2019
Progenitor-derived human endothelial cells evade alloimmunity by CRISPR/Cas9-mediated complete ablation of MHC expression
Merola J, Reschke M, Pierce RW, Qin L, Spindler S, Baltazar T, Manes TD, Lopez-Giraldez F, Li G, Bracaglia LG, Xie C, Kirkiles-Smith N, Saltzman WM, Tietjen GT, Tellides G, Pober JS. Progenitor-derived human endothelial cells evade alloimmunity by CRISPR/Cas9-mediated complete ablation of MHC expression. JCI Insight 2019, 4 PMID: 31527312, PMCID: PMC6824302, DOI: 10.1172/jci.insight.129739.Peer-Reviewed Original ResearchMeSH KeywordsAllograftsAnimalsbeta 2-MicroglobulinCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell DifferentiationCells, CulturedCRISPR-Cas SystemsDisease Models, AnimalEndothelial CellsEndothelial Progenitor CellsFemaleFetal BloodGene Knockout TechniquesGraft RejectionHealthy VolunteersHumansIsoantibodiesKiller Cells, NaturalLymphocyte ActivationMiceMicrovesselsNuclear ProteinsOrgan TransplantationPrimary Cell CultureTissue EngineeringTrans-ActivatorsConceptsDonor-specific antibodiesClass II transactivatorEndothelial cellsMHC expressionAllogeneic natural killer (NK) cellsT effector memory cellsEffector memory T cellsClass IClass II major histocompatibility complex moleculesEffector memory cellsMHC molecule expressionMemory T cellsNatural killer cellsAlloreactive cytotoxic T lymphocytesAllogeneic endothelial cellsMajor histocompatibility complex moleculesCytotoxic T lymphocytesClass I MHC moleculesHistocompatibility complex moleculesI MHC moleculesAllogeneic CD4Donor leukocytesHuman endothelial cellsGraft perfusionKiller cells
2016
Blocking MHC class II on human endothelium mitigates acute rejection
Abrahimi P, Qin L, Chang WG, Bothwell AL, Tellides G, Saltzman WM, Pober JS. Blocking MHC class II on human endothelium mitigates acute rejection. JCI Insight 2016, 1: e85293. PMID: 26900601, PMCID: PMC4756651, DOI: 10.1172/jci.insight.85293.Peer-Reviewed Original ResearchClass II MHC moleculesCytotoxic T lymphocytesII MHC moleculesClass I MHC moleculesMHC moleculesI MHC moleculesEndothelial cellsAcute rejectionT cellsEffector memory T cellsT cell-mediated destructionAcute allograft rejectionCell-mediated destructionGraft endothelial cellsMemory T cellsAlloreactive cytotoxic T lymphocytesExperimental rodent modelsMajor histocompatibility complex moleculesSecondary lymphoid organsMHC class IIClass I major histocompatibility complex moleculesAllogeneic human lymphocytesHistocompatibility complex moleculesPrevents CD4Artery graft
2011
Differential but Competitive Binding of Nogo Protein and Class I Major Histocompatibility Complex (MHCI) to the PIR-B Ectodomain Provides an Inhibition of Cells*
Matsushita H, Endo S, Kobayashi E, Sakamoto Y, Kobayashi K, Kitaguchi K, Kuroki K, Söderhäll A, Maenaka K, Nakamura A, Strittmatter SM, Takai T. Differential but Competitive Binding of Nogo Protein and Class I Major Histocompatibility Complex (MHCI) to the PIR-B Ectodomain Provides an Inhibition of Cells*. Journal Of Biological Chemistry 2011, 286: 25739-25747. PMID: 21636572, PMCID: PMC3138294, DOI: 10.1074/jbc.m110.157859.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsbeta 2-MicroglobulinBinding, CompetitiveFemaleHistocompatibility Antigens Class IHLA AntigensHLA-G AntigensHumansImmunologic FactorsInterleukin-6LipopolysaccharidesMast CellsMiceMice, Inbred C57BLMyelin ProteinsMyelin-Associated GlycoproteinNeurotransmitter AgentsNogo ProteinsProtein Structure, TertiaryRatsReceptors, ImmunologicSubstrate SpecificityConceptsMajor histocompatibility complexRecent unexpected findingsClass I major histocompatibility complexI major histocompatibility complexInterleukin-6 releaseClass I MHC moleculesC-terminal ectodomainNovel inhibitory roleCultured mast cellsI MHC moleculesTerminal domainPeripheral toleranceInhibitory receptorsInhibition of cellMast cellsOutgrowth inhibitorB cellsMyeloid cellsImmune systemMHC moleculesNeurite regenerationNovel mechanismNogo proteinEctodomainInhibitory role
2001
CD8 Binding to MHC Class I Molecules Is Influenced by T Cell Maturation and Glycosylation
Daniels M, Devine L, Miller J, Moser J, Lukacher A, Altman J, Kavathas P, Hogquist K, Jameson S. CD8 Binding to MHC Class I Molecules Is Influenced by T Cell Maturation and Glycosylation. Immunity 2001, 15: 1051-1061. PMID: 11754824, DOI: 10.1016/s1074-7613(01)00252-7.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsATP Binding Cassette Transporter, Subfamily B, Member 2ATP-Binding Cassette TransportersCD3 ComplexCD4-Positive T-LymphocytesCD8 AntigensCD8-Positive T-LymphocytesCell AdhesionCell DifferentiationCellular SenescenceGlycosylationH-2 AntigensHistocompatibility Antigen H-2DLigandsMacromolecular SubstancesMembrane GlycoproteinsMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutN-Acetylneuraminic AcidNeuraminidaseOvalbuminPeptide FragmentsProtein BindingProtein Processing, Post-TranslationalReceptors, Antigen, T-Cell, alpha-betaRheologySolubilityT-Lymphocyte SubsetsThymus GlandConceptsGlycosylation stateT cell maturationCell maturationT cell adhesionDevelopmental regulationDouble-positive thymocytesCell adhesionT cell activationClass I MHC tetramersAdhesion moleculesCell activationMHC class I moleculesMaturationClass I moleculesClass I MHC moleculesI MHC moleculesI moleculesMoleculesGlycosylationMHC ligandsRegulationMHC moleculesClass I MHCBindingSialylationThe Clonotypic T Cell Receptor Is a Source of Tumor‐associated Antigens in Cutaneous T Cell Lymphoma
BERGER C, LONGLEY J, HANLON D, GIRARDI M, EDELSON R. The Clonotypic T Cell Receptor Is a Source of Tumor‐associated Antigens in Cutaneous T Cell Lymphoma. Annals Of The New York Academy Of Sciences 2001, 941: 106-122. PMID: 11594564, DOI: 10.1111/j.1749-6632.2001.tb03715.x.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAntigens, NeoplasmCancer VaccinesCD8-Positive T-LymphocytesCell LineCells, CulturedHumansHybridomasImmunoglobulin IdiotypesLymphocyte ActivationLymphoma, T-Cell, CutaneousMiceNeoplasm TransplantationPeptidesReceptors, Antigen, T-CellSkin NeoplasmsSurvival RateT-Lymphocytes, CytotoxicTransfectionConceptsCutaneous T-cell lymphomaT-cell lymphomaT cell receptorClonotypic T cell receptorCell lymphomaAutologous CD8 T cellsCD8 T cell linesCell receptorBeta chainCD8 T cell recognitionImmunogenic tumor peptidesCD8 T cellsCell surface TCR expressionClass I MHC moleculesSource of tumorsT cell recognitionT-cell malignanciesTCR beta chainI MHC moleculesT cell linesTCR epitopesTumor epitopesDendritic cellsSurface TCR expressionCancer vaccines
2000
Cytoprotection of Human Umbilical Vein Endothelial Cells Against Apoptosis and CTL-Mediated Lysis Provided by Caspase-Resistant Bcl-2 Without Alterations in Growth or Activation Responses
Zheng L, Dengler T, Kluger M, Madge L, Schechner J, Maher S, Pober J, Bothwell A. Cytoprotection of Human Umbilical Vein Endothelial Cells Against Apoptosis and CTL-Mediated Lysis Provided by Caspase-Resistant Bcl-2 Without Alterations in Growth or Activation Responses. The Journal Of Immunology 2000, 164: 4665-4671. PMID: 10779771, DOI: 10.4049/jimmunol.164.9.4665.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisCaspasesCell DivisionCell Line, TransformedCells, CulturedCulture Media, ConditionedCytotoxicity, ImmunologicEndothelial Growth FactorsEndothelium, VascularGenetic VectorsGreen Fluorescent ProteinsHumansLuminescent ProteinsProto-Oncogene Proteins c-bcl-2RetroviridaeT-Lymphocytes, CytotoxicTransduction, GeneticTransfectionUmbilical VeinsConceptsGraft endothelial cellsAllograft rejectionBcl-2Endothelial cellsAcute allograft rejectionClass I MHC moleculesNF-kappaB activationHuman umbilical vein endothelial cellsI MHC moleculesUmbilical vein endothelial cellsHost CTLVein endothelial cellsEndothelial injuryAnti-apoptotic gene Bcl-2MHC moleculesGene Bcl-2Induction of apoptosisBcl-2-transduced cellsClass IActivation responseApoptotic effectsCTLHUVECTNFGrowth factor withdrawal
1998
Natural killer activating receptors trigger interferon γ secretion from T cells and natural killer cells
Mandelboim O, Kent S, Davis D, Wilson S, Okazaki T, Jackson R, Hafler D, Strominger J. Natural killer activating receptors trigger interferon γ secretion from T cells and natural killer cells. Proceedings Of The National Academy Of Sciences Of The United States Of America 1998, 95: 3798-3803. PMID: 9520447, PMCID: PMC19917, DOI: 10.1073/pnas.95.7.3798.Peer-Reviewed Original ResearchConceptsNatural killer cell activating receptorsT cellsNK cellsInterferon γ secretionSubset of CD8Target cellsHuman class I major histocompatibility complex (MHC) moleculesNatural killer cellsInterferon-gamma secretionGammadelta T cellsMajor histocompatibility complex moleculesAlphabeta T cellsClass I MHC moleculesClass I major histocompatibility complex moleculesTypes of lymphocytesMHC class IHistocompatibility complex moleculesI MHC moleculesT cell receptorEnhancement of proliferationΓ secretionGamma secretionNatural killerKiller cellsActivating receptors
1995
Ubiquitin, proteasomes, and the regulation of intracellular protein degradation
Hochstrasser M. Ubiquitin, proteasomes, and the regulation of intracellular protein degradation. Current Opinion In Cell Biology 1995, 7: 215-223. PMID: 7612274, DOI: 10.1016/0955-0674(95)80031-x.Peer-Reviewed Original ResearchConceptsCellular regulatory mechanismsIntracellular protein degradationCell cycle progressionProtein ubiquitinationUbiquitin systemProtein degradationRegulatory mechanismsCycle progressionSpecific proteinsForeign proteinsLarge familyCell proliferationProteasomeRapid degradationProteinClass I MHC moleculesUbiquitinationDeubiquitinationUbiquitinI MHC moleculesProteolysisEnzymeKey stepDegradationRegulation
1993
HUMAN CD4+ T CELLS PROLIFERATE TO HLA-DR+ ALLOGENEIC VASCULAR ENDOTHELIUM
SAVAGE C, HUGHES C, MCINTYRE B, PICARD J, POBER J. HUMAN CD4+ T CELLS PROLIFERATE TO HLA-DR+ ALLOGENEIC VASCULAR ENDOTHELIUM. Transplantation 1993, 56: 128-134. PMID: 7687392, DOI: 10.1097/00007890-199307000-00024.Peer-Reviewed Original ResearchMeSH KeywordsAntibodies, MonoclonalAntigens, CDAntigens, Differentiation, T-LymphocyteCD2 AntigensCD4 AntigensCD58 AntigensCells, CulturedEndothelium, VascularFlow CytometryHistocompatibility Antigens Class IHLA-DR AntigensHumansInterferon-gammaLymphocyte ActivationMembrane GlycoproteinsPolymerase Chain ReactionReceptors, ImmunologicRecombinant ProteinsT-Lymphocyte SubsetsTransplantation, HomologousUmbilical VeinsConceptsHLA-DR expressing cellsT cellsHLA-DRPolymerase chain reactionEC culturesAllogeneic class II MHC moleculesMHC moleculesLFA-1 beta chainLFA-1Peripheral blood CD4VLA-4 alphaMHC class II moleculesT cell responsesClass II MHC moleculesT cell surface moleculesT cell proliferationClass I MHC moleculesExpressing cellsClass II moleculesBeta chainII MHC moleculesDe novo expressionI MHC moleculesAllogeneic proliferationBlood CD4Four different classes of inhibitors of receptor-mediated endocytosis decrease tumor necrosis factor-induced gene expression in human endothelial cells.
Bradley JR, Johnson DR, Pober JS. Four different classes of inhibitors of receptor-mediated endocytosis decrease tumor necrosis factor-induced gene expression in human endothelial cells. The Journal Of Immunology 1993, 150: 5544-55. PMID: 8390537, DOI: 10.4049/jimmunol.150.12.5544.Peer-Reviewed Original ResearchConceptsIFN-gamma-mediated inductionELAM-1Human endothelial cellsEndothelial cellsMHC moleculesReceptor-mediated endocytosisCytokine-inducible moleculesAnti-inflammatory therapyIL-1-induced increaseClass II MHC moleculesICAM-1 expressionClass I MHC moleculesVCAM-1 expressionCultured human endothelial cellsII MHC moleculesI MHC moleculesNew potential targetsICAM-1VCAM-1Levels of mRNADensity lipoproteinExposure of cellsTNFGene expressionTNF induction
1991
Tumor necrosis factor induction of endothelial cell surface antigens is independent of protein kinase C activation or inactivation. Studies with phorbol myristate acetate and staurosporine.
Ritchie AJ, Johnson DR, Ewenstein BM, Pober JS. Tumor necrosis factor induction of endothelial cell surface antigens is independent of protein kinase C activation or inactivation. Studies with phorbol myristate acetate and staurosporine. The Journal Of Immunology 1991, 146: 3056-62. PMID: 1707932, DOI: 10.4049/jimmunol.146.9.3056.Peer-Reviewed Original ResearchMeSH Keywords1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineAlkaloidsCell Adhesion MoleculesCell CompartmentationEndothelium, VascularEnzyme ActivationE-SelectinHistocompatibility Antigens Class IHumansIn Vitro TechniquesIntercellular Adhesion Molecule-1IsoquinolinesPhosphoproteinsPiperazinesProtein BiosynthesisProtein Kinase CRNA, MessengerSignal TransductionStaurosporineTetradecanoylphorbol AcetateTumor Necrosis Factor-alphaConceptsAdhesion molecule-1Intercellular adhesion molecule-1Molecule-1Endothelial leukocyte adhesion molecule-1 expressionProtein kinase CAdhesion molecule-1 expressionEndothelial leukocyte adhesion molecule-1Leukocyte adhesion molecule-1Surface Ag expressionMolecule-1 expressionClass I MHC moleculesClass I MHCEndothelial cell surface antigensAction of TNFI MHC moleculesCell surface antigensNecrosis factor inductionMechanism of actionPhorbol myristate acetatePKC activationTNF effectsI MHCSurface antigenProtein kinase C activationActivation of PKC
1990
IFN-gamma enhances endothelial activation induced by tumor necrosis factor but not IL-1.
Doukas J, Pober JS. IFN-gamma enhances endothelial activation induced by tumor necrosis factor but not IL-1. The Journal Of Immunology 1990, 145: 1727-33. PMID: 1697308, DOI: 10.4049/jimmunol.145.6.1727.Peer-Reviewed Original ResearchMeSH KeywordsBlotting, NorthernCell Adhesion MoleculesDrug SynergismEndothelium, VascularE-SelectinFluorescent Antibody TechniqueGene ExpressionHistocompatibility Antigens Class IHumansIn Vitro TechniquesIntercellular Adhesion Molecule-1Interferon-gammaInterleukin-1Recombinant ProteinsRNA, MessengerTumor Necrosis Factor-alphaConceptsEndothelial leukocyte adhesion molecule-1ELAM-1 expressionIL-1 betaIFN-gammaIL-1Endothelial cellsEC activationIL-1 beta responseIntercellular adhesion molecule-1 expressionAdhesion molecule-1 expressionMHC Ag expressionLeukocyte adhesion molecule-1Treatment of ECICAM-1 expressionMolecule-1 expressionClass I MHC moleculesTumor necrosis factorAdhesion molecule-1ICAM-1 mRNAClass I MHCI MHC moleculesIFN-gamma effectELAM-1 mRNACultured endothelial cellsIncrease TNFInvariant chain association with HLA-DR molecules inhibits immunogenic peptide binding
Roche P, Cresswell P. Invariant chain association with HLA-DR molecules inhibits immunogenic peptide binding. Nature 1990, 345: 615-618. PMID: 2190094, DOI: 10.1038/345615a0.Peer-Reviewed Original ResearchConceptsClass II moleculesImmunogenic peptidesMHC moleculesClass II major histocompatibility complex moleculesClass II MHC moleculesMajor histocompatibility complex moleculesClass I MHC moleculesHLA-DR moleculesII MHC moleculesHistocompatibility complex moleculesI MHC moleculesClass I moleculesIntracellular class II moleculesCell surface expressionT lymphocytesPresent immunogenic peptidesClass IIProtein antigensClass IInvariant chain associationI moleculesCell surface glycoproteinSurface expressionInvariant chainFunctional dichotomy
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