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
2004
Perforin and Fas Ligand Are Required for the Regulation of Alloreactive CD8+ T Cells.
Maeda Y, Levy R, Reddy P, Liu C, Teshima T, Ferrara J. Perforin and Fas Ligand Are Required for the Regulation of Alloreactive CD8+ T Cells. Blood 2004, 104: 3052. DOI: 10.1182/blood.v104.11.3052.3052.Peer-Reviewed Original ResearchDonor T cellsT cellsDonor CD8WT T cellsAlloreactive CD8Day 10Day 30Host antigen presenting cellsFas ligandSingle MHC class IHost dendritic cellsModel of graftT cell populationsAntigen presenting cellsT cell homeostasisFas ligand pathwayMHC class IAllogeneic CD8Bm1 miceLethal GVHDSevere GVHDSignificant GVHDHost diseaseBMT recipientsEpithelial target cellsBoth perforin and Fas ligand are required for the regulation of alloreactive CD8+ T cells during acute graft-versus-host disease
Maeda Y, Levy R, Reddy P, Liu C, Clouthier S, Teshima T, Ferrara J. Both perforin and Fas ligand are required for the regulation of alloreactive CD8+ T cells during acute graft-versus-host disease. Blood 2004, 105: 2023-2027. PMID: 15466930, DOI: 10.1182/blood-2004-08-3036.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsBone Marrow TransplantationCD8-Positive T-LymphocytesCell Culture TechniquesFas Ligand ProteinGraft vs Host DiseaseHistocompatibilityHistocompatibility Antigens Class ILymphocyte TransfusionMembrane GlycoproteinsMiceMice, Inbred StrainsModels, AnimalPerforinPore Forming Cytotoxic ProteinsTransplantation, HomologousConceptsT cellsHost diseaseAllogeneic bone marrow transplantationT cell-mediated cytotoxicityTumor necrosis factor alphaMajor histocompatibility complex class IGreater serum levelsDonor T cellsBone marrow transplantationCell-mediated cytotoxicityHistocompatibility complex class IWild-type T cellsNecrosis factor alphaComplex class ILethal GVHDAcute graftAlloreactive CD8Histopathologic damageMarrow transplantationSerum levelsAlloantigen stimulationIrradiated murine modelFactor alphaCD8Murine modelIncreasing T-cell age reduces effector activity but preserves proliferative capacity in a murine allogeneic major histocompatibility complex-mismatched bone marrow transplant model
Friedman J, Alpdogan O, van den Brink M, Liu C, Hurwitz D, Boyd A, Kupper T, Burakoff S. Increasing T-cell age reduces effector activity but preserves proliferative capacity in a murine allogeneic major histocompatibility complex-mismatched bone marrow transplant model. Transplantation And Cellular Therapy 2004, 10: 448-460. PMID: 15205666, DOI: 10.1016/j.bbmt.2004.03.005.Peer-Reviewed Original ResearchConceptsOld T cellsT cellsSurface antigen expressionCD8 cellsAntigen expressionEffector activityT cell receptor repertoireBone marrow transplant modelCD4 T cell expansionT-cell doseSeverity of GVHDType 1 cytokinesT cell expansionAntigen-driven proliferationT-cell groupAdult T-cellT-cell ageSuccinimidyl ester labelingYoung T cellsAge-dependent declineLethal GVHDHost diseasePathologic evidenceTransplant modelCytolytic function