2022
Super‐killer CTLs are generated by single gene deletion of Bach2
Barton P, Davenport A, Hukelmann J, Cantrell D, Stinchcombe J, Richard A, Griffiths G. Super‐killer CTLs are generated by single gene deletion of Bach2. European Journal Of Immunology 2022, 52: 1776-1788. PMID: 36086884, PMCID: PMC9828676, DOI: 10.1002/eji.202249797.Peer-Reviewed Original ResearchConceptsCD8<sup>+</sup> T cellsT cellsEffector CTLSplenic CD8<sup>+</sup> T cellsT cell-mediated immune regulationMurine CD8<sup>+</sup> T cellsCentral memory T cellsWild-type CTLMemory T cellsNaive T cellsGene deletionAbsence of Bach2In vitro activityCytolytic capacityBach2 deficiencyNaive cellsEnhanced cytotoxicityImmune regulationCytolytic granulesCytotoxic advantageCTLBach2Wild-typeDifferentiation stateGranule contents
2017
Inducible T Cell Kinase Regulates the Acquisition of Cytolytic Capacity and Degranulation in CD8+ CTLs
Kapnick S, Stinchcombe J, Griffiths G, Schwartzberg P. Inducible T Cell Kinase Regulates the Acquisition of Cytolytic Capacity and Degranulation in CD8+ CTLs. The Journal Of Immunology 2017, 198: 2699-2711. PMID: 28213500, PMCID: PMC5360469, DOI: 10.4049/jimmunol.1601202.Peer-Reviewed Original ResearchConceptsInducible T-cell kinaseT-cell kinaseITK deficiencyCD8<sup>+</sup> T cell functionCD8<sup>+</sup> T cellsAcquisition of effector functionsExposure to IL-2CD8<sup>+</sup> CTLsCD8+ CTLT cell functionSusceptibility to viral infectionsCTL expansionCytolytic capacityCytolytic effectorsT cellsIL-12IL-2Effector functionsMurine CTLTCR signalingViral infectionMurine cellsDefective functionCTLCytokine signaling
2014
The Transcription Factor FoxO1 Sustains Expression of the Inhibitory Receptor PD-1 and Survival of Antiviral CD8+ T Cells during Chronic Infection
Staron MM, Gray SM, Marshall HD, Parish IA, Chen JH, Perry CJ, Cui G, Li MO, Kaech SM. The Transcription Factor FoxO1 Sustains Expression of the Inhibitory Receptor PD-1 and Survival of Antiviral CD8+ T Cells during Chronic Infection. Immunity 2014, 41: 802-814. PMID: 25464856, PMCID: PMC4270830, DOI: 10.1016/j.immuni.2014.10.013.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, BlockingAntibodies, MonoclonalCD28 AntigensCD8-Positive T-LymphocytesCell DifferentiationCell Line, TumorChronic DiseaseForkhead Box Protein O1Forkhead Transcription FactorsGranzymesHumansInterferon-gammaJurkat CellsLymphocyte ActivationLymphocytic ChoriomeningitisLymphocytic choriomeningitis virusMiceMice, Inbred C57BLMice, TransgenicProgrammed Cell Death 1 ReceptorProto-Oncogene Proteins c-aktReceptors, Antigen, T-CellSirolimusT-Lymphocytes, CytotoxicTOR Serine-Threonine KinasesConceptsChronic viral infectionsVirus-specific CTLPD-1Viral infectionMurine lymphocytic choriomeningitis virus infectionInhibitory receptor PD-1Lymphocytic choriomeningitis virus infectionCell death protein 1Receptor PD-1Death protein 1MTOR inhibitor rapamycinExhausted CTLsAntiviral CD8Activation of AktInhibitory receptorsTranscription factor FOXO1Chronic infectionT cellsT lymphocytesTherapeutic effectVirus infectionPersistent infectionPositive feedback pathwayInfectionCTL
2003
Adaptor protein 3–dependent microtubule-mediated movement of lytic granules to the immunological synapse
Clark R, Stinchcombe J, Day A, Blott E, Booth S, Bossi G, Hamblin T, Davies E, Griffiths G. Adaptor protein 3–dependent microtubule-mediated movement of lytic granules to the immunological synapse. Nature Immunology 2003, 4: 1111-1120. PMID: 14566336, DOI: 10.1038/ni1000.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Protein Complex 3Adaptor Protein Complex beta SubunitsAntigens, CDBase SequenceCytoplasmic GranulesHermanski-Pudlak SyndromeHumansImmune SystemMembrane Transport ProteinsMicrotubulesMolecular Sequence DataMutationPlatelet Membrane GlycoproteinsProteinsTetraspanin 30T-Lymphocytes, CytotoxicConceptsAP-3Hermansky-Pudlak syndromeLytic granulesImmunological synapseAP-3 deficiencyAdaptor protein 3Hermansky-Pudlak syndrome type 2Lysosomal sortingSecretory domainPolarized secretionAutosomal recessive diseaseCytotoxic T lymphocyte (CTL)-mediated cytotoxicityRare autosomal recessive diseasePlasma membraneProtein CD63Recessive diseaseOculocutaneous albinismProtein 3Platelet defectsSynapseType 2AdaptorMicrotubulesCTLMutations
2002
Porcine Endothelial Cells, Unlike Human Endothelial Cells, Can Be Killed by Human CTL Via Fas Ligand and Cannot Be Protected by Bcl-2
Zheng L, Ben LH, Pober JS, Bothwell AL. Porcine Endothelial Cells, Unlike Human Endothelial Cells, Can Be Killed by Human CTL Via Fas Ligand and Cannot Be Protected by Bcl-2. The Journal Of Immunology 2002, 169: 6850-6855. PMID: 12471117, DOI: 10.4049/jimmunol.169.12.6850.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, HeterophileApoptosisCD8-Positive T-LymphocytesCell LineCell Line, TransformedCoculture TechniquesCytotoxicity Tests, ImmunologicCytotoxicity, ImmunologicEndothelium, VascularEpitopes, T-LymphocyteFas Ligand Proteinfas ReceptorGenetic VectorsGranzymesHistocompatibility Antigens Class IHumansImmunity, InnateIsoantigensLigandsMembrane GlycoproteinsPerforinPore Forming Cytotoxic ProteinsProto-Oncogene Proteins c-bcl-2Serine EndopeptidasesSwineT-Lymphocytes, CytotoxicConceptsHuman endothelial cellsPorcine endothelial cellsEndothelial cellsBcl-2MHC class I restrictionClass I restrictionPorcine aortic endothelial cellsTarget cell recognitionAnti-Fas ligand AbAortic endothelial cellsHost CTLAcute rejectionCTL responsesDrug-induced apoptosisHuman CTLPorcine targetsTarget cell typeHuman xenotransplantationFAS expressionFas ligandPorcine cellsCTLMajor effectorCell recognitionMajor targetBreakdown of CTL Tolerance to Self HLA-B*2705 Induced by Exposure to Chlamydia trachomatis
Popov I, Dela Cruz CS, Barber BH, Chiu B, Inman RD. Breakdown of CTL Tolerance to Self HLA-B*2705 Induced by Exposure to Chlamydia trachomatis. The Journal Of Immunology 2002, 169: 4033-4038. PMID: 12244206, DOI: 10.4049/jimmunol.169.7.4033.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, Genetically ModifiedAutoantigensCells, CulturedChlamydia trachomatisCoculture TechniquesCytotoxicity, ImmunologicEpitopes, T-LymphocyteHLA-B AntigensHLA-B27 AntigenHumansL CellsLymphocyte ActivationLymphocyte Culture Test, MixedMiceRatsRats, Inbred LewSelf ToleranceT-Lymphocytes, CytotoxicTransfectionConceptsB27-transgenic ratsSuch immunized animalsGeneration of CTLMHC class IArthritogenic pathogensSelf-HLASeronegative arthritisCTL toleranceHLA-B27Arthritogenic peptidesCTL recognitionImmunized animalsRestriction elementsTransgenic ratsChlamydia trachomatisB27Disease pathogenesisSplenocytesClass IStrong associationCTLIntracellular bacteriaImmunizationChlamydiaRats
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
1999
Specificity of CTL interactions with peptide-MHC class I tetrameric complexes is temperature dependent.
Whelan J, Dunbar P, Price D, Purbhoo M, Lechner F, Ogg G, Griffiths G, Phillips R, Cerundolo V, Sewell A. Specificity of CTL interactions with peptide-MHC class I tetrameric complexes is temperature dependent. The Journal Of Immunology 1999, 163: 4342-8. PMID: 10510374, DOI: 10.4049/jimmunol.163.8.4342.Peer-Reviewed Original ResearchConceptsTetramer stainingPopulation of CTLTCR/peptide-MHC interactionCD8+ cellsPeptide-MHC class I complexesClass I ligandsPolyclonal cell populationsClass I complexesEarly endocytic compartmentEpitope variantsEffect of incubation temperatureImmune responseStaining intensityDegree of promiscuityI ligandsReceptor internalizationDegrees CCell populationsCTLEndocytic compartmentsStainingPeptide variantsConfocal microscopyWell-characterized setIncubation temperatureHuman vascular endothelial cells favor clonal expansion of unusual alloreactive CTL.
Biedermann B, Pober J. Human vascular endothelial cells favor clonal expansion of unusual alloreactive CTL. The Journal Of Immunology 1999, 162: 7022-30. PMID: 10358144, DOI: 10.4049/jimmunol.162.12.7022.Peer-Reviewed Original ResearchConceptsTarget cell contactB lymphoblastoid cellsLittle IFN-gammaIFN-gammaEndothelial cellsCTL clonesClass I MHC-restricted CTLAbsence of ECExpression of CD40LAllogeneic endothelial cellsIFN-gamma secretionIL-4 secretionCell contactHuman vascular endothelial cellsVascular endothelial cellsCTL subsetsCD40L expressionCTL linesCD40 ligandT cellsAlloreactive CTLArterial intimaClonal expansionCTLCultured HUVECs
1998
Human endothelial cells induce and regulate cytolytic T cell differentiation.
Biedermann B, Pober J. Human endothelial cells induce and regulate cytolytic T cell differentiation. The Journal Of Immunology 1998, 161: 4679-87. PMID: 9794397, DOI: 10.4049/jimmunol.161.9.4679.Peer-Reviewed Original ResearchConceptsB lymphoblastoid cellsEndothelial cellsHuman endothelial cellsSame donorT cellsProliferation of CD8IFN-gamma secretionCultured human endothelial cellsT cell differentiationT cell growthAllogeneic CD8CTL responsesPerforin expressionCTL differentiationPresence of ECT lymphocytesAllospecific CTLCD8CTLEfficient stimulatorsLymphoblastoid cellsCell numberReproducible frequencyCell growthInput cell numberIL-18 augments perforin-dependent cytotoxicity of liver NK-T cells.
Dao T, Mehal W, Crispe I. IL-18 augments perforin-dependent cytotoxicity of liver NK-T cells. The Journal Of Immunology 1998, 161: 2217-22. PMID: 9725214, DOI: 10.4049/jimmunol.161.5.2217.Peer-Reviewed Original ResearchMeSH KeywordsAdjuvants, ImmunologicAnimalsCytokinesCytotoxicity, ImmunologicHumansInterferon InducersInterferon-gammaInterleukin-18Jurkat CellsKiller Cells, NaturalLiverLymphoproliferative DisordersMembrane GlycoproteinsMiceMice, Inbred C57BLMice, Inbred StrainsMice, KnockoutPerforinPore Forming Cytotoxic ProteinsT-Lymphocyte SubsetsT-Lymphocytes, CytotoxicTumor Necrosis Factor-alphaConceptsNK T cellsLiver NK T cellsIL-18NK cellsIntrahepatic lymphocyte subpopulationsNK cell activityPerforin-dependent cytotoxicityPerforin-dependent pathwayTNF-alpha productionSoluble TNF-alphaT cell linesLymphocyte subpopulationsCytotoxic cellsTNF-alphaT cellsCell activityExact mechanismNKCell populationsCell linesLiverCytotoxicityCellsCytokinesCTL
1997
Protein sorting and secretion during CTL killing
Griffiths G. Protein sorting and secretion during CTL killing. Seminars In Immunology 1997, 9: 109-115. PMID: 9194221, DOI: 10.1006/smim.1997.0059.Peer-Reviewed Original Research
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