2025
Decreased T helper 1 cell function underlies recurrent sinopulmonary infections in the 17q12 deletion syndrome
Shin J, Shin H, Gutierrez A, Yoo N, Par-Young J, Osmani L, Shin M, Sanchez-Lara P, Bucala R, Soffer G, Kang I. Decreased T helper 1 cell function underlies recurrent sinopulmonary infections in the 17q12 deletion syndrome. EBioMedicine 2025, 112: 105578. PMID: 39891996, PMCID: PMC11840234, DOI: 10.1016/j.ebiom.2025.105578.Peer-Reviewed Original ResearchConceptsCD4<sup>+</sup> T cellsRecurrent sinopulmonary infectionsT cell functionRNA-seq analysisT cellsHealthy controlsSinopulmonary infectionsRNA-seqT-betIFN-gFrequency of CD4<sup>+</sup> T cellsCD4<sup>+</sup> T cell functionTh1 transcription factor T-betDeletion syndromeFlow cytometryCompared to age-matched healthy controlsTranscription factor T-betDecreased T-betUrinary tract abnormalitiesAge-matched healthy controlsMultiplex assayDownstream effector cytokinesEffector cytokinesRecurrent infectionsTh17 cytokines
2024
JAK Inhibitors as Immunomodulators
Peterson D, Damsky W, King B. JAK Inhibitors as Immunomodulators. 2024, 57-71. DOI: 10.1007/978-3-031-66590-5_5.Peer-Reviewed Original Research
2023
Regulatory T cells in peripheral tissue tolerance and diseases
Cheru N, Hafler D, Sumida T. Regulatory T cells in peripheral tissue tolerance and diseases. Frontiers In Immunology 2023, 14: 1154575. PMID: 37197653, PMCID: PMC10183596, DOI: 10.3389/fimmu.2023.1154575.Peer-Reviewed Original ResearchConceptsTissue-resident TregsRegulatory T cellsT cellsResident TregsTissue TregsAutoimmune diseasesCommon human autoimmune diseasesAutoreactive T cellsHuman autoimmune diseasesNon-immune cellsNon-lymphoid tissuesTissue-resident cellsTreg poolTreg studiesEffector cytokinesPeripheral toleranceTreg functionIPEX syndromeImmune homeostasisSpecific tissue environmentsTregsSuppressive functionLoss of functionResident cellsGene signatureTargeting TBK1 to overcome resistance to cancer immunotherapy
Sun Y, Revach O, Anderson S, Kessler E, Wolfe C, Jenney A, Mills C, Robitschek E, Davis T, Kim S, Fu A, Ma X, Gwee J, Tiwari P, Du P, Sindurakar P, Tian J, Mehta A, Schneider A, Yizhak K, Sade-Feldman M, LaSalle T, Sharova T, Xie H, Liu S, Michaud W, Saad-Beretta R, Yates K, Iracheta-Vellve A, Spetz J, Qin X, Sarosiek K, Zhang G, Kim J, Su M, Cicerchia A, Rasmussen M, Klempner S, Juric D, Pai S, Miller D, Giobbie-Hurder A, Chen J, Pelka K, Frederick D, Stinson S, Ivanova E, Aref A, Paweletz C, Barbie D, Sen D, Fisher D, Corcoran R, Hacohen N, Sorger P, Flaherty K, Boland G, Manguso R, Jenkins R. Targeting TBK1 to overcome resistance to cancer immunotherapy. Nature 2023, 615: 158-167. PMID: 36634707, PMCID: PMC10171827, DOI: 10.1038/s41586-023-05704-6.Peer-Reviewed Original ResearchConceptsOvercome resistance to cancer immunotherapyResistance to cancer immunotherapyPD-1 blockadeCancer immunotherapyImmune-evasion genesResponse to PD-1 blockadePatient-derived tumor modelsPatient-derived organoidsEffective treatment strategiesTBK1 inhibitionPD-1Effector cytokinesConcordant findingsTumor cellsTumor modelCaspase-dependent cell deathResponse to TNFTreatment strategiesTargeting TBK1ImmunotherapyPharmacological toolsBlockadeTumor spheroidsCell deathTBK1
2022
The AIM2 inflammasome is activated in astrocytes during the late phase of EAE
Barclay WE, Aggarwal N, Deerhake ME, Inoue M, Nonaka T, Nozaki K, Luzum NA, Miao EA, Shinohara ML. The AIM2 inflammasome is activated in astrocytes during the late phase of EAE. JCI Insight 2022, 7: e155563. PMID: 35451371, PMCID: PMC9089781, DOI: 10.1172/jci.insight.155563.Peer-Reviewed Original ResearchConceptsExperimental autoimmune encephalomyelitisCentral nervous systemInflammasome activationInflammasome-mediated inflammationRole of inflammasomesApoptosis-associated speck-like proteinIL-1β releaseAIM2 inflammasome activationSpeck-like proteinAutoimmune encephalomyelitisEffector cytokinesAutoimmune conditionsIL-18Multiple sclerosisIL-1βDisease peakInflammatory responseSpinal cordMelanoma 2Mouse modelAnimal modelsReporter miceNervous systemMyeloid cellsAIM2 inflammasome
2014
Engineering Human Peripheral Blood Stem Cell Grafts that Are Depleted of Naïve T Cells and Retain Functional Pathogen-Specific Memory T Cells
Bleakley M, Heimfeld S, Jones LA, Turtle C, Krause D, Riddell SR, Shlomchik W. Engineering Human Peripheral Blood Stem Cell Grafts that Are Depleted of Naïve T Cells and Retain Functional Pathogen-Specific Memory T Cells. Transplantation And Cellular Therapy 2014, 20: 705-716. PMID: 24525279, PMCID: PMC3985542, DOI: 10.1016/j.bbmt.2014.01.032.Peer-Reviewed Original ResearchConceptsPeripheral blood stem cellsHematopoietic cell transplantationMemory T cellsStem cell graftsT cellsCell graftsPathogen-specific memory T cellsPeripheral blood stem cell graftsAllogeneic stem cell graftsBlood stem cell graftsNaïve T cell subsetsAllogeneic hematopoietic cell transplantationFrequent major complicationCentral memory phenotypeT cell subsetsBlood stem cellsNaïve T cellsOpportunistic pathogenCommon opportunistic pathogenStem cellsHost diseaseHCT outcomesEffector cytokinesMajor complicationsMemory phenotype
2013
Rapamycin-treated human endothelial cells preferentially activate allogeneic regulatory T cells
Wang C, Yi T, Qin L, Maldonado RA, von Andrian UH, Kulkarni S, Tellides G, Pober JS. Rapamycin-treated human endothelial cells preferentially activate allogeneic regulatory T cells. Journal Of Clinical Investigation 2013, 123: 1677-1693. PMID: 23478407, PMCID: PMC3613923, DOI: 10.1172/jci66204.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsArteriesB7-H1 AntigenCD4-Positive T-LymphocytesCell ProliferationCells, CulturedCoculture TechniquesFemaleGene ExpressionGene Knockdown TechniquesHuman Umbilical Vein Endothelial CellsHumansImmunosuppression TherapyInterleukin-6Lymphocyte ActivationMiceMice, SCIDProgrammed Cell Death 1 Ligand 2 ProteinRegulatory-Associated Protein of mTORRNA, Small InterferingSirolimusT-Lymphocytes, RegulatoryTOR Serine-Threonine KinasesTranscriptional ActivationTransplantation, HomologousConceptsEffect of rapamycinT cellsEndothelial cellsAllograft rejectionHuman endothelial cellsPD-L1PD-L2Allogeneic regulatory T cellsHuman-mouse chimeric modelInhibitory molecule PD-L1Inflammatory cytokines IL-6Alloantigen-specific mannerAllograft endothelial cellsHuman arterial allograftsImmune-mediated rejectionGraft endothelial cellsEffector T cellsRegulatory T cellsMemory T cellsT cell responsesAntigen-presenting cellsCytokines IL-6Mock-treated cellsAllogeneic CD4Effector cytokines
2012
IL-13 receptor α2-arginase 2 pathway mediates IL-13-induced pulmonary hypertension
Cho WK, Lee CM, Kang MJ, Huang Y, Giordano FJ, Lee PJ, Trow TK, Homer RJ, Sessa WC, Elias JA, Lee CG. IL-13 receptor α2-arginase 2 pathway mediates IL-13-induced pulmonary hypertension. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2012, 304: l112-l124. PMID: 23125252, PMCID: PMC3543640, DOI: 10.1152/ajplung.00101.2012.Peer-Reviewed Original ResearchConceptsPulmonary hypertensionIL-13Human pulmonary artery smooth muscle cellsDevelopment of PHPulmonary artery smooth muscle cellsRight ventricle systolic pressurePathogenesis of PHArtery smooth muscle cellsExpression of ARG2Pulmonary arterial hypertensionPulmonary vascular remodelingVentricle systolic pressurePotential therapeutic targetIL-13 treatmentSmooth muscle cellsNull mutant miceArterial hypertensionEffector cytokinesMedial thickeningSystolic pressureHemodynamic changesPulmonary arterySmall-interfering RNAVascular remodelingArginase-2
2010
Human IL-7Rαlow memory CD8+ T cells have defect in the calcium signaling pathway in response to TCR triggering, leading to impaired IL-2 production and proliferation. (132.34)
Lee H, Yu M, Lee D, Kang J, Hwang Y, Lee W, Kang I, Kim H. Human IL-7Rαlow memory CD8+ T cells have defect in the calcium signaling pathway in response to TCR triggering, leading to impaired IL-2 production and proliferation. (132.34). The Journal Of Immunology 2010, 184: 132.34-132.34. DOI: 10.4049/jimmunol.184.supp.132.34.Peer-Reviewed Original ResearchIL-2 productionMemory CD8T cellsCytokine productionIL-7Effector cytokine productionT cell subsetsAnergic T cellsPMA/ionomycin treatmentAnti-CD3 AbTCR triggeringEffector cytokinesAnergic phenotypeCell subsetsHuman CD8IL-2CD8Calcium fluxTCR stimulationIonomycin treatmentCell survival responseMAPK pathwayCellular characteristicsProliferationCells
2008
The Role of ICOS in Peripheral Inflammation in Lupus
Eardley L, Odegard J, Craft J. The Role of ICOS in Peripheral Inflammation in Lupus. The FASEB Journal 2008, 22: 668.18-668.18. DOI: 10.1096/fasebj.22.1_supplement.668.18.Peer-Reviewed Original ResearchCostimulatory molecule ICOST cellsPeripheral inflammationDendritic cellsChemokine receptorsMRL/Faslpr miceExpression of CCR6Role of ICOSChemokine receptor expressionMajority of CD4Role of CD4Lupus-prone miceSevere renal diseaseFaslpr miceIndependent cytokinesLupus nephritisEffector cytokinesIL-10Lupus miceRenal diseaseCellular infiltrateChemokine productionSuch inflammationIL-5Certain chemokines
2007
Dual Roles of IL-15 in Maintaining IL-7RαlowCCR7− Memory CD8+ T Cells in Humans via Recovering the Phosphatidylinositol 3-Kinase/AKT Pathway
Kim HR, Hwang KA, Kang I. Dual Roles of IL-15 in Maintaining IL-7RαlowCCR7− Memory CD8+ T Cells in Humans via Recovering the Phosphatidylinositol 3-Kinase/AKT Pathway. The Journal Of Immunology 2007, 179: 6734-6740. PMID: 17982063, DOI: 10.4049/jimmunol.179.10.6734.Peer-Reviewed Original ResearchMeSH KeywordsCD8-Positive T-LymphocytesCell ProliferationCell SurvivalEnzyme ActivationGene Expression RegulationHumansImmunologic MemoryInfectionsInterleukin-15Interleukin-2 Receptor beta SubunitInterleukin-7NeoplasmsPerforinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Antigen, T-CellReceptors, CCR7Receptors, Interleukin-17Signal TransductionConceptsIL-15T cellsPI3K/Akt pathwayAkt pathwayIL-7Memory T cell survivalProliferation of ILIL-15 signalingHuman peripheral bloodT cell survivalEffector cytokinesMemory CD8Peripheral bloodEffector functionsIL-7REnhanced gene expressionProliferative functionIndependent mechanismsILTCR triggeringCell survivalSuch cellsSurvivalTranscriptional factorsDual roleCCR2 identifies first responders among human CD4+ memory T cells: long-lived, apoptosis-resistant, antigen-responsive cells with enhanced migration potential, a low threshold for activation, and immediate effector capabilities (85.5)
Farber J, Song K, Zhang H, Rabin R, Hill B, Sereti I, Prussin C, Siegel R, Douek D, Roederer M. CCR2 identifies first responders among human CD4+ memory T cells: long-lived, apoptosis-resistant, antigen-responsive cells with enhanced migration potential, a low threshold for activation, and immediate effector capabilities (85.5). The Journal Of Immunology 2007, 178: s119-s119. DOI: 10.4049/jimmunol.178.supp.85.5.Peer-Reviewed Original ResearchMemory T cellsT cellsEffector capabilitiesExpression of chemokine receptors CCR5Memory CD4+ T cellsCD4+ memory T cellsCD4+ T cellsLong-lived memory cellsHuman memory CD4+ T cellsCCR2+ cellsCD4+ subsetHuman CD4+ memory T cellsChemokine receptor CCR5Antigen-responsive cellsChemokine receptor typeResistance to apoptosisSecrete high levelsCells co-expressingSusceptibility to apoptosisReduced proliferative potentialEffector cytokinesExcision circlesEnhanced migration potentialReceptor CCR5Peripheral blood
2005
Endothelial Cells Promote Human Immunodeficiency Virus Replication in Nondividing Memory T Cells via Nef-, Vpr-, and T-Cell Receptor-Dependent Activation of NFAT
Choi J, Walker J, Talbert-Slagle K, Wright P, Pober JS, Alexander L. Endothelial Cells Promote Human Immunodeficiency Virus Replication in Nondividing Memory T Cells via Nef-, Vpr-, and T-Cell Receptor-Dependent Activation of NFAT. Journal Of Virology 2005, 79: 11194-11204. PMID: 16103171, PMCID: PMC1193601, DOI: 10.1128/jvi.79.17.11194-11204.2005.Peer-Reviewed Original ResearchConceptsMemory T cellsHuman immunodeficiency virus (HIV) replicationImmunodeficiency virus replicationT cellsViral replicationEndothelial cellsAntiretroviral therapyHIV replicationSuboptimal T cell receptor (TCR) stimulationHIV Type 1 ReplicationVirus replicationMajor histocompatibility complex (MHC) class II moleculesType 1 replicationTumor necrosis factorMHC class IIClass II moleculesT cell receptor stimulationVirus-producing cellsReceptor-dependent activationNef-dependent mannerEffector cytokinesHuman endothelial cellsHLA-DRIL-6Presence of EC
2004
Asthma: Mechanisms of Disease Persistence and Progression
Cohn L, Elias JA, Chupp GL. Asthma: Mechanisms of Disease Persistence and Progression. Annual Review Of Immunology 2004, 22: 789-815. PMID: 15032597, DOI: 10.1146/annurev.immunol.22.012703.104716.BooksConceptsIL-13Key effector cytokineAnti-inflammatory therapyIL-13 productionProduction of chemokinesProgression of diseaseAirway fibrosisAllergic asthmaAirway remodelingEffector cytokinesEosinophilic inflammationPersistent diseaseTh2 cytokinesEpithelial damageDisease progressionInflammatory responseTh2 cellsMucus productionSmooth muscleBronchial airwaysMatrix metalloproteinasesAnimal dataAsthmaDisease persistenceInflammation
1998
Endotoxin downregulates rat hepatic ntcp gene expression via decreased activity of critical transcription factors.
Trauner M, Arrese M, Lee H, Boyer J, Karpen S. Endotoxin downregulates rat hepatic ntcp gene expression via decreased activity of critical transcription factors. Journal Of Clinical Investigation 1998, 101: 2092-2100. PMID: 9593765, PMCID: PMC508797, DOI: 10.1172/jci1680.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBile Acids and SaltsCarrier ProteinsCells, CulturedCholestasisDNA-Binding ProteinsDown-RegulationEndotoxinsGene Expression RegulationHepatocyte Nuclear Factor 1Hepatocyte Nuclear Factor 1-alphaHepatocyte Nuclear Factor 1-betaLiverMaleMembrane Transport ProteinsNuclear ProteinsOrganic Anion Transporters, Sodium-DependentPromoter Regions, GeneticRatsRats, Sprague-DawleyRNA, MessengerSepsisSymportersTranscription FactorsConceptsNuclear binding activityNtcp mRNA levelsMRNA levelsHepatobiliary transportersMRNA expressionCritical transcription factorTime pointsSepsis-associated cholestasisNuclear factor-kappaBSodium-dependent uptakeEffector cytokinesSequential time pointsEndotoxin administrationPretreatment levelsBinding activityMaximal decreaseBile acidsFactor-kappaBHepatocyte nuclear factor 1Normal levelsHepatic basolateral membraneNuclear factorMarked reductionCoordinated downregulationEndotoxin
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply