2013
Long-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
2011
Kinase inhibitor Sorafenib modulates immunosuppressive cell populations in a murine liver cancer model
Cao M, Xu Y, Youn J, Cabrera R, Zhang X, Gabrilovich D, Nelson D, Liu C. Kinase inhibitor Sorafenib modulates immunosuppressive cell populations in a murine liver cancer model. Laboratory Investigation 2011, 91: 598-608. PMID: 21321535, PMCID: PMC3711234, DOI: 10.1038/labinvest.2010.205.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBenzenesulfonatesBone Marrow CellsCarcinoma, HepatocellularCell DivisionCell Line, TumorDisease ProgressionImmunity, CellularLiver NeoplasmsMiceMice, Inbred BALB CMyeloid CellsNiacinamidePhenylurea CompoundsProtein Kinase InhibitorsPyridinesSorafenibSpleenT-Lymphocytes, RegulatoryConceptsMyeloid-derived suppressor cellsImmunosuppressive cell populationsAnti-tumor immunityTumor-bearing hostsImmune cell populationsLiver cancer modelMurine liver cancer modelHepatocellular carcinomaCell populationsCancer modelNovel multi-kinase inhibitorSuppressive immune cell populationBALB/c miceDepletion of TregsImpact of sorafenibRegulatory T cellsAdvanced hepatocellular carcinomaTreatment of sorafenibKinase inhibitor sorafenibMulti-kinase inhibitorHCC cell growthSuppressor cellsTumor burdenC miceCancer patients
2008
IL-17 contributes to CD4-mediated graft-versus-host disease
Kappel L, Goldberg G, King C, Suh D, Smith O, Ligh C, Holland A, Grubin J, Mark N, Liu C, Iwakura Y, Heller G, van den Brink M. IL-17 contributes to CD4-mediated graft-versus-host disease. Blood 2008, 113: 945-952. PMID: 18931341, PMCID: PMC2630280, DOI: 10.1182/blood-2008-08-172155.Peer-Reviewed Original ResearchConceptsRecipients of ILT cellsGVHD mortalityHost diseaseIL-17Proinflammatory cytokinesAllogeneic bone marrow transplantAllogeneic BMT modelIL-17 contributesDonor T cellsBone marrow transplantWhole T cellsT-cell recipientsAcute graftGVHD developmentGVT activityAllograft rejectionTh17 cellsIL-17FIL-22Interleukin-17Marrow transplantAutoimmune diseasesTh1 cellsLymphoid organs
2004
Blockade of CXCR3 Receptor:Ligand Interactions Reduces Leukocyte Recruitment to the Lung and the Severity of Experimental Idiopathic Pneumonia Syndrome
Hildebrandt G, Corrion L, Olkiewicz K, Lu B, Lowler K, Duffner U, Moore B, Kuziel W, Liu C, Cooke K. Blockade of CXCR3 Receptor:Ligand Interactions Reduces Leukocyte Recruitment to the Lung and the Severity of Experimental Idiopathic Pneumonia Syndrome. The Journal Of Immunology 2004, 173: 2050-2059. PMID: 15265940, DOI: 10.4049/jimmunol.173.3.2050.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Marrow CellsBronchoalveolar Lavage FluidCells, CulturedChemokine CXCL10Chemokine CXCL9Chemokines, CXCChemotaxis, LeukocyteCrosses, GeneticFemaleHematopoietic Stem Cell TransplantationInterferon-gammaLigandsLungLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutPneumoniaReceptors, CCR5Receptors, ChemokineReceptors, CXCR3SpleenT-Lymphocytes, CytotoxicTransplantation, HomologousTumor Necrosis Factor-alphaConceptsIdiopathic pneumonia syndromeDonor T cellsPneumonia syndromeIP-10TNF-alphaT cellsIFN-gammaCXCR3 receptorDevelopment of IPSExperimental Idiopathic Pneumonia SyndromeIP-10 protein levelsAllogeneic stem cell transplantationAllo-SCT recipientsInfiltration of IFNStandard immunosuppressive therapyT cell subsetsBronchoalveolar lavage fluidStem cell transplantationT cell recruitmentControl-treated animalsImmunosuppressive therapyLigand MigAllo-SCTFatal complicationLung injury
2003
Repifermin (keratinocyte growth factor-2) reduces the severity of graft-versus-host disease while preserving a graft-versus-leukemia effect
Clouthier S, Cooke K, Teshima T, Lowler K, Liu C, Connolly K, Ferrara J. Repifermin (keratinocyte growth factor-2) reduces the severity of graft-versus-host disease while preserving a graft-versus-leukemia effect. Transplantation And Cellular Therapy 2003, 9: 592-603. PMID: 14506661, DOI: 10.1016/s1083-8791(03)00230-1.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Marrow TransplantationCD4 Lymphocyte CountCD8-Positive T-LymphocytesCell DivisionCell Line, TumorDisease Models, AnimalFemaleFibroblast Growth Factor 10Fibroblast Growth FactorsGraft vs Host DiseaseGraft vs Leukemia EffectHumansInterferon-gammaInterleukin-2IntestinesLipopolysaccharidesLiverLymphocyte CountMiceMice, Inbred C57BLMice, Inbred StrainsRecombinant ProteinsSpleenT-LymphocytesT-Lymphocytes, CytotoxicTransplantation, HomologousTumor Necrosis Factor-alphaConceptsBone marrow transplantationAllogeneic bone marrow transplantationAllogeneic BMT recipientsSystemic GVHDGVL effectHost diseaseBMT recipientsTumor necrosis factor alphaBeneficial GVL effectInduction of GVHDSeverity of graftToxicity of GVHDMurine BMT modelBone marrow inoculumNecrosis factor alphaT cell proliferationRecombinant human keratinocyte growth factorHuman keratinocyte growth factorKeratinocyte growth factorLeukemia effectLeukemia responseSerum levelsMarrow transplantationControl miceOrgan histopathologyImpaired thymic negative selection causes autoimmune graft-versus-host disease
Teshima T, Reddy P, Liu C, Williams D, Cooke K, Ferrara J. Impaired thymic negative selection causes autoimmune graft-versus-host disease. Blood 2003, 102: 429-435. PMID: 12663438, DOI: 10.1182/blood-2003-01-0266.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsAutoimmune DiseasesBone Marrow TransplantationCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCells, CulturedClonal DeletionDendritic CellsEpithelial CellsFemaleGraft vs Host DiseaseInflammation MediatorsInterleukin-1MiceMice, Inbred C57BLRadiation ChimeraRadiation ToleranceSelf ToleranceSkinSpleenThymectomyThymus GlandT-Lymphocyte SubsetsTumor Necrosis Factor-alphaVisceraConceptsThymic negative selectionSystemic autoimmune diseaseAntigen-presenting cellsAutoimmune diseasesHost diseaseT cellsAutoreactive T cell repertoireClass IIThymic antigen-presenting cellsMajor histocompatibility complex class IIHistocompatibility complex class IIImpaired negative selectionLethal autoimmune diseaseBone marrow chimerasPeripheral regulatory mechanismsT cell repertoireMHC class IIMHC class INegative selectionAcute graftAcute GVHDAutoimmune graftPeripheral CD4Adoptive transferNaive miceEarly changes in gene expression profiles of hepatic GVHD uncovered by oligonucleotide microarrays
Ichiba T, Teshima T, Kuick R, Misek D, Liu C, Takada Y, Maeda Y, Reddy P, Williams D, Hanash S, Ferrara J. Early changes in gene expression profiles of hepatic GVHD uncovered by oligonucleotide microarrays. Blood 2003, 102: 763-771. PMID: 12663442, DOI: 10.1182/blood-2002-09-2748.Peer-Reviewed Original ResearchMeSH KeywordsAcute-Phase ProteinsAnimalsAntigen PresentationApoptosisBone Marrow TransplantationChemotaxis, LeukocyteExpressed Sequence TagsFemaleGene Expression ProfilingGene Expression RegulationGraft vs Host DiseaseInflammationIntercellular Adhesion Molecule-1Interferon-gammaLiverLymphocyte ActivationMiceMice, Inbred C57BLOligonucleotide Array Sequence AnalysisOrgan SpecificityRadiation ChimeraSpleenT-LymphocytesTransplantation, HomologousTransplantation, IsogeneicConceptsBone marrow transplantationAllogeneic bone marrow transplantationHepatic GVHDAcute GVHDSyngeneic bone marrow transplantationMajor histocompatibility class II moleculesDonor T cellsMajor target organAcute phase proteinsClass II moleculesGene expression profilesIFN-gamma proteinNew potential molecular targetsPotential molecular targetsAcute graftHost diseaseMajor complicationsMarrow transplantationHistologic changesGVHDT cellsEndocrine functionIFN-gammaGastrointestinal tractInterferon gamma