2011
Cross-Presentation by Host CD8α+dendritic Cells Augments Graft-Versus-Tumor Effect without Aggravating Graft-Versus-Host Disease After Allogeneic BMT
Toubai T, Sun Y, Tawara I, Liu C, Reddy P. Cross-Presentation by Host CD8α+dendritic Cells Augments Graft-Versus-Tumor Effect without Aggravating Graft-Versus-Host Disease After Allogeneic BMT. Blood 2011, 118: 310. DOI: 10.1182/blood.v118.21.310.310.Peer-Reviewed Original ResearchAntigen presenting cellsTumor-specific antigensProfessional antigen presenting cellsGVT responseAllogeneic animalsGraft-VersusSyngeneic B6APC subsetsTumor cellsPoly IToll-like receptor 3Induction of GVHDGVHD target organsWild-type B6Acute GVHDAllo-BMTCD8α- DCsAllogeneic BMTGVHD modelGVHD severityGVT effectHost diseaseTumor effectTLR-3Allo-antigenCeacam1 Separates Graft-versus-Host-Disease from Graft-versus-Tumor Activity after Experimental Allogeneic Bone Marrow Transplantation
Lu S, Kappel L, Charbonneau-Allard A, Atallah R, Holland A, Turbide C, Hubbard V, Rotolo J, Smith M, Suh D, King C, Rao U, Yim N, Bautista J, Jenq R, Penack O, Na I, Liu C, Murphy G, Alpdogan O, Blumberg R, Macian F, Holmes K, Beauchemin N, van den Brink M. Ceacam1 Separates Graft-versus-Host-Disease from Graft-versus-Tumor Activity after Experimental Allogeneic Bone Marrow Transplantation. PLOS ONE 2011, 6: e21611. PMID: 21760897, PMCID: PMC3130781, DOI: 10.1371/journal.pone.0021611.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Marrow TransplantationCarcinoembryonic AntigenCD8-Positive T-LymphocytesCell PolarityCell ProliferationCytotoxicity, ImmunologicDendritic CellsGraft vs Host DiseaseGraft vs Tumor EffectHumansIntegrinsIntestine, SmallLymphocyte ActivationLymphocyte CountLymphoid TissueMiceOrgan SpecificityRadiation Injuries, ExperimentalRadiation, IonizingTransplantation, HomologousConceptsAllogeneic bone marrow transplantationBone marrow transplantationDonor T cellsCD8 T cellsT cellsMarrow transplantationGVHD mortalityTumor activityExperimental allogeneic bone marrow transplantationInflammatory bowel disease modelCell adhesion molecule-1GVHD target tissuesRegulation of GVHDTarget tissuesT cell numbersAlloreactive T cellsAdhesion molecule-1T cell activationVariety of physiologicAllo-BMTSystemic GVHDHost diseaseSmall intestinal cryptsDonor graftsAllogeneic transplantation
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 vasculatureSecondary Lymphoid Organs Contribute to, but Are Not Required for the Induction of Graft-versus-Host Responses following Allogeneic Bone Marrow Transplantation: A shifting Paradigm for T Cell Allo-activation
Silva I, Olkiewicz K, Askew D, Fisher J, Chaudhary M, Vannella K, Deurloo D, Choi S, Pierce E, Clouthier S, Liu C, Cooke K. Secondary Lymphoid Organs Contribute to, but Are Not Required for the Induction of Graft-versus-Host Responses following Allogeneic Bone Marrow Transplantation: A shifting Paradigm for T Cell Allo-activation. Transplantation And Cellular Therapy 2010, 16: 598-611. PMID: 20117226, PMCID: PMC3838892, DOI: 10.1016/j.bbmt.2009.12.007.Peer-Reviewed Original ResearchConceptsSecondary lymphoid organsDonor T cellsAllogeneic bone marrow transplantationAly/aly miceBone marrow transplantationAntigen-presenting cellsPeyer's patchesT cellsAllo-BMTLymph nodesMarrow transplantationAly miceLymphoid organsAllogeneic T-cell responsesHost antigen-presenting cellsInduction of GVHDInduction of graftT cell responsesT cell activationDisparate donorsHost diseaseBMT recipientsMajor complicationsTumor burdenLeukemia activity
2009
TRAIL/ 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 cFLIP
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
2003
A critical role for CCR2/MCP-1 interactions in the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation
Hildebrandt G, Duffner U, Olkiewicz K, Corrion L, Willmarth N, Williams D, Clouthier S, Hogaboam C, Reddy P, Moore B, Kuziel W, Liu C, Yanik G, Cooke K. A critical role for CCR2/MCP-1 interactions in the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation. Blood 2003, 103: 2417-2426. PMID: 14615370, DOI: 10.1182/blood-2003-08-2708.Peer-Reviewed Original ResearchConceptsMonocyte chemoattractant protein-1Idiopathic pneumonia syndromeAllogeneic bone marrow transplantationBone marrow transplantationChemokine receptor 2CCR2/MCPAllo-BMTPneumonia syndromeMarrow transplantationBronchoalveolar lavage fluid cellularityExperimental Idiopathic Pneumonia SyndromeBAL fluid levelsMouse BMT modelSoluble p55 TNF receptorTime of diagnosisPreliminary clinical findingsChemoattractant protein-1P55 TNF receptorDonor leukocytesLung injuryMajor complicationsAllogeneic recipientsBAL fluidLethal complicationPulmonary expression