2001
INHIBITION OF INTERFERON-γ–MEDIATED MICROVASCULAR ENDOTHELIAL CELL MAJOR HISTOCOMPATIBILITY COMPLEX CLASS II GENE ACTIVATION BY HMG-COA REDUCTASE INHIBITORS1
Sadeghi M, Tiglio A, Sadigh K, O’Donnell L, Collinge M, Pardi R, Bender J. INHIBITION OF INTERFERON-γ–MEDIATED MICROVASCULAR ENDOTHELIAL CELL MAJOR HISTOCOMPATIBILITY COMPLEX CLASS II GENE ACTIVATION BY HMG-COA REDUCTASE INHIBITORS1. Transplantation 2001, 71: 1262-1268. PMID: 11397960, DOI: 10.1097/00007890-200105150-00014.Peer-Reviewed Original ResearchConceptsMicrovascular endothelial cellsClass II transactivatorInhibitory effectVascular diseaseSimvastatin pretreatmentIFN-gammaReductase inhibitorsClass II major histocompatibility complex moleculesCardiac transplant patientsGraft vascular diseaseLate graft failureHMG-CoA reductase inhibitorsHuman leukocyte antigenEffect of simvastatinMajor histocompatibility complex moleculesHLA-DR inductionSTAT-1 phosphorylationCoA reductase inhibitorsHistocompatibility complex moleculesHuman microvascular endothelial cellsInhibition of interferonTranscription-polymerase chain reaction analysisCardiac transplantationTransplant patientsGraft failure
2000
CD28 and LFA‐1 contribute to cyclosporin A‐resistant T cell growth by stabilizing the IL‐2 mRNA through distinct signaling pathways
Geginat J, Clissi B, Moro M, Dellabona P, Bender J, Pardi R. CD28 and LFA‐1 contribute to cyclosporin A‐resistant T cell growth by stabilizing the IL‐2 mRNA through distinct signaling pathways. European Journal Of Immunology 2000, 30: 1136-1144. PMID: 10760803, DOI: 10.1002/(sici)1521-4141(200004)30:4<1136::aid-immu1136>3.0.co;2-3.Peer-Reviewed Original ResearchMeSH KeywordsAntigens, CDB7-2 AntigenCalcineurinCD28 AntigensCells, CulturedCyclosporineCytoskeletonDendritic CellsDNA-Binding ProteinsDrug SynergismHumansIntercellular Adhesion Molecule-1Interleukin-2Lymphocyte ActivationLymphocyte Function-Associated Antigen-1Membrane GlycoproteinsMitogen-Activated Protein KinasesNF-kappa BNFATC Transcription FactorsNuclear ProteinsPromoter Regions, GeneticProtein BindingRNA StabilityRNA, MessengerSignal TransductionSuperantigensT-LymphocytesTranscription FactorsConceptsIL-2 mRNALFA-1ICAM-1IL-2 dependentT cell proliferationSubsequent T cell proliferationCostimulatory molecule CD28TCR-induced proliferationSignaling pathwaysT cell growthIL-2 transcriptsGraft rejectionDendritic cellsIL-2Clinical transplantationT lymphocytesMolecule CD28Primary T lymphocytesNF-kappaBCD28Distinct signaling pathwaysLower transcriptional rateDifferent signaling pathwaysProtein kinase activationCell proliferation
1995
Contact-dependent endothelial class II HLA gene activation induced by NK cells is mediated by IFN-gamma-dependent and -independent mechanisms.
Watson C, Petzelbauer P, Zhou J, Pardi R, Bender J. Contact-dependent endothelial class II HLA gene activation induced by NK cells is mediated by IFN-gamma-dependent and -independent mechanisms. The Journal Of Immunology 1995, 154: 3222-33. PMID: 7897208, DOI: 10.4049/jimmunol.154.7.3222.Peer-Reviewed Original ResearchMeSH KeywordsAntigens, Differentiation, B-LymphocyteBase SequenceBlotting, NorthernCell AdhesionCells, CulturedEndothelium, VascularGene Expression RegulationHistocompatibility Antigens Class IIHLA-DR AntigensHumansInterferon-gammaKiller Cells, NaturalMolecular Sequence DataOrgan Culture TechniquesPromoter Regions, GeneticSkinTranscriptional ActivationTransfectionConceptsNK cellsNK lymphocytesEndothelial cellsIFN-gammaMHC class II AgIFN-gamma dependenceT cell recruitmentClass II HLAClass II expressionHLA-DR inductionClass II AgT cell proliferationMembrane expressionTrans-well experimentsReceptor AbEndothelial activationImmune amplificationCell recruitmentMicrovessel endotheliumHuman IFN-gammaPromoter constructsClonal expansionCoculture modelCell proliferationChinese hamster ovary cells