2012
Immune modulation of effector CD4+ and regulatory T cell function by sorafenib in patients with hepatocellular carcinoma
Cabrera R, Ararat M, Xu Y, Brusko T, Wasserfall C, Atkinson M, Chang L, Liu C, Nelson D. Immune modulation of effector CD4+ and regulatory T cell function by sorafenib in patients with hepatocellular carcinoma. Cancer Immunology, Immunotherapy 2012, 62: 737-746. PMID: 23223899, PMCID: PMC3863727, DOI: 10.1007/s00262-012-1380-8.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsCarcinoma, HepatocellularCase-Control StudiesCD4-Positive T-LymphocytesCoculture TechniquesCytokinesDose-Response Relationship, ImmunologicEnzyme-Linked Immunosorbent AssayHumansInterleukin-2 Receptor alpha SubunitLiver NeoplasmsNiacinamidePhenylurea CompoundsSorafenibT-Lymphocytes, RegulatoryConceptsEffect of sorafenibHepatocellular carcinomaTeff activationT cellsLow dosesTeff responsesTumor immunityRegulatory T cell functionImpact of sorafenibEffector T cellsRegulatory T cellsTreg suppressive functionPeripheral mononuclear cellsCD25 surface expressionT cell functionNovel combination treatmentTreg suppressionEffector CD4Treg functionPharmacologic dosesTeff proliferationImmune reactivitySystemic drugsCD25 expressionMononuclear cells
2011
Hepatocyte growth factor upregulation promotes carcinogenesis and epithelial-mesenchymal transition in hepatocellular carcinoma via Akt and COX-2 pathways
Ogunwobi O, Liu C. Hepatocyte growth factor upregulation promotes carcinogenesis and epithelial-mesenchymal transition in hepatocellular carcinoma via Akt and COX-2 pathways. Clinical & Experimental Metastasis 2011, 28: 721-731. PMID: 21744257, PMCID: PMC3732749, DOI: 10.1007/s10585-011-9404-x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCadherinsCarcinoma, HepatocellularCell AdhesionCell DifferentiationCell Line, TumorCell MovementCell ProliferationCyclooxygenase 2Enzyme-Linked Immunosorbent AssayEpithelial-Mesenchymal TransitionExtracellular Signal-Regulated MAP KinasesHepatocyte Growth FactorLiver Neoplasms, ExperimentalMiceMice, Inbred BALB CNeoplasm InvasivenessPhosphorylationProto-Oncogene Proteins c-aktReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSignal TransductionUp-RegulationVimentinConceptsEpithelial-mesenchymal transitionHepatocyte growth factorCyclooxygenase-2Hepatocellular carcinomaBNL cellsMarkers of EMTDevelopment of HCCAdvanced hepatocellular carcinomaCOX-2 pathwayMetastatic hepatocellular carcinomaUpregulation of HGFMesenchymal characteristicsGrowth factor upregulationE-cadherinCharacteristic epithelial morphologyCancer mortalitySubsequent metastasisEMT markersImportant causeMigratory capacityHCC cellsBNL CLCancer progressionCollagen 1Growth factor
2009
Hepatocellular Carcinoma Immunopathogenesis: Clinical Evidence for Global T Cell Defects and an Immunomodulatory Role for Soluble CD25 (sCD25)
Cabrera R, Ararat M, Cao M, Xu Y, Wasserfall C, Atkinson M, Liu C, Nelson D. Hepatocellular Carcinoma Immunopathogenesis: Clinical Evidence for Global T Cell Defects and an Immunomodulatory Role for Soluble CD25 (sCD25). Digestive Diseases And Sciences 2009, 55: 484-495. PMID: 19714465, PMCID: PMC3161029, DOI: 10.1007/s10620-009-0955-5.Peer-Reviewed Original ResearchConceptsT cell responsesHCC patientsHepatocellular carcinomaCell responsesTumor burdenImpaired T cell responsesLower IFN-γ productionEffector T cell responsesIL-2 receptor alpha chainATP production assaysLevels of sCD25Tolerogenic tumor environmentIFN-γ ELISPOTEffector T cellsT cell immunityT cell reactivityIFN-γ productionIL-2 supplementationT cell defectsDose-dependent mannerReceptor alpha chainIL-2 signalingSerum sCD25Soluble CD25Worse survival
2008
Combined Th2 cytokine deficiency in donor T cells aggravates experimental acute graft-vs-host disease
Tawara I, Maeda Y, Sun Y, Lowler K, Liu C, Toubai T, McKenzie A, Reddy P. Combined Th2 cytokine deficiency in donor T cells aggravates experimental acute graft-vs-host disease. Experimental Hematology 2008, 36: 988-996. PMID: 18410989, PMCID: PMC2603625, DOI: 10.1016/j.exphem.2008.02.010.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsBone Marrow TransplantationCD4-Positive T-LymphocytesCell ProliferationDisease Models, AnimalEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryGraft vs Host DiseaseImmunologic TestsInterleukin-2 Receptor alpha SubunitInterleukinsMajor Histocompatibility ComplexMiceMice, Inbred BALB CMice, Inbred C57BLSurvival RateT-LymphocytesTh2 CellsTransplantation, HomologousConceptsDonor T cellsT cellsWT T cellsTh2 cytokinesAcute graftAllogeneic bone marrow transplantationAllogeneic antigen-presenting cellsT cell proliferative responsesAnti-CD3 monoclonal antibodyEnhanced T cell proliferationExperimental acute graftNumber of immunoregulatoryTarget organ damageTh2 cytokine secretionBone marrow transplantationT helper 1Antigen-presenting cellsWild-type T cellsT cell proliferationGreater clinical severityBALB/cB6 recipientsGVHD mortalityHost diseaseIL-17
2005
Absence of β7 integrin results in less graft-versus-host disease because of decreased homing of alloreactive T cells to intestine
Waldman E, Lu S, Hubbard V, Kochman A, Eng J, Terwey T, Muriglan S, Kim T, Heller G, Murphy G, Liu C, Alpdogan O, van den Brink M. Absence of β7 integrin results in less graft-versus-host disease because of decreased homing of alloreactive T cells to intestine. Blood 2005, 107: 1703-1711. PMID: 16291587, PMCID: PMC1895413, DOI: 10.1182/blood-2005-08-3445.Peer-Reviewed Original ResearchConceptsHematopoietic stem cell transplantationLess GVHD morbidityT cell infiltrationT cellsGVHD morbidityGVT activityHost diseaseDonor T-cell infiltrationDonor T cellsAlloreactive T cellsStem cell transplantationWild-type T cellsOverall significant decreaseIntestinal graftIntestinal GVHDLess graftBeta7 integrinCell transplantationCytokine productionAlpha4beta7 integrinIntact activationTumor experimentsMorbidityClinical potentialGraftStimulation 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