2025
Transcriptional signatures of endothelial cells shape immune responses in cardiopulmonary health and disease
Fließer E, Jandl K, Chen S, Wang M, Schupp J, Kuebler W, Baker A, Kwapiszewska G. Transcriptional signatures of endothelial cells shape immune responses in cardiopulmonary health and disease. JCI Insight 2025, 10: e191059. PMID: 40401523, PMCID: PMC12128986, DOI: 10.1172/jci.insight.191059.Peer-Reviewed Original ResearchConceptsEndothelial cellsCardiopulmonary vasculatureImmune responseImmune cell recruitmentRegulation of immune responsesFunction of endothelial cellsImmunoregulatory roleAntigen presentationCytokine secretionCell recruitmentCardiopulmonary healthDelivery of oxygenSingle-cell RNA sequencingImmunomodulatory propertiesCardiopulmonary diseaseClearance functionDisease pathogenesisTherapy targetTranscriptional signatureEC subpopulationsImmunomodulatory activityDiseaseLungVasculatureHeartActivation of macrophages by extracellular vesicles derived from Babesia-infected red blood cells
Hagos B, Brasov I, Branscome H, Rashid S, Bradford R, Leonelli J, Kashanchi F, Mamoun C, Molestina R. Activation of macrophages by extracellular vesicles derived from Babesia-infected red blood cells. Infection And Immunity 2025, 93: e00333-24. PMID: 40172538, PMCID: PMC12070731, DOI: 10.1128/iai.00333-24.Peer-Reviewed Original ResearchConceptsInfected red blood cellsPrimary cause of human babesiosisRed blood cellsExtracellular vesiclesActivated macrophagesResponse to <i>B.Host-pathogen interactionsModulation of pro-inflammatory cytokinesBlood cellsElimination of parasitesPro-inflammatory cytokinesActivation of NF-kBActivation of macrophagesRelease of extracellular vesiclesInnate immune responseIncubation of macrophagesUninfected RBCsCo-culture experimentsHuman babesiosisProtozoan parasitesCytokine secretionImmune responseMacrophage activationBabesiosisEV fractions
2024
New applications of clioquinol in the treatment of inflammation disease by directly targeting arginine 335 of NLRP3
Chen P, Wang Y, Tang H, Zhou C, Liu Z, Gao S, Wang T, Xu Y, Ji S. New applications of clioquinol in the treatment of inflammation disease by directly targeting arginine 335 of NLRP3. Journal Of Pharmaceutical Analysis 2024, 15: 101069. PMID: 39902456, PMCID: PMC11788862, DOI: 10.1016/j.jpha.2024.101069.Peer-Reviewed Original ResearchNOD-like receptor protein 3Innate immune-mediated inflammationExperimental acute peritonitisInhibition of nod-like receptor protein 3Treatment of inflammation diseasesTumor necrosis factor-aImmune-mediated inflammationLowered serum levelsNOD-like receptor protein 3 inflammasomeReduced cytokine secretionNLRP3 inflammasome assemblyTarget arginineNACHT domainComponent proteinsReceptor protein 3Inflammasome assemblyAcute peritonitisSerum levelsCytokine secretionTreatment strategiesInterleukin-1bTNF-aInhibitory concentrationIL-1BInhibiting NLRP3 activationCaspase-4/11 promotes hyperlipidemia and chronic kidney disease-accelerated vascular inflammation by enhancing trained immunity
Sun Y, Lu Y, Liu L, Saaoud F, Shao Y, Xu K, Drummer C, Cueto R, Shan H, Jiang X, Zhao H, Wang H, Yang X. Caspase-4/11 promotes hyperlipidemia and chronic kidney disease-accelerated vascular inflammation by enhancing trained immunity. JCI Insight 2024, 9: e177229. PMID: 39024553, PMCID: PMC11343595, DOI: 10.1172/jci.insight.177229.Peer-Reviewed Original ResearchChronic kidney diseaseTrained immunityAortic endothelial cellsVascular inflammationEndothelial cellsRecruitment of macrophagesIL-1b levelsHuman aortic endothelial cellsHigh-fat dietMembrane expressionN-terminal gasdermin DCytokine secretionPathological analysisIL-1BKidney diseaseNeointima hyperplasiaCaspase-4/11HyperlipidemiaInflammationCytosolic lipopolysaccharideCaspase-11RNA sequencingGasdermin DImmunityLipopolysaccharideTLR5-deficiency controls dendritic cell subset development in an autoimmune diabetes-susceptible model
Pearson J, Hu Y, Peng J, Wong F, Wen L. TLR5-deficiency controls dendritic cell subset development in an autoimmune diabetes-susceptible model. Frontiers In Immunology 2024, 15: 1333967. PMID: 38482010, PMCID: PMC10935730, DOI: 10.3389/fimmu.2024.1333967.Peer-Reviewed Original ResearchConceptsToll-like receptor 5Antigen-presenting cellsDendritic cellsType 1 diabetesTLR5-deficientDC developmentCytokine secretionCD4<sup>+</sup> T cell proliferationPathogenesis of type 1 diabetesT cell responsesEnhanced cytokine secretionT cell proliferationWild-type miceSusceptibility to obesitySusceptibility to T1DProinflammatory cytokine secretionGut microbiotaSpontaneous T1DNOD miceAutoimmune diabetesNon-obeseHuman T1DReceptor 5Autoimmune diseasesHyper-secretion
2023
Core Needle Biopsies as an Alternative Source for Ex Vivo Expanded TIL for Adoptive Cell Therapy in Triple-Negative Breast Cancer
Coman M, Pusztai L, Hooley R, Andreveja L, Kim L, Joshi N, Bersenev A, Krause D, Park T. Core Needle Biopsies as an Alternative Source for Ex Vivo Expanded TIL for Adoptive Cell Therapy in Triple-Negative Breast Cancer. Journal Of Immunotherapy 2023, 47: 49-53. PMID: 37991241, DOI: 10.1097/cji.0000000000000495.Peer-Reviewed Original ResearchTumor-infiltrating lymphocytesCore needle biopsyTriple-negative breast cancerNeedle biopsyBreast cancerEx vivoT-cell receptor clonalityUltrasound-guided core needle biopsyTriple negative breast cancer tumorsMorbidity of surgeryAdoptive cell therapyBreast cancer tumorsTIL generationAdoptive transferTIL culturesMultiple lesionsCytokine secretionMetastatic cancerSame patientTumor tissueCell therapyPatientsCancer tumorsCancerSurgeryCellular allostatic load is linked to increased energy expenditure and accelerated biological aging
Bobba-Alves N, Sturm G, Lin J, Ware S, Karan K, Monzel A, Bris C, Procaccio V, Lenaers G, Higgins-Chen A, Levine M, Horvath S, Santhanam B, Kaufman B, Hirano M, Epel E, Picard M. Cellular allostatic load is linked to increased energy expenditure and accelerated biological aging. Psychoneuroendocrinology 2023, 155: 106322. PMID: 37423094, PMCID: PMC10528419, DOI: 10.1016/j.psyneuen.2023.106322.Peer-Reviewed Original ResearchConceptsCellular agingCellular energy expenditureDNA methylation clockMitochondrial oxidative phosphorylationStress adaptationMtDNA instabilityOXPHOS activityMethylation clockOxidative phosphorylationMetabolic shiftEnergetic costHuman fibroblast lineCellular basisPhysiological responsesFibroblast linesStress triggersPotential driversBiological agingEnergy expenditureChronic activationLifespanDamaging effectsPrimary human fibroblast linesCytokine secretionPhosphorylation
2021
Malignant T Cell Activation by a Bacillus Species Isolated from Cutaneous T-Cell Lymphoma Lesions
Dehner CA, Ruff WE, Greiling T, Pereira MS, Redanz S, McNiff J, Girardi M, Kriegel MA. Malignant T Cell Activation by a Bacillus Species Isolated from Cutaneous T-Cell Lymphoma Lesions. JID Innovations 2021, 2: 100084. PMID: 35199089, PMCID: PMC8844718, DOI: 10.1016/j.xjidi.2021.100084.Peer-Reviewed Original ResearchCutaneous T-cell lymphomaT cell activationSkin microbiotaAppropriate genetic backgroundCell activationBacillus speciesCutaneous T-cell lymphoma lesionsUnique microbiotaHuman commensalGenetic backgroundCell explantsClonal T-cell proliferationSkin-homing CD4T-cell lymphomaAdaptive immune responsesCell interactionsT cell proliferationT cell interactionsEnvironmental factorsMicrobial triggersMicrobiotaCommensalCTCL lesionsLymphoma lesionsCytokine secretionImmunomodulatory functions of TRPM7 and its implications in autoimmune diseases
Liang H, Chen Y, Wei X, Ma G, Ding J, Lu C, Zhou R, Hu W. Immunomodulatory functions of TRPM7 and its implications in autoimmune diseases. Immunology 2021, 165: 3-21. PMID: 34558663, DOI: 10.1111/imm.13420.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutoimmune DiseasesAutoimmunityBiomarkersDisease SusceptibilityDrug DevelopmentGene Expression RegulationHumansImmune SystemImmunomodulationIon Channel GatingOrgan SpecificityProtein Kinase InhibitorsProtein Serine-Threonine KinasesSignal TransductionStructure-Activity RelationshipTRPM Cation ChannelsConceptsAutoimmune diseasesRole of TRPM7New treatment targetsPotential therapeutic targetReceptor ion channelsImmune toleranceRheumatoid arthritisMultiple sclerosisSystemic disordersBody of evidenceImmune cellsCytokine secretionImmunoreactive substancesFunctional damageImmunomodulatory functionsTherapeutic targetTreatment targetsDiseaseEffective interventionsPharmacological propertiesOne-tissueTRPM7Physiologic conditionsInappropriate responsesCell migrationUbiquitination of ATF6 by disease-associated RNF186 promotes the innate receptor-induced unfolded protein response
Ranjan K, Hedl M, Sinha S, Zhang X, Abraham C. Ubiquitination of ATF6 by disease-associated RNF186 promotes the innate receptor-induced unfolded protein response. Journal Of Clinical Investigation 2021, 131: e145472. PMID: 34623328, PMCID: PMC8409591, DOI: 10.1172/jci145472.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 6AnimalsEndoplasmic Reticulum StressGenetic VariationHost Microbial InteractionsHumansImmunity, InnateInflammatory Bowel DiseasesMacrophagesMiceMice, Inbred C57BLMice, KnockoutNod2 Signaling Adaptor ProteinReceptors, Pattern RecognitionRisk FactorsSignal TransductionUbiquitin-Protein LigasesUbiquitinationUnfolded Protein ResponseConceptsPattern recognition receptorsUnfolded protein responseInflammatory bowel diseaseER stress sensorsHuman macrophagesIntestinal immune homeostasisProtein responseInnate immune systemRisk variantsKey macrophage functionsBowel diseaseOral challengeTranscription factor 6Immune homeostasisCytokine secretionColonic tissueMacrophage functionStress sensorImmune systemRecognition receptorsEffective clearanceMicrobial responsesWeight lossMacrophagesUbiquitinationSingle-cell secretion analysis reveals a dual role for IL-10 in restraining and resolving the TLR4-induced inflammatory response
Alexander AF, Kelsey I, Forbes H, Miller-Jensen K. Single-cell secretion analysis reveals a dual role for IL-10 in restraining and resolving the TLR4-induced inflammatory response. Cell Reports 2021, 36: 109728. PMID: 34551303, PMCID: PMC8995750, DOI: 10.1016/j.celrep.2021.109728.Peer-Reviewed Original Research
2020
Exploring the molecular approach of COX and LOX in Alzheimer’s and Parkinson’s disorder
Kumar A, Behl T, Jamwal S, Kaur I, Sood A, Kumar P. Exploring the molecular approach of COX and LOX in Alzheimer’s and Parkinson’s disorder. Molecular Biology Reports 2020, 47: 9895-9912. PMID: 33263931, DOI: 10.1007/s11033-020-06033-x.Peer-Reviewed Original ResearchConceptsParkinson's diseaseDocosahexaenoic acidAlzheimer's diseaseArachidonic acidLipid mediatorsAnti-inflammatory actionAppropriate therapeutic optionPro-inflammatory eicosanoidsProduction of eicosanoidsResolution of inflammationRole of AACOX-2 enzymeLOX pathwayNeuroinflammatory responseNeuroinflammatory eventsTherapeutic optionsAD patientsCytokine secretionEpidemiological studiesLeukocyte traffickingNF-κBEicosanoid productionBrain disordersNeurological disordersCyclooxygenase
2019
PSEN1ΔE9, APPswe, and APOE4 Confer Disparate Phenotypes in Human iPSC-Derived Microglia
Konttinen H, Cabral-da-Silva M, Ohtonen S, Wojciechowski S, Shakirzyanova A, Caligola S, Giugno R, Ishchenko Y, Hernández D, Fazaludeen M, Eamen S, Budia M, Fagerlund I, Scoyni F, Korhonen P, Huber N, Haapasalo A, Hewitt A, Vickers J, Smith G, Oksanen M, Graff C, Kanninen K, Lehtonen S, Propson N, Schwartz M, Pébay A, Koistinaho J, Ooi L, Malm T. PSEN1ΔE9, APPswe, and APOE4 Confer Disparate Phenotypes in Human iPSC-Derived Microglia. Stem Cell Reports 2019, 13: 669-683. PMID: 31522977, PMCID: PMC6829767, DOI: 10.1016/j.stemcr.2019.08.004.Peer-Reviewed Original ResearchConceptsInduced pluripotent stem cellsPluripotent stem cellsErythromyeloid progenitorsDisparate phenotypesIsogenic controlsSignature genesMicroglia-like cellsHuman microglia-like cellsGenetic backgroundHuman iPSCStem cellsMicroglial signature genesYolk sacIPSC linesIntracellular CaImpairs phagocytosisIMGLsMetabolic activitySmall moleculesHigh-yield protocolCellsAPPswe mutationMinor alterationsCytokine secretionGenesTIGIT signaling restores suppressor function of Th1 Tregs
Lucca LE, Axisa PP, Singer ER, Nolan NM, Dominguez-Villar M, Hafler DA. TIGIT signaling restores suppressor function of Th1 Tregs. JCI Insight 2019, 4: e124427. PMID: 30728325, PMCID: PMC6413794, DOI: 10.1172/jci.insight.124427.Peer-Reviewed Original ResearchIL-12Multiple sclerosisHuman autoimmune disordersT-bet expressionProinflammatory cytokine secretionProduction of IFNType 1 diabetesReduced suppressor activitySuppressor functionRepression of AktFOXO1 nuclear localizationTh1 programTIGIT pathwayCoinhibitory receptorsImmunomodulatory therapyTh17 responsesAutoimmune disordersAutoimmune diseasesSuppressor defectCytokine secretionTregsTIGITProtective effectFunctional inhibitionAkt pathwayHigh ambient temperature dampens adaptive immune responses to influenza A virus infection
Moriyama M, Ichinohe T. High ambient temperature dampens adaptive immune responses to influenza A virus infection. Proceedings Of The National Academy Of Sciences Of The United States Of America 2019, 116: 3118-3125. PMID: 30718396, PMCID: PMC6386664, DOI: 10.1073/pnas.1815029116.Peer-Reviewed Original ResearchConceptsAdaptive immune responsesHeat-exposed miceVirus-specific adaptive immune responsesInfluenza virus infectionImmune responseVirus infectionVirus-specific CD8 T cellsRespiratory influenza virus infectionDietary short chain fatty acidCD8 T cellsDendritic cell migrationExposure of miceAdministration of glucoseThrombocytopenia syndrome phlebovirusCommensal microbiota compositionInflammasome-dependent cytokine secretionShort-chain fatty acidsAntibody responseCytokine secretionLung tissueSevere feverT cellsViral infectionInduction of autophagyMicrobiota composition
2017
Human LACC1 increases innate receptor-induced responses and a LACC1 disease-risk variant modulates these outcomes
Lahiri A, Hedl M, Yan J, Abraham C. Human LACC1 increases innate receptor-induced responses and a LACC1 disease-risk variant modulates these outcomes. Nature Communications 2017, 8: 15614. PMID: 28593945, PMCID: PMC5472760, DOI: 10.1038/ncomms15614.Peer-Reviewed Original ResearchMeSH KeywordsBacteriaCells, CulturedCrohn DiseaseCytokinesElectron Transport Complex IIExtracellular Signal-Regulated MAP KinasesHumansImmunity, InnateIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesMacrophagesNF-kappa BNod2 Signaling Adaptor Proteinp38 Mitogen-Activated Protein KinasesProteinsReactive Oxygen SpeciesReceptors, Pattern RecognitionRNA InterferenceRNA, Small InterferingSuccinate DehydrogenaseConceptsBacterial clearanceCytokine secretionDisease risk variantsReceptor-induced responsesMyeloid-derived cellsNOD2 stimulationRecognition receptorsHuman macrophagesSuccinate dehydrogenaseMtROS productionMitochondrial ROS productionROS productionOutcomesSDH activityMacrophagesSecretionFunctional consequencesClearanceLACC1PRRImportant contributorCellsDisease-associated lociReceptorsAdipose tissue macrophages impair preadipocyte differentiation in humans
Liu LF, Craig CM, Tolentino LL, Choi O, Morton J, Rivas H, Cushman SW, Engleman EG, McLaughlin T. Adipose tissue macrophages impair preadipocyte differentiation in humans. PLOS ONE 2017, 12: e0170728. PMID: 28151993, PMCID: PMC5289462, DOI: 10.1371/journal.pone.0170728.Peer-Reviewed Original ResearchConceptsImpaired adipocyte differentiationSystemic insulin resistanceInsulin resistanceAdipocyte differentiationPreadipocyte differentiationMacrophage removalImpaired preadipocyte differentiationProinflammatory immune cellsAdipose tissue inflammationAbsence of CD14Insulin-resistant humansAdipose tissue samplesOil Red ODifferentiation of preadipocytesBariatric surgeryProinflammatory cytokinesInflammatory cytokinesTissue inflammationImmune cellsCytokine secretionAdiponectin secretionAdipogenic gene expressionPhysiologic mechanismsAdipose tissueVAT adipocytes
2016
JAK2 Disease-Risk Variants Are Gain of Function and JAK Signaling Threshold Determines Innate Receptor-Induced Proinflammatory Cytokine Secretion in Macrophages
Hedl M, Proctor DD, Abraham C. JAK2 Disease-Risk Variants Are Gain of Function and JAK Signaling Threshold Determines Innate Receptor-Induced Proinflammatory Cytokine Secretion in Macrophages. The Journal Of Immunology 2016, 197: 3695-3704. PMID: 27664279, PMCID: PMC5127452, DOI: 10.4049/jimmunol.1600845.Peer-Reviewed Original ResearchConceptsInflammatory bowel diseaseAnti-inflammatory cytokinesImmune-mediated diseasesOligomerization domain 2Proinflammatory cytokinesMyeloid cellsJAK2 expressionJAK inhibitorsIntestinal myeloid cellsThymic stromal lymphopoietinUlcerative colitis patientsProinflammatory cytokine secretionPattern recognition receptorsHuman myeloid cellsLower JAK2Cell typesColitis patientsBowel diseaseIL-10IL-22Peripheral macrophagesIL-4Cytokine secretionAA carriersDecreased responseInflammatory processes are specifically enhanced in endothelial cells by placental-derived TNF-α: Implications in preeclampsia (PE)
Shaw J, Tang Z, Schneider H, Saljé K, Hansson SR, Guller S. Inflammatory processes are specifically enhanced in endothelial cells by placental-derived TNF-α: Implications in preeclampsia (PE). Placenta 2016, 43: 1-8. PMID: 27324092, DOI: 10.1016/j.placenta.2016.04.015.Peer-Reviewed Original ResearchConceptsPro-inflammatory cytokine secretionMaternal perfusateCytokine secretionEndothelial dysfunctionActivation markersEndothelial cellsTNF-α blocking antibodyDual perfusion modelMaternal endothelial dysfunctionPro-inflammatory cytokinesMCP-1 secretionTNF-α actionEndothelial cell linePlacental pathophysiologyEndothelial activationIL-6IL-8Maternal endotheliumInflammatory processDual perfusionMaternal circulationBlocking antibodiesPreeclampsiaTNFPerfusion model
2015
MTMR3 risk allele enhances innate receptor-induced signaling and cytokines by decreasing autophagy and increasing caspase-1 activation
Lahiri A, Hedl M, Abraham C. MTMR3 risk allele enhances innate receptor-induced signaling and cytokines by decreasing autophagy and increasing caspase-1 activation. Proceedings Of The National Academy Of Sciences Of The United States Of America 2015, 112: 10461-10466. PMID: 26240347, PMCID: PMC4547281, DOI: 10.1073/pnas.1501752112.Peer-Reviewed Original ResearchMeSH KeywordsAllelesAutophagyCaspase 1CytokinesEnzyme ActivationGene Expression RegulationGenetic Predisposition to DiseaseGenotypeHomeostasisHumansInflammationInflammatory Bowel DiseasesLeukocytes, MononuclearLigandsMacrophagesMonocytesProtein Structure, TertiaryProtein Tyrosine Phosphatases, Non-ReceptorRisk FactorsRNA, Small InterferingSignal TransductionToll-Like ReceptorsConceptsPattern recognition receptorsCaspase-1 activationInflammatory bowel diseaseMTMR3 expressionReceptor-induced signalingHost pattern recognition receptorsCytokine secretionMultiple genetic lociPhosphatase domainMicrobial interactionsGenetic lociMTMR3Undefined roleAutophagyIL-1β secretionRecognition receptorsHuman macrophagesAutophagy levelEnhanced autophagyProtein 3Bowel diseaseCytokine productionRisk polymorphismsRisk allelesAltered function
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