDRecipient macrophagesIkaros-Notch axis in host hematopoietic cells regulates experimental graft-versus-host disease
Toubai T, Sun Y, Tawara I, Friedman A, Liu C, Evers R, Nieves E, Malter C, Chockley P, Maillard I, Winandy S, Reddy P. Ikaros-Notch axis in host hematopoietic cells regulates experimental graft-versus-host disease. Blood 2011, 118: 192-204. PMID: 21471527, PMCID: PMC3139384, DOI: 10.1182/blood-2010-12-324616.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigen-Presenting CellsCD8-Positive T-LymphocytesCells, CulturedDendritic CellsDisease Models, AnimalFemaleGraft vs Host DiseaseHematopoiesisIkaros Transcription FactorImmunophenotypingMaleMiceMice, Inbred BALB CMice, Inbred C3HMice, Inbred C57BLMice, Mutant StrainsReceptor, Notch1Signal TransductionConceptsDendritic cellsAcute GVHDDonor T cell expansionExperimental bone marrow transplantationHost hematopoietic cellsInduction of GVHDAllogeneic T cellsBone marrow transplantationT cell expansionRelevant murine modelGvH responseAllostimulatory capacityHost diseaseWild-type controlsDC biologyMarrow transplantationPotent APCsActivation markersTLR stimulationT cellsMurine modelGVHDExperimental graftEnhanced stimulationIkaros deficiencyRoles of CD28, CTLA4, and Inducible Costimulator in Acute Graft-versus-Host Disease in Mice
Li J, Semple K, Suh W, Liu C, Chen F, Blazar B, Yu X. Roles of CD28, CTLA4, and Inducible Costimulator in Acute Graft-versus-Host Disease in Mice. Transplantation And Cellular Therapy 2011, 17: 962-969. PMID: 21447398, PMCID: PMC3131782, DOI: 10.1016/j.bbmt.2011.01.018.Peer-Reviewed Original ResearchMeSH KeywordsAbataceptAcute DiseaseAnimalsAntigens, CDAntigens, Differentiation, T-LymphocyteB7-1 AntigenB7-2 AntigenBone Marrow TransplantationCD28 AntigensCTLA-4 AntigenFas Ligand ProteinGraft vs Host DiseaseImmune ToleranceImmunoconjugatesInducible T-Cell Co-Stimulator ProteinInterferon-gammaLymphocyte ActivationMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutRadiation ChimeraT-Lymphocyte SubsetsTransplantation, HomologousTumor Necrosis Factor-alphaConceptsAllogeneic bone marrow transplantationBone marrow transplantationInducible costimulatorRole of CD28T cellsCTLA4 signalsHost diseaseMarrow transplantationMyeloablative allogeneic bone marrow transplantationPathogenic T cell responsesDevelopment of GVHDSeverity of GVHDT cell responsesT cell toleranceAbsence of B7T cell activationAcute graftAcute GVHDICOS signalingPrevents GVHDCTLA4-IgCD28 familyGVHDEffector functionsCell tolerance