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 contentstRNA-m1A modification promotes T cell expansion via efficient MYC protein synthesis
Liu Y, Zhou J, Li X, Zhang X, Shi J, Wang X, Li H, Miao S, Chen H, He X, Dong L, Lee GR, Zheng J, Liu RJ, Su B, Ye Y, Flavell RA, Yi C, Wu Y, Li HB. tRNA-m1A modification promotes T cell expansion via efficient MYC protein synthesis. Nature Immunology 2022, 23: 1433-1444. PMID: 36138184, DOI: 10.1038/s41590-022-01301-3.Peer-Reviewed Original ResearchConceptsCell expansionKey functional proteinsVivo physiological roleDe novo protein productionCell cycle arrestTranslational controlRNA modificationsMyc proteinFunctional proteinsTranslation efficiencyKey proteinsCell homeostasisProtein productionPhysiological roleProtein synthesisProliferative stateCycle arrestConditional deletionT cell homeostasisNaive T cellsProteinQuiescent stateSpecific subsetT cellsCellsNaive T-Cell Depletion to Prevent Chronic Graft-Versus-Host Disease
Bleakley M, Sehgal A, Seropian S, Biernacki MA, Krakow EF, Dahlberg A, Persinger H, Hilzinger B, Martin PJ, Carpenter PA, Flowers ME, Voutsinas J, Gooley TA, Loeb K, Wood BL, Heimfeld S, Riddell SR, Shlomchik WD. Naive T-Cell Depletion to Prevent Chronic Graft-Versus-Host Disease. Journal Of Clinical Oncology 2022, 40: 1174-1185. PMID: 35007144, PMCID: PMC8987226, DOI: 10.1200/jco.21.01755.Peer-Reviewed Original ResearchConceptsChronic GVHDAcute GVHDHost diseaseNonrelapse mortalityT cellsPeripheral blood stem cell graftsBlood stem cell graftsGrade II acute GVHDGrade III acute GVHDNaive T-cell depletionAllogeneic hematopoietic cell transplantationPhase II clinical trialChronic Graft-VersusUnrelated donor graftsT-cell depletionHematopoietic cell transplantationTotal body irradiationMemory T cellsRelapse-free survivalStem cell graftsNaive T cellsApparent excess riskCell transplantation approachesGastrointestinal GVHDGraft-Versus
2021
Inherited human c-Rel deficiency disrupts myeloid and lymphoid immunity to multiple infectious agents
Lévy R, Langlais D, Béziat V, Rapaport F, Rao G, Lazarov T, Bourgey M, Zhou Y, Briand C, Moriya K, Ailal F, Avery D, Markle J, Lim A, Ogishi M, Yang R, Pelham S, Emam M, Migaud M, Deswarte C, Habib T, Saraiva L, Moussa E, Guennoun A, Boisson B, Belkaya S, Martinez-Barricarte R, Rosain J, Belkadi A, Breton S, Payne K, Benhsaien I, Plebani A, Lougaris V, Di Santo J, Neven B, Abel L, S. C, Bousfiha A, Marr N, Bustamante J, Liu K, Gros P, Geissmann F, Tangye S, Casanova J, Puel A. Inherited human c-Rel deficiency disrupts myeloid and lymphoid immunity to multiple infectious agents. Journal Of Clinical Investigation 2021, 131: e150143. PMID: 34623332, PMCID: PMC8409595, DOI: 10.1172/jci150143.Peer-Reviewed Original ResearchConceptsCD4+ T cellsMemory CD4+ T cellsC-Rel deficiencyT cellsMyeloid cellsLymphoid cellsB cellsC-RelMultiple infectious agentsNaive CD4+ T cellsCD8+ T cellsAntigen-presenting cell functionConventional DC1sFrequency of NKMemory B cellsNaive T cellsNaive B cellsFunctional deficitsReduced IL-2 productionProduction of Th1Infectious agentsIL-23 productionIL-2 productionInduction of CD86 expressionB cell survival
2020
Risk associated alterations in marrow T cells in pediatric leukemia
Bailur JK, McCachren SS, Pendleton K, Vasquez JC, Lim H, Duffy A, Doxie D, Kaushal A, Foster C, DeRyckere D, Castellino S, Kemp ML, Qiu P, Dhodapkar M, Dhodapkar K. Risk associated alterations in marrow T cells in pediatric leukemia. JCI Insight 2020, 5: e140179. PMID: 32692727, PMCID: PMC7455136, DOI: 10.1172/jci.insight.140179.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentBone MarrowCase-Control StudiesChildChild, PreschoolFemaleGene Expression ProfilingHumansInfantKiller Cells, NaturalLeukemia, Myeloid, AcuteMalePrecursor Cell Lymphoblastic Leukemia-LymphomaReproducibility of ResultsRisk FactorsSingle-Cell AnalysisT-LymphocytesTumor MicroenvironmentConceptsAcute lymphoblastic leukemiaNaive T cellsT cellsDisease riskChildhood leukemiaLymphoblastic leukemiaStem-like memory T cellsTerminal effector T cellsB-cell acute lymphoblastic leukemiaChronic immune activationCell acute lymphoblastic leukemiaEffector T cellsMarrow T cellsMemory T cellsAcute myelogenous leukemiaEvidence of dysfunctionStem-like genesImmune signaturesNK cellsClinical featuresImmune environmentImmune landscapeImmune therapyImmune activationImmune microenvironmentStimulation strength controls the rate of initiation but not the molecular organization of TCR-induced signalling
Y C, Marioni J, Griffiths G, Richard A. Stimulation strength controls the rate of initiation but not the molecular organization of TCR-induced signalling. ELife 2020, 9: e53948. PMID: 32412411, PMCID: PMC7308083, DOI: 10.7554/elife.53948.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD8-Positive T-LymphocytesCells, CulturedFemaleFlow CytometryInterferon Regulatory FactorsKineticsLigandsLymphocyte ActivationMaleMice, Inbred C57BLMice, TransgenicNuclear Receptor Subfamily 4, Group A, Member 1OvalbuminPeptide FragmentsPhosphorylationReceptors, Antigen, T-CellRibosomal Protein S6Signal TransductionSingle-Cell AnalysisConceptsT cellsMurine CD8<sup>+</sup> T cellsStrength of TCR stimulationCD8<sup>+</sup> T cellsDistal signaling eventsStimulation strengthTCR-induced signalsNaive T cellsMultiple signaling pathwaysT cell activationRibosomal protein S6Signaling eventsPeptide-MHC ligandsIntracellular machineryTCR stimulationProtein S6Signaling pathwayMass cytometrySignaling resultsStimulationMolecular organizationTranscriptionAlbumin fusion with granulocyte-macrophage colony-stimulating factor acts as an immunotherapy against chronic tuberculosis
Chuang YM, He L, Pinn ML, Tsai YC, Cheng MA, Farmer E, Karakousis PC, Hung CF. Albumin fusion with granulocyte-macrophage colony-stimulating factor acts as an immunotherapy against chronic tuberculosis. Cellular & Molecular Immunology 2020, 18: 2393-2401. PMID: 32382128, PMCID: PMC8484439, DOI: 10.1038/s41423-020-0439-2.Peer-Reviewed Original ResearchConceptsTuberculosis infectionChronic tuberculosis infectionPotent immune responsesGM-CSFLymph nodesDendritic cellsImmune responseChronic Mycobacterium tuberculosis infectionHigher IL-1β levelsAlbumin fusionLung bacillary burdenTB treatment regimensDendritic cell populationsDrug-resistant TBIL-1β levelsGM-CSF administrationMycobacterium tuberculosis infectionNaive T cellsIL-1β releaseBacillary burdenChronic tuberculosisNovel immunotherapiesTreatment regimensVaccination platformSubcutaneous administrationGinsenoside F2 attenuates chronic-binge ethanol-induced liver injury by increasing regulatory T cells and decreasing Th17 cells
Kim M, Kim H, Jeong J, Shim Y, Lee J, Kim Y, Ryu T, Yang K, Kim K, Jeon B, Kim S, Jung J, Choi J, Lee Y, Byun J, Jeong W. Ginsenoside F2 attenuates chronic-binge ethanol-induced liver injury by increasing regulatory T cells and decreasing Th17 cells. Journal Of Ginseng Research 2020, 44: 815-822. PMID: 33192125, PMCID: PMC7655498, DOI: 10.1016/j.jgr.2020.03.002.Peer-Reviewed Original ResearchAttenuates alcoholic liver injuryDifferentiation of naive T cellsAlcoholic liver injuryRegulatory T cellsNaive T cellsT cellsTh17 cellsLiver injuryFrequency of Foxp3<sup>+</sup> regulatory T cellsIL-10Foxp3<sup>+</sup> regulatory T cellsIL-17-producing TInduce alcoholic liver injuryIncreased regulatory T cellsIL-10 KO miceInfiltration of inflammatory macrophagesDecreased IL-17 expressionMRNA expressionIL-17 mRNA expressionAlcoholic liver inflammationInterleukin (IL)-10 knockoutMice compared to controlsDecreased Th17 cellsIncreased IL-10 expressionEthanol-induced liver injury
2019
Safety and pharmacodynamics of anti‐CD2 monoclonal antibody treatment in cynomolgus macaques – an experimental study
Berglund E, Alonso‐Guallart P, Danton M, Sellberg F, Binder C, Fröbom R, Berglund D, Llore N, Sakai H, Iuga A, Ekanayake‐Alper D, Reimann K, Sachs D, Sykes M, Griesemer A. Safety and pharmacodynamics of anti‐CD2 monoclonal antibody treatment in cynomolgus macaques – an experimental study. Transplant International 2019, 33: 98-107. PMID: 31523849, PMCID: PMC7017722, DOI: 10.1111/tri.13524.Peer-Reviewed Original ResearchConceptsAnti-CD2 treatmentT cellsStudy drug-related adverse eventsCynomolgus macaquesDrug-related adverse eventsEarly immune reconstitutionMemory T cellsLymph node examinationTreat transplant rejectionNaive T cellsMonoclonal antibody treatmentSecondary lymphoid organsMixed lymphocyte reactionAnti-CD2 monoclonal antibodiesImmune reconstitutionMLR inhibitionMemory subsetsNode examinationAntibody treatmentPeripheral bloodCD2 expressionLymphocyte reactionSafety profilePharmacodynamic profileTransplant rejectionAdaptive Immunity: Effector Functions, Regulation, and Vaccination
Kavathas P, Krause P, Ruddle N. Adaptive Immunity: Effector Functions, Regulation, and Vaccination. 2019, 75-95. DOI: 10.1007/978-3-030-25553-4_5.ChaptersAntigen-presenting cellsT cellsB cellsImmune responseInnate cellsEffector cellsInnate antigen-presenting cellsCD4 T helper cellsEffector T cellsB memory cellsT helper cellsSecondary lymphoid organsNaive T cellsBalanced immune responsePathogen-infected host cellsCD4 subsetCytokine milieuHelper cellsLymphoid organsEffector TPlasma cellsEffector functionsAdaptive immuneTypes of pathogensMacrophage responseInflammasomes and autoimmune and rheumatic diseases: A comprehensive review
Shin J, Lee K, Joo Y, Lee J, Jeon J, Jung H, Shin M, Cho S, Kim T, Park S, Jeon B, Jeong H, Lee K, Kang K, Oh M, Lee H, Lee S, Kwon Y, Oh G, Kronbichler A. Inflammasomes and autoimmune and rheumatic diseases: A comprehensive review. Journal Of Autoimmunity 2019, 103: 102299. PMID: 31326231, DOI: 10.1016/j.jaut.2019.06.010.Peer-Reviewed Original ResearchConceptsSystemic lupus erythematosusAutoimmune diseasesAnti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitisPolarization of naive T cellsAntibody (ANCA)-associated vasculitisRheumatoid arthritisNaive T cellsDevelopment of tailored therapiesInterleukin (IL)-1bDiagnosis of autoimmune diseasesInnate immune systemIgA vasculitisBehcet's diseaseSjogren's syndromeT cellsLupus erythematosusTailored therapyInflammatory cascadeAdaptive immunityIL-18Rheumatic diseasesImmune systemInflammasome activationVasculitisInflammasome
2018
T cell cytolytic capacity is independent of initial stimulation strength
Richard A, Lun A, Lau W, Göttgens B, Marioni J, Griffiths G. T cell cytolytic capacity is independent of initial stimulation strength. Nature Immunology 2018, 19: 849-858. PMID: 30013148, PMCID: PMC6300116, DOI: 10.1038/s41590-018-0160-9.Peer-Reviewed Original ResearchConceptsGenome-wide RNASignaling machineryIntercellular variabilityTranscriptional pathwaysEnvironmental fluctuationsMyriad stimuliLigand potencyCD8+ T cells in vitroActivation pathwaySingle cellsT cells in vitroNaive T cellsMachineryActive cellsCellsStimulation strengthPathwayCytolytic capacityT cellsRNAActivityProteinPhenotype
2016
Bridging channel dendritic cells induce immunity to transfused red blood cells
Calabro S, Gallman A, Gowthaman U, Liu D, Chen P, Liu J, Krishnaswamy JK, Nascimento MS, Xu L, Patel SR, Williams A, Tormey CA, Hod EA, Spitalnik SL, Zimring JC, Hendrickson JE, Stowell SR, Eisenbarth SC. Bridging channel dendritic cells induce immunity to transfused red blood cells. Journal Of Experimental Medicine 2016, 213: 887-896. PMID: 27185856, PMCID: PMC4886363, DOI: 10.1084/jem.20151720.Peer-Reviewed Original ResearchConceptsSplenic dendritic cellsDendritic cellsRBC transfusionT cellsImmune responseRed blood cell transfusionBlood cell transfusionT cell primingConventional dendritic cellsDetrimental immune responsesB cell responsesNaive T cellsT cell helpMurine transfusion modelRBC transfusion supportTime of transfusionRBC alloantigensCell transfusionDC subsetsAllogeneic RBCsRed blood cellsRenal failureTransfusion supportMajor complicationsCell priming
2015
Outcomes of acute leukemia patients transplanted with naive T cell–depleted stem cell grafts
Bleakley M, Heimfeld S, Loeb KR, Jones LA, Chaney C, Seropian S, Gooley TA, Sommermeyer F, Riddell SR, Shlomchik WD. Outcomes of acute leukemia patients transplanted with naive T cell–depleted stem cell grafts. Journal Of Clinical Investigation 2015, 125: 2677-2689. PMID: 26053664, PMCID: PMC4563691, DOI: 10.1172/jci81229.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAdolescentAdrenal Cortex HormonesAdultAnimalsChronic DiseaseDisease-Free SurvivalFemaleGraft vs Host DiseaseHematopoietic Stem Cell TransplantationHistocompatibility TestingHumansKaplan-Meier EstimateLeukemiaLymphocyte DepletionMaleMiceMiddle AgedMyelodysplastic SyndromesT-Lymphocyte SubsetsTissue DonorsTransplantation ConditioningTransplantation, HomologousYoung AdultConceptsHematopoietic stem cell transplantationStem cell graftsChronic GVHDT cellsCell graftsT-cell-depleted stem cell graftsPeripheral blood stem cell graftsAllogeneic hematopoietic stem cell transplantationBlood stem cell graftsFunctional T-cell memoryT-cell-replete graftsPathogen-specific T cellsSingle-arm clinical trialT-cell recoveryVirus-specific immunityStem cell allograftsTotal body irradiationMemory T cellsStem cell transplantationT cell memoryAcute leukemia patientsHigh-risk leukemiaNaive T cellsAcute GVHDSevere GVHDChitinase like protein BRP-39 suppress Th1 differentiation via regulation of IFNγ-STAT1 axis (LYM8P.633)
Kim D, Park H, Lee J, Kang M, Lee C, Elias J, Choi J. Chitinase like protein BRP-39 suppress Th1 differentiation via regulation of IFNγ-STAT1 axis (LYM8P.633). The Journal Of Immunology 2015, 194: 201.9-201.9. DOI: 10.4049/jimmunol.194.supp.201.9.Peer-Reviewed Original ResearchT cell immunityBRP-39Th1 cellsT cellsTCR stimuliUp-regulate T-betExpression of PTPN2Naive CD4 T cellsIncreased production of IL-2Production of IL-2CD4 T cellsNaive T cellsT cell activationEnzyme sitesChitinase activityParasite life cycleAnti-parasite immune responsesSignaling pathwayRegulatory roleChitinaseTh2 cellsInnate immunityT-betTh1 differentiationIFN-gT Cell–Extrinsic CD18 Attenuates Antigen-Dependent CD4+ T Cell Activation In Vivo
Wu X, Lahiri A, Sarin R, Abraham C. T Cell–Extrinsic CD18 Attenuates Antigen-Dependent CD4+ T Cell Activation In Vivo. The Journal Of Immunology 2015, 194: 4122-4129. PMID: 25801431, PMCID: PMC4404034, DOI: 10.4049/jimmunol.1401328.Peer-Reviewed Original ResearchConceptsT cell activationCell proliferationAg-dependent T cell activationCell activationCell-extrinsic roleHematopoietic cellsEssential roleT cell proliferationCritical roleAdhesion moleculesΒ2 integrinsProliferationT cellsCellsActivationVivoActivation profilesAPCNaive T cellsSecondary lymphoid organsLeukocyte adhesion moleculesTraffickingRoleIntegrinsCD11b blockadeMHC Class II Presentation Is Controlled by the Lysosomal Small GTPase, Arl8b
Michelet X, Garg S, Wolf B, Tuli A, Ricciardi-Castagnoli P, Brenner M. MHC Class II Presentation Is Controlled by the Lysosomal Small GTPase, Arl8b. The Journal Of Immunology 2015, 194: 2079-2088. PMID: 25637027, DOI: 10.4049/jimmunol.1401072.Peer-Reviewed Original ResearchMeSH KeywordsADP-Ribosylation FactorsAnimalsAntigen PresentationAntigensBone Marrow CellsCD4-Positive T-LymphocytesCell LineChickensDendritic CellsEndosomesGene Expression RegulationHistocompatibility Antigens Class IILysosomesMiceMice, Inbred C57BLOvalbuminPrimary Cell CultureProtein TransportRNA, Small InterferingSignal TransductionSpleenConceptsDendritic cellsMHC-II presentationMHC II-peptide complexesII presentationII-peptide complexesT cellsCell surfaceCD4(+) T cellsPrime naive T cellsAg-presenting moleculesMHC class II presentationNaive T cellsMHC class IIT cell recognitionMHC II compartmentsGTPase Rab5Small GTPasesClass II presentationMHC II moleculesEndocytic vesiclesComplex formationArl8bAg deliveryRegulate formationExogenous Ag
2014
An age-related decline of CD62L and vaccine response
Shin J, Bayry J. An age-related decline of CD62L and vaccine response. Human Vaccines & Immunotherapeutics 2014, 10: 1404-1405. PMID: 24401614, PMCID: PMC4896605, DOI: 10.4161/hv.27665.Peer-Reviewed Original Research
2013
PD-L1 and PD-L2 Protect The Heart In a T-Cell Receptor Transgenic Model Of Graft-Versus Host Disease
Juchem K, Anderson B, Zhang C, Sharpe A, McNiff J, Demetris A, Shlomchik M, Shlomchik W. PD-L1 and PD-L2 Protect The Heart In a T-Cell Receptor Transgenic Model Of Graft-Versus Host Disease. Blood 2013, 122: 4479. DOI: 10.1182/blood.v122.21.4479.4479.Peer-Reviewed Original ResearchDonor bone marrowPD-L1PD-L1/2T cellsBone marrowLate weight lossWeight lossHost diseasePD-1Graft Versus Host DiseaseInhibitory molecules PD-1Effector memory T cellsT cell receptor transgenic modelAllogeneic stem cell transplantationT-cell-mediated pathogenesisMore chronic phasesPD-L1/2 expressionRadioresistant stromal cellsDays post transplantHost T cellsCD4 T cellsMemory T cellsStem cell transplantationNaive T cellsEarly weight lossThe CD226/CD155 Interaction Regulates the Proinflammatory (Th1/Th17)/Anti-Inflammatory (Th2) Balance in Humans
Lozano E, Joller N, Cao Y, Kuchroo VK, Hafler DA. The CD226/CD155 Interaction Regulates the Proinflammatory (Th1/Th17)/Anti-Inflammatory (Th2) Balance in Humans. The Journal Of Immunology 2013, 191: 3673-3680. PMID: 23980210, PMCID: PMC3819731, DOI: 10.4049/jimmunol.1300945.Peer-Reviewed Original ResearchConceptsNaive T cellsT cellsInflammatory balanceIL-13IL-17-producing cellsRole of CD226IL-17 productionIL-17 secretionHuman autoimmune diseasesIFN-γ productionIL-13 secretionIFN-γ expressionProduction of IFNSTAT-6 phosphorylationT cell activationHuman T cellsLigand CD155Th17 cellsIL-17Autoimmune diseasesIL-4T-betTh1 differentiationTh17 conditionsTherapeutic approaches
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