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
2013
Reversible epigenetic down-regulation of MHC molecules by devil facial tumour disease illustrates immune escape by a contagious cancer
Siddle H, Kreiss A, Tovar C, Yuen C, Cheng Y, Belov K, Swift K, Pearse A, Hamede R, Jones M, Skjødt K, Woods G, Kaufman J. Reversible epigenetic down-regulation of MHC molecules by devil facial tumour disease illustrates immune escape by a contagious cancer. Proceedings Of The National Academy Of Sciences Of The United States Of America 2013, 110: 5103-5108. PMID: 23479617, PMCID: PMC3612627, DOI: 10.1073/pnas.1219920110.Peer-Reviewed Original ResearchConceptsDFTD cellsDown-regulation of MHC moleculesMHC class I moleculesClass I moleculesDevil facial tumour diseaseExpression of MHC class I moleculesI moleculesMHC moleculesTumor diseaseMHC class II transactivatorAssociated with up-regulationIn vivoClass II transactivatorTransporter associated with antigen processingLoss of gene expressionCells in vitroDown-regulationAntigen processing pathwayHost immune responseFacial tumour diseaseContagious cancerImmune escapeUnusual pathogenLymphocytic infiltrationT cells
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
1998
Class II transactivator-independent endothelial cell MHC class II gene activation induced by lymphocyte adhesion.
Collinge M, Pardi R, Bender J. Class II transactivator-independent endothelial cell MHC class II gene activation induced by lymphocyte adhesion. The Journal Of Immunology 1998, 161: 1589-93. PMID: 9712019, DOI: 10.4049/jimmunol.161.4.1589.Peer-Reviewed Original ResearchConceptsClass II transactivatorNK cellsIFN-gamma-dependent mechanismIFN-gamma-independent mannerLymphocyte adhesionMHC class II expressionHLA-DR alpha mRNAHLA-DR expressionMHC class II moleculesNK cell activationAllogeneic endothelial cellsClass II expressionIFN-gamma-induced MHC class II expressionClass II moleculesAlpha mRNA expressionCell linesHLA-DRIFN-gammaCell activationMRNA expressionEndothelial cellsAlpha mRNACellsPromoter constructsActivation
1997
Protective antibodies develop, and murine Lyme arthritis regresses, in the absence of MHC class II and CD4+ T cells.
Fikrig E, Barthold SW, Chen M, Chang CH, Flavell RA. Protective antibodies develop, and murine Lyme arthritis regresses, in the absence of MHC class II and CD4+ T cells. The Journal Of Immunology 1997, 159: 5682-6. PMID: 9548512, DOI: 10.4049/jimmunol.159.11.5682.Peer-Reviewed Original ResearchConceptsMHC class IIT cellsClass IINaive C3H/HeN miceC3H/HeN miceC57/BL6 miceCIITA-deficient miceRegression of arthritisResolution of arthritisResolution of carditisDevelopment of arthritisMurine Lyme borreliosisMHC class II transactivatorClass II moleculesClass II transactivatorIgG2b AbsProtective antibodiesBL6 miceHeN miceDeficient miceProtective AbsSCID micePersistent infectionArthritisCD4 repertoire
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