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 CellsT-LymphocytesThymus GlandTNF-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 reconstitutionTRAIL/ DR5 Interactions Are Important for Thymic Damage After Allogeneic Bone Marrow Transplantation.
Na I, Lu S, Yim N, Goldberg G, Tsai J, Rao U, Smith O, King C, Suh D, Hirschhorn-Cymerman D, Palomba M, Penack O, Holland A, Jenq R, Ghosh A, Tran H, Merghoub T, Liu C, Sempowski G, Ventevogel M, Beauchemin N, Furie B, van den Brink M. TRAIL/ DR5 Interactions Are Important for Thymic Damage After Allogeneic Bone Marrow Transplantation. Blood 2009, 114: 234. DOI: 10.1182/blood.v114.22.234.234.Peer-Reviewed Original ResearchAlloreactive T cellsDonor alloreactive T cellsAllogeneic bone marrow transplantationT-cell dosePost-transplant periodBone marrow transplantationAllo-BMTT cellsThymic damageThymic cellularityMarrow transplantationCell doseThymic stromaDay 28Early post-transplant periodAllo-BMT recipientsPeri-transplant periodDonor T cellsFas/Fas ligandOvert clinical diseaseSignificant weight lossExpression of DR5TRAIL/DR5 pathwayRole of TRAILAnti-apoptotic protein cFLIPNOD2 regulates hematopoietic cell function during graft-versus-host disease
Penack O, Smith O, Cunningham-Bussel A, Liu X, Rao U, Yim N, Na I, Holland A, Ghosh A, Lu S, Jenq R, Liu C, Murphy G, Brandl K, van den Brink M. NOD2 regulates hematopoietic cell function during graft-versus-host disease. Journal Of Experimental Medicine 2009, 206: 2101-2110. PMID: 19737867, PMCID: PMC2757869, DOI: 10.1084/jem.20090623.Peer-Reviewed Original ResearchConceptsAntigen-presenting cellsNOD2 deficiencyHost diseaseCrohn's diseaseExperimental allogeneic bone marrow transplantationAllogeneic bone marrow transplantationHost antigen-presenting cellsAllo-BMT recipientsDevelopment of GVHDExperimental colitis modelHematopoietic cellsHost hematopoietic cellsDonor T cellsIndependent risk factorBone marrow chimerasBone marrow transplantationChimeric recipientsIntestinal inflammationProinflammatory stateColitis modelMarrow transplantationNOD2 mutationsRisk factorsT cellsPaneth cells
2008
Depletion of Vascular Endothelial Progenitor Cells Inhibits Inflammation
Penack O, Henke E, Suh D, King C, Smith M, Na I, Holland A, Ghosh A, Lu S, Jenq R, Liu C, Murphy G, Lu T, May C, Scheinberg D, Gao D, Mittal V, Benezra R, Van Den Brink M. Depletion of Vascular Endothelial Progenitor Cells Inhibits Inflammation. Blood 2008, 112: 694. DOI: 10.1182/blood.v112.11.694.694.Peer-Reviewed Original ResearchDepletion of EPCsAllo-BMT recipientsEndothelial progenitor cellsDonor T cellsRole of EPCsDay of BMTGVHD target organsDonor BM cellsAllo-BMTT cellsTumor growthImproved survivalA20 lymphomaInflamed colonPeripheral bloodEndothelial cellsInflammatory diseasesBM cellsTarget organsBM-derived endothelial progenitor cellsAllogeneic hematopoietic stem cell transplantationDay 0Donor endothelial progenitor cellsAllogeneic bone marrow transplantationBALB/c recipients
2006
Secondary Lymphoid Tissues Are Not Required for the Induction of GVHD Following Allogeneic BMT: A Shifting Paradigm for T Cell Allo-Activation.
Silva I, Olkiewicz K, Fisher J, Chaudhary M, Vannella K, Deurloo D, Choi S, Liu C, Cooke K. Secondary Lymphoid Tissues Are Not Required for the Induction of GVHD Following Allogeneic BMT: A Shifting Paradigm for T Cell Allo-Activation. Blood 2006, 108: 3170. DOI: 10.1182/blood.v108.11.3170.3170.Peer-Reviewed Original ResearchBone marrow transplantationAllo-BMT recipientsAntigen presenting cellsHost antigen presenting cellsAllogeneic bone marrow transplantationAly/aly miceInduction of GVHDSecondary lymphoid tissuesPeyer's patchesAllo-BMTAly miceLymphoid tissueT cellsLittermate controlsDonor T cell activationDonor T cell expansionWild-type B6 recipientsAllo-stimulatory capacitySyngeneic BMT recipientsDonor T cellsOnly curative optionSeverity of GVHDBALB/c T cellsIFN-γ productionT cell expansion
2004
Donor-derived TNF-α regulates pulmonary chemokine expression and the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation
Hildebrandt G, Olkiewicz K, Corrion L, Chang Y, Clouthier S, Liu C, Cooke K. Donor-derived TNF-α regulates pulmonary chemokine expression and the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation. Blood 2004, 104: 586-593. PMID: 15069018, DOI: 10.1182/blood-2003-12-4259.Peer-Reviewed Original ResearchConceptsDevelopment of IPSIdiopathic pneumonia syndromeAllogeneic bone marrow transplantationBone marrow transplantationTNF-alphaT cell-derived TNF-alphaPneumonia syndromeMarrow transplantationT cellsBronchoalveolar lavage fluid levelsTNF-alpha-deficient miceAllo-BMT recipientsPulmonary chemokine expressionLavage fluid levelsSignificant lung injuryInflammatory chemokine productionTNF-alpha secretionSignificant effector moleculesAllo-BMTBMT recipientsLung injuryChemokine expressionChemokine productionSyngeneic controlsTumor necrosis