2008
A 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
IFN-γ and Fas Ligand Are Required for Graft-versus-Tumor Activity against Renal Cell Carcinoma in the Absence of Lethal Graft-versus-Host Disease
Ramirez-Montagut T, Chow A, Kochman A, Smith O, Suh D, Sindhi H, Lu S, Borsotti C, Grubin J, Patel N, Terwey T, Kim T, Heller G, Murphy G, Liu C, Alpdogan O, van den Brink M. IFN-γ and Fas Ligand Are Required for Graft-versus-Tumor Activity against Renal Cell Carcinoma in the Absence of Lethal Graft-versus-Host Disease. The Journal Of Immunology 2007, 179: 1669-1680. PMID: 17641033, DOI: 10.4049/jimmunol.179.3.1669.Peer-Reviewed Original ResearchConceptsRenal cell carcinomaMurine renal cell carcinomaT cellsCell carcinomaGVT activityHost diseaseRenca cellsIFN-gammaTumor activityAllogeneic bone marrow transplantation modelFas ligandAbsence of graftRecipients of IFNBone marrow transplantation modelMechanism of graftMembrane-bound TNF-alphaTumor-bearing miceLethal graftLethal GVHDSevere GVHDTNF-alphaTransplantation modelTransplanted miceLytic capacitySolid tumors
2005
Stimulation of Host NKT Cells by Synthetic Glycolipid Regulates Acute Graft-versus-Host Disease by Inducing Th2 Polarization of Donor T Cells
Hashimoto D, Asakura S, Miyake S, Yamamura T, Van Kaer L, Liu C, Tanimoto M, Teshima T. Stimulation of Host NKT Cells by Synthetic Glycolipid Regulates Acute Graft-versus-Host Disease by Inducing Th2 Polarization of Donor T Cells. The Journal Of Immunology 2005, 174: 551-556. PMID: 15611282, DOI: 10.4049/jimmunol.174.1.551.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CD1Antigens, CD1dBone Marrow TransplantationEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryGalactosylceramidesGlycolipidsGraft vs Host DiseaseMiceMice, KnockoutSTAT6 Transcription FactorT-Lymphocyte SubsetsT-LymphocytesTh2 CellsTrans-ActivatorsTumor Necrosis Factor-alphaConceptsHost NKT cellsDonor T cellsNKT cellsT cellsTh2 polarizationAcute GVHDAcute graftHost diseaseAlpha-GalCerAllogeneic bone marrow transplantationImmunoregulatory T-cell populationsMortality of GVHDTh2 cytokine responsesSerum TNF-alphaNKT cell ligandBone marrow transplantationSTAT6-dependent mechanismT cell populationsNKT ligandCytokine responsesMarrow transplantationIL-4Recipient miceTNF-alphaGVHD
2004
A Role for Tumor Necrosis Factor-&agr;-Mediated Endothelial Apoptosis in the Development of Experimental Idiopathic Pneumonia Syndrome
Gerbitz A, Nickoloff B, Olkiewicz K, Willmarth N, Hildebrandt G, Liu C, Kobzik L, Eissner G, Holler E, Ferrara J, Cooke K. A Role for Tumor Necrosis Factor-&agr;-Mediated Endothelial Apoptosis in the Development of Experimental Idiopathic Pneumonia Syndrome. Transplantation 2004, 78: 494-502. PMID: 15446306, DOI: 10.1097/01.tp.0000128839.13674.02.Peer-Reviewed Original ResearchConceptsExperimental Idiopathic Pneumonia SyndromeAllogeneic bone marrow transplantationIdiopathic pneumonia syndromeBone marrow transplantationTumor necrosis factorLung injuryTNF-alphaPneumonia syndromeNecrosis factorVascular endotheliumBronchoalveolar lavage fluid tumor necrosis factorDevelopment of IPSPulmonary vascular endothelial cell apoptosisAlloreactive donor T cellsInflammatory mediators TNF-alphaMinor histocompatibility antigenic differencesMurine BMT systemPulmonary vascular endotheliumDonor T cellsEC apoptosisVascular endothelial cell apoptosisEndothelial cell apoptosisHost diseaseLung histopathologyPulmonary histopathologyBlockade 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 injuryDonor-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 necrosisDonor T cell-derived TNF alpha regulates pulmonary chemokine expression and the development of idiopathic pneumonia syndrome after allogeneic stem cell transplantation
Hildebrandt G, Olkiewicz K, Corrion L, Chang Y, Liu C, Ferrara J, Cooke K. Donor T cell-derived TNF alpha regulates pulmonary chemokine expression and the development of idiopathic pneumonia syndrome after allogeneic stem cell transplantation. Transplantation And Cellular Therapy 2004, 10: 20. DOI: 10.1016/j.bbmt.2003.12.078.Peer-Reviewed Original Research
2003
CD8+ T‐cell interaction with HCV replicon cells: Evidence for both cytokine‐ and cell‐mediated antiviral activity
Liu C, Zhu H, Tu Z, Xu Y, Nelson D. CD8+ T‐cell interaction with HCV replicon cells: Evidence for both cytokine‐ and cell‐mediated antiviral activity. Hepatology 2003, 37: 1335-1342. PMID: 12774012, DOI: 10.1053/jhep.2003.50207.Peer-Reviewed Original ResearchConceptsHepatitis C virusHCV replicon cellsAntiviral activityReplicon cellsHCV repliconMechanisms of HCVAnti-tumor necrosis factor alphaHCV subgenomic replicon systemAnti-interferon gammaDirect cytolytic effectHLA-A11 alleleNecrosis factor alphaHLA class IHost immune responseSubgenomic replicon systemT cell interactionsT-cell bindingHCV nonstructural proteinsCytolytic functionHCV interactionC virusSpecific lysisInfected hepatocytesTNF-alphaAntiviral effect