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 AgPresentationCellsTransplantationAbsenceInfusionAntigenRecipients
2010
Inhibition of Neovascularization to Simultaneously Ameliorate Graft-vs-Host Disease and Decrease Tumor Growth
Penack O, Henke E, Suh D, King C, Smith O, Na I, Holland A, Ghosh A, Lu S, Jenq R, Liu C, Murphy G, Lu T, May C, Scheinberg D, Gao D, Mittal V, Heller G, Benezra R, van den Brink M. Inhibition of Neovascularization to Simultaneously Ameliorate Graft-vs-Host Disease and Decrease Tumor Growth. Journal Of The National Cancer Institute 2010, 102: 894-908. PMID: 20463307, PMCID: PMC2886094, DOI: 10.1093/jnci/djq172.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis InhibitorsAnimalsAntibodies, MonoclonalAntigens, CDBone Marrow TransplantationCadherinsFemaleFlow CytometryFluorescent Antibody TechniqueGraft vs Host DiseaseHematopoietic Stem Cell TransplantationMiceMice, Inbred C57BLNeoplasmsNeovascularization, PathologicTransplantation, HomologousConceptsTumor growthAllo-BMTHost diseaseAllogeneic hematopoietic stem cell transplantationHematopoietic stem cell transplantationEndothelial cellsAllo-BMT recipientsGVHD target tissuesAllogeneic BM transplantationStem cell transplantationEndothelial progenitor cellsDecreases tumor growthInhibition of neovascularizationTumor-bearing miceTissue endothelial cellsAmeliorate graftDonor BMBM transplantationCell transplantationGVHDBone marrowTherapeutic targetingNeovascularizationOverall outcomeTumor vasculature
2009
The cytolytic molecules Fas ligand and TRAIL are required for murine thymic graft-versus-host disease
Na I, Lu S, Yim N, Goldberg G, Tsai J, Rao U, Smith O, King C, Suh D, Hirschhorn-Cymerman D, Palomba L, Penack O, Holland A, Jenq R, Ghosh A, Tran H, Merghoub T, Liu C, Sempowski G, Ventevogel M, Beauchemin N, van den Brink M. The cytolytic molecules Fas ligand and TRAIL are required for murine thymic graft-versus-host disease. Journal Of Clinical Investigation 2009, 120: 343-356. PMID: 19955659, PMCID: PMC2798682, DOI: 10.1172/jci39395.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Marrow TransplantationCASP8 and FADD-Like Apoptosis Regulating ProteinCell MovementFas Ligand ProteinGraft vs Host DiseaseLymphocyte ActivationMiceMice, Inbred BALB CMice, Inbred C57BLReceptors, OX40Receptors, TNF-Related Apoptosis-Inducing LigandStromal CellsThymus GlandT-LymphocytesTNF-Related Apoptosis-Inducing LigandTransplantation, HomologousConceptsAlloreactive T cellsDonor alloreactive T cellsThymic stromal cellsHost diseaseT cellsDeath receptor 5Thymic graftsProfound T-cell deficiencySelectin glycoprotein ligand-1Stromal cellsPeripheral T cell functionCell adhesion molecule-1Allo-BMT recipientsAllogeneic BM transplantationT-cell reconstitutionT cell deficiencyT cell functionDeath receptor FasAdhesion molecule-1Fas/FasLApoptosis-inducing ligandBMT conditioningSystemic graftP-selectin glycoprotein ligand-1Cell reconstitution
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 inhibition