2009
T helper17 Cells Are Sufficient But Not Necessary to Induce Acute Graft-Versus-Host Disease
Iclozan C, Yu Y, Liu C, Liang Y, Yi T, Anasetti C, Yu X. T helper17 Cells Are Sufficient But Not Necessary to Induce Acute Graft-Versus-Host Disease. Transplantation And Cellular Therapy 2009, 16: 170-178. PMID: 19804837, PMCID: PMC3876952, DOI: 10.1016/j.bbmt.2009.09.023.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalBody WeightBone Marrow TransplantationCD3 ComplexCells, CulturedGraft vs Host DiseaseGraft vs Host ReactionInterferon-gammaInterleukin-17MiceMice, Inbred StrainsMice, TransgenicNuclear Receptor Subfamily 1, Group F, Member 3Severity of Illness IndexSurvival AnalysisTh1 CellsTime FactorsT-Lymphocyte SubsetsT-Lymphocytes, Helper-InducerTumor Necrosis Factor-alphaWhole Body ImagingConceptsHost diseaseBALB/c recipientsBone marrow transplantation settingAcute Graft-VersusT helper17 cellsGVHD target organsInduction of graftPathogenesis of GVHDCD4 T cellsGraft-VersusGVHD developmentC recipientsT helperTh17 cellsAllogeneic recipientsAutoimmune diseasesC57BL/6 miceSyngeneic recipientsTransplantation settingGVHDT cellsIFN-gammaTarget organsSuperior expansionDisease
2008
Histone deacetylase inhibition modulates indoleamine 2,3-dioxygenase–dependent DC functions and regulates experimental graft-versus-host disease in mice
Reddy P, Sun Y, Toubai T, Duran-Struuck R, Clouthier S, Weisiger E, Maeda Y, Tawara I, Krijanovski O, Gatza E, Liu C, Malter C, Mascagni P, Dinarello C, Ferrara J. Histone deacetylase inhibition modulates indoleamine 2,3-dioxygenase–dependent DC functions and regulates experimental graft-versus-host disease in mice. Journal Of Clinical Investigation 2008, 118: 2562-2573. PMID: 18568076, PMCID: PMC2430497, DOI: 10.1172/jci34712.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDBone Marrow TransplantationCytokinesDendritic CellsEnzyme InhibitorsFemaleGene ExpressionGraft vs Host DiseaseHistone Deacetylase InhibitorsHumansHydroxamic AcidsIndoleamine-Pyrrole 2,3,-DioxygenaseLipopolysaccharidesLymphocyte ActivationMiceMice, Inbred BALB CMice, Inbred C3HMice, Inbred C57BLMice, Inbred StrainsMice, KnockoutRNA, Small InterferingSurvival AnalysisT-LymphocytesVorinostatConceptsDC functionHDAC inhibitorsSuberoylanilide hydroxamic acidHost diseaseExperimental graftBlockade of IDOPretreatment of DCsAllogeneic BM transplantationBM-derived cellsImmune-mediated diseasesExpression of CD40Expression of indoleamineBM transplantation modelExposure of DCsInduction of IDOVivo functional roleHistone deacetylase inhibitionHistone deacetylase inhibitorsMechanism of actionProinflammatory cytokinesBM transplantationWT DCsTransplantation modelImmunomodulatory functionsDeacetylase inhibitionA Role for TNF Receptor Type II in Leukocyte Infiltration into the Lung during Experimental Idiopathic Pneumonia Syndrome
Hildebrandt G, Olkiewicz K, Corrion L, Clouthier S, Pierce E, Liu C, Cooke K. A Role for TNF Receptor Type II in Leukocyte Infiltration into the Lung during Experimental Idiopathic Pneumonia Syndrome. Transplantation And Cellular Therapy 2008, 14: 385-396. PMID: 18342780, PMCID: PMC2390587, DOI: 10.1016/j.bbmt.2008.01.004.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBronchoalveolar Lavage FluidFemaleGraft SurvivalGraft vs Host DiseaseLungMiceMice, Inbred C57BLMice, Inbred StrainsPneumoniaReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IIStem Cell TransplantationSyndromeTransplantation, HomologousTumor Necrosis Factor-alphaConceptsIdiopathic pneumonia syndromeTNF-alphaPneumonia syndromeAllo-SCTLeukocyte infiltrationPulmonary vascular endothelial cell apoptosisBronchoalveolar lavage fluid levelsExperimental Idiopathic Pneumonia SyndromePulmonary ICAM-1 expressionWild-type B6 miceAllogeneic stem cell transplantationTNF receptor type IIType II TNF receptorLavage fluid levelsStem cell transplantationICAM-1 expressionVascular endothelial cell apoptosisReceptor type IIMHC class IEndothelial cell apoptosisDonor leukocytesFatal complicationPulmonary inflammationSyngeneic donorsWT mice
2007
Absence of donor T-cell–derived soluble TNF decreases graft-versus-host disease without impairing graft-versus-tumor activity
Borsotti C, Franklin A, Lu S, Kim T, Smith O, Suh D, King C, Chow A, Liu C, Alpdogan O, van den Brink M. Absence of donor T-cell–derived soluble TNF decreases graft-versus-host disease without impairing graft-versus-tumor activity. Blood 2007, 110: 783-786. PMID: 17395784, PMCID: PMC1924485, DOI: 10.1182/blood-2006-10-054510.Peer-Reviewed Original ResearchConceptsT cellsTNF-alpha converting enzymeGVT activityHost diseaseTumor activityAllogeneic bone marrow transplantationDonor T cellsBone marrow transplantationMurine BMT modelWild-type T cellsLess GVHDMarrow transplantationBMT modelNecrosis factorEndogenous TNFSoluble TNFGVHDConverting enzymeGraftTNFDiseaseRecipientsSoluble moleculesCellsMemTNF
2004
Both perforin and Fas ligand are required for the regulation of alloreactive CD8+ T cells during acute graft-versus-host disease
Maeda Y, Levy R, Reddy P, Liu C, Clouthier S, Teshima T, Ferrara J. Both perforin and Fas ligand are required for the regulation of alloreactive CD8+ T cells during acute graft-versus-host disease. Blood 2004, 105: 2023-2027. PMID: 15466930, DOI: 10.1182/blood-2004-08-3036.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsBone Marrow TransplantationCD8-Positive T-LymphocytesCell Culture TechniquesFas Ligand ProteinGraft vs Host DiseaseHistocompatibilityHistocompatibility Antigens Class ILymphocyte TransfusionMembrane GlycoproteinsMiceMice, Inbred StrainsModels, AnimalPerforinPore Forming Cytotoxic ProteinsTransplantation, HomologousConceptsT cellsHost diseaseAllogeneic bone marrow transplantationT cell-mediated cytotoxicityTumor necrosis factor alphaMajor histocompatibility complex class IGreater serum levelsDonor T cellsBone marrow transplantationCell-mediated cytotoxicityHistocompatibility complex class IWild-type T cellsNecrosis factor alphaComplex class ILethal GVHDAcute graftAlloreactive CD8Histopathologic damageMarrow transplantationSerum levelsAlloantigen stimulationIrradiated murine modelFactor alphaCD8Murine model
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 histopathology