2025
Subcellular proteomics and iPSC modeling uncover reversible mechanisms of axonal pathology in Alzheimer’s disease
Cai Y, Kanyo J, Wilson R, Bathla S, Cardozo P, Tong L, Qin S, Fuentes L, Pinheiro-de-Sousa I, Huynh T, Sun L, Mansuri M, Tian Z, Gan H, Braker A, Trinh H, Huttner A, Lam T, Petsalaki E, Brennand K, Nairn A, Grutzendler J. Subcellular proteomics and iPSC modeling uncover reversible mechanisms of axonal pathology in Alzheimer’s disease. Nature Aging 2025, 5: 504-527. PMID: 40065072, PMCID: PMC11922768, DOI: 10.1038/s43587-025-00823-3.Peer-Reviewed Original ResearchMeSH KeywordsAlzheimer DiseaseAnimalsAxonsDisease Models, AnimalHumansInduced Pluripotent Stem CellsMiceProteomicsSignal TransductionTOR Serine-Threonine KinasesConceptsAlzheimer's diseaseProximity labeling approachIPSC-derived neuronsSubcellular proteomicsCytoskeleton dynamicsPhosphorylated mTOR levelsDystrophic neuritesLipid transportBiological processesProtein turnoverAD modelHuman induced pluripotent stem cellsAmyloid depositsIPSC modelsProteomicsInduced pluripotent stem cellsPluripotent stem cellsMTOR inhibitionTherapeutic targetAxonal pathologyLabeling approachMTOR levelsMouse brainSpheroid formationAlzheimerOxytocin improves maternal licking behavior deficits in autism-associated Shank3 mutant dogs
Lyu W, Li Y, Yao A, Tan Q, Zhang R, Zhao J, Guo K, Jiang Y, Tian R, Zhang Y. Oxytocin improves maternal licking behavior deficits in autism-associated Shank3 mutant dogs. Translational Psychiatry 2025, 15: 76. PMID: 40050270, DOI: 10.1038/s41398-025-03296-5.Peer-Reviewed Original ResearchConceptsAutism spectrum disorderMutant damsWild-typeMaternal behaviorASD risk genesLicking behaviorAbundant scaffolding proteinImpaired social interactionEffects of oxytocinCRISPR/Cas9 methodologyRisk genesMutant dogsNursing frequencyOXT treatmentBehavioral deficitsRepetitive behaviorsPotential therapeutic strategySpectrum disorderFGF21 Signaling Exerts Antifibrotic Properties during Pulmonary Fibrosis.
Ghanem M, Archer G, Justet A, Jaillet M, Vasarmidi E, Mordant P, Castier Y, Mal H, Cazes A, Poté N, Crestani B, Mailleux A. FGF21 Signaling Exerts Antifibrotic Properties during Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2025, 211: 486-498. PMID: 39637324, DOI: 10.1164/rccm.202311-2021oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisWild-type littermatesPlasma of patientsPulmonary fibrosisAntifibrotic propertiesIntratracheal injection of bleomycinDevelopment of pulmonary fibrosisDecreased fibrosis markersEffects of FGF21Increased sensitivity to bleomycinInjection of bleomycinPulmonary fibrosis developmentSensitivity to bleomycinDecrease of BaxConcentrations of FGF21Human lung fibroblastsTherapeutic optionsFibrosis markersAntifibrotic effectsControl subjectsInjury scoreIntratracheal injectionLiver fibrosisLung fibrogenesisFibroblast growth factorDevelopment of Syngeneic Murine Glioma Models with Somatic Mismatch Repair Deficiency to Study Therapeutic Responses to Alkylating Agents and Immunotherapy
Bhatt D, Sundaram R, López K, Lee T, Gueble S, Vasquez J. Development of Syngeneic Murine Glioma Models with Somatic Mismatch Repair Deficiency to Study Therapeutic Responses to Alkylating Agents and Immunotherapy. Current Protocols 2025, 5: e70097. PMID: 39995104, DOI: 10.1002/cpz1.70097.Peer-Reviewed Original ResearchConceptsImproved response to immune checkpoint blockadeGlioma modelResponse to immune checkpoint blockadeAlkylating agentsImmune checkpoint blockadeIncrease tumor immunogenicityMurine glioma modelMurine glioma cell lineResponse to alkylating agentsResistance to temozolomideDNA repair genotypesMMR deficiencyAntitumor immunityCheckpoint blockadeTumor immunogenicityMedian survivalImmunocompetent modelDismal prognosisMismatch repairMismatch repair deficiencyGlioma cell linesIntracranial tumorsAlkylating chemotherapySomatic lossSomatic acquisitionCD103+ dendritic cell — fibroblast crosstalk via TLR9, TDO2, and AHR signaling drives lung fibrogenesis
Carter H, Costa R, Adams T, Gilchrist T, Emch C, Bame M, Oldham J, Huang S, Linderholm A, Noth I, Kaminski N, Moore B, Gurczynski S. CD103+ dendritic cell — fibroblast crosstalk via TLR9, TDO2, and AHR signaling drives lung fibrogenesis. JCI Insight 2025, 10 PMID: 39964756, PMCID: PMC11949071, DOI: 10.1172/jci.insight.177072.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDBasic Helix-Loop-Helix Transcription FactorsBleomycinDendritic CellsDisease Models, AnimalFibroblastsHumansIdiopathic Pulmonary FibrosisIntegrin alpha ChainsInterleukin-6LungMaleMiceMice, Inbred C57BLReceptors, Aryl HydrocarbonSignal TransductionToll-Like Receptor 9Tryptophan OxygenaseConceptsIdiopathic pulmonary fibrosisAhR signalingMice treated with BLMIL-17+ cellsCD103+ DCLoss of lung functionStudies of human samplesLimited treatment optionsTreated ex vivoProduction of IL-6Inflammatory cytokine productionExon 2 deletionExpression of TDO2IL-6 productionAdoptive transferCD11c-CreCD11c+ cellsImmunological changesPulmonary fibrosisTLR agonistsProgressive scarringTreatment optionsCytokine productionLung fibrogenesisAryl hydrocarbon receptorShort-term disruption of TGFβ signaling in adult mice renders the aorta vulnerable to hypertension-induced dissection
Jiang B, Ren P, He C, Wang M, Murtada S, Ruiz-Rodríguez M, Chen Y, Ramachandra A, Li G, Qin L, Assi R, Schwartz M, Humphrey J, Tellides G. Short-term disruption of TGFβ signaling in adult mice renders the aorta vulnerable to hypertension-induced dissection. JCI Insight 2025, 10 PMID: 39932797, PMCID: PMC11949005, DOI: 10.1172/jci.insight.182629.Peer-Reviewed Original ResearchConceptsSmooth muscle cellsBlood pressureAortic dissectionAdult miceInherited connective tissue disorderConnective tissue disordersTGF-b signalingAccumulation of bloodHigh blood pressureAortic phenotypeTissue disordersMolecule expressionTGFB signalingMuscle cellsRisk factorsSynthesis of extracellular matrixSustained increaseTransient increaseBlood extravasationDissectionMedial injuryExtracellular matrix productionVascular degenerationExperimental modelMiceHuman and mouse proteomics reveals the shared pathways in Alzheimer’s disease and delayed protein turnover in the amyloidome
Yarbro J, Han X, Dasgupta A, Yang K, Liu D, Shrestha H, Zaman M, Wang Z, Yu K, Lee D, Vanderwall D, Niu M, Sun H, Xie B, Chen P, Jiao Y, Zhang X, Wu Z, Chepyala S, Fu Y, Li Y, Yuan Z, Wang X, Poudel S, Vagnerova B, He Q, Tang A, Ronaldson P, Chang R, Yu G, Liu Y, Peng J. Human and mouse proteomics reveals the shared pathways in Alzheimer’s disease and delayed protein turnover in the amyloidome. Nature Communications 2025, 16: 1533. PMID: 39934151, PMCID: PMC11814087, DOI: 10.1038/s41467-025-56853-3.Peer-Reviewed Original ResearchConceptsAlzheimer's diseaseProtein turnoverMouse model of amyloidosisMulti-omics analysisMurine model of Alzheimer's diseaseModel of Alzheimer's diseaseModel of amyloidosisProteome turnoverMouse proteomeGenetic incorporationAD pathwayAmyloid formationBrain proteomeMulti-omicsProteomic strategyAD progressionProteomicsProtein alterationsProteinDisease mechanismsAmyloidPathwayPotential targetMouse brainTurnoverDeletion of sphingosine 1-phosphate receptor 1 in myeloid cells reduces hepatic inflammatory macrophages and attenuates MASH
Parthasarathy G, Venkatesan N, Sidhu G, Song M, Liao C, Barrow F, Mauer A, Sehrawat T, Nakao Y, Daniel P, Dasgupta D, Pavelko K, Revelo X, Malhi H. Deletion of sphingosine 1-phosphate receptor 1 in myeloid cells reduces hepatic inflammatory macrophages and attenuates MASH. Hepatology Communications 2025, 9: e0613. PMID: 39899672, DOI: 10.1097/hc9.0000000000000613.Peer-Reviewed Original ResearchConceptsMyeloid cellsMonocyte-derived macrophagesHigh-fatLiver injuryProinflammatory monocyte-derived macrophagesReceptor 1Cell-specific knockout miceMass cytometryT cell subsetsSphingosine 1-phosphate receptor 1Cardiometabolic risk factorsS1P receptor 1Accumulation of monocyte-derived macrophagesImmune cell typesWild-typeLiver inflammatory infiltrationGene ontology pathway analysisWild-type controlsDevelopment of steatohepatitisSphingosine 1-phosphateMitogen-activated protein kinase pathwayT cellsIntrahepatic macrophagesInflammatory infiltrateKnockout miceCCL21-CCR7 blockade prevents neuroinflammation and degeneration in Parkinson’s disease models
Leser F, Júnyor F, Pagnoncelli I, Delgado A, Medeiros I, Nóbrega A, Andrade B, de Lima M, da Silva N, Jacob L, Boyé K, Geraldo L, de Souza A, Maron-Gutierrez T, Castro-Faria-Neto H, Follmer C, Braga C, Neves G, Eichmann A, Romão L, Lima F. CCL21-CCR7 blockade prevents neuroinflammation and degeneration in Parkinson’s disease models. Journal Of Neuroinflammation 2025, 22: 31. PMID: 39894839, PMCID: PMC11789347, DOI: 10.1186/s12974-024-03318-x.Peer-Reviewed Original ResearchConceptsMouse model of PDModel of PDMouse modelDopaminergic neuronsNeuron-microglia communicationNeuron-glia communicationParkinson's diseaseCCR7-dependent mannerMicroglial cell activationCCR7 expressionCCL21-CCR7Progressive degenerative diseaseCCR7 receptorMicroglial cell migrationInflammatory profileChemokine CCL21Cell activationCCL21Therapeutic strategiesChemokine inhibitorsTherapeutic implicationsMicroglial activationReceptor pathwayCCR7Behavioral deficitsThe fungal microbiota modulate neonatal oxygen-induced lung injury
Martin I, Silverberg M, Abdelgawad A, Tanaka K, Halloran B, Nicola T, Myers E, Desai J, White C, Karabayir I, Akbilgic O, Tipton L, Gentle S, Ambalavanan N, Peters B, Vu L, Jain V, Lal C, Cormier S, Pierre J, Jilling T, Talati A, Willis K. The fungal microbiota modulate neonatal oxygen-induced lung injury. Microbiome 2025, 13: 24. PMID: 39871397, PMCID: PMC11773857, DOI: 10.1186/s40168-025-02032-x.Peer-Reviewed Original ResearchConceptsBronchopulmonary dysplasiaLung injury severityLung injuryDevelopment of bronchopulmonary dysplasiaSeverity of lung injuryAugmented lung injuryMorbidities of prematurityVery preterm infantsOxygen-induced lung injuryChronic lung diseaseIntestinal microbiomeMicrobiome of infantsPotential therapeutic strategyPreterm infantsNeonatal microbiomePremature infantsPremature neonatesInjury severityMurine modelNeonatal healthLung diseaseMouse modelTherapeutic strategiesLoss of function approachesFungal communitiesPharmacological blocking of microfibrillar-associated protein 4 reduces retinal neoangiogenesis and vascular leakage
Schlosser A, Pilecki B, Allen C, Benest A, Lynch A, Hua J, Ved N, Blackley Z, Andersen T, Hennig D, Graversen J, Möller S, Skallerup S, Ormhøj M, Lange C, Agostini H, Grauslund J, Heegaard S, Dacheva I, Koss M, Hu W, Iglesias B, Lawrence M, Beck H, Steffensen L, Laursen N, Andersen G, Holmskov U, Bates D, Sorensen G. Pharmacological blocking of microfibrillar-associated protein 4 reduces retinal neoangiogenesis and vascular leakage. Molecular Therapy 2025, 33: 1048-1072. PMID: 39863929, PMCID: PMC11897753, DOI: 10.1016/j.ymthe.2025.01.038.Peer-Reviewed Original ResearchConceptsMicrofibrillar-associated protein 4Vascular leakageNeovascular age-related macular degenerationAge-related macular degenerationChoroidal neovascularization mouse modelDiabetic macular edemaProtein 4Treatment of neovascularizationLaser-induced choroidal neovascularization mouse modelVascular leakage areaDuration of efficacyVascular endothelial cellsRetinal neoangiogenesisMacular edemaRetinal neovascularizationMacular degenerationVision lossRetinal diseasesPharmacological blockMuller cellsRetinal astrocytesVascular permeabilityVascular mural cellsEndothelial cell motilityMouse modelBridging animal models and humans: neuroimaging as intermediate phenotypes linking genetic or stress factors to anhedonia
Guo H, Xiao Y, Dong S, Yang J, Zhao P, Zhao T, Cai A, Tang L, Liu J, Wang H, Hua R, Liu R, Wei Y, Sun D, Liu Z, Xia M, He Y, Wu Y, Si T, Womer F, Xu F, Tang Y, Wang J, Zhang W, Zhang X, Wang F. Bridging animal models and humans: neuroimaging as intermediate phenotypes linking genetic or stress factors to anhedonia. BMC Medicine 2025, 23: 38. PMID: 39849528, PMCID: PMC11755933, DOI: 10.1186/s12916-025-03850-4.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnhedoniaAnimalsBrainDepressionDisease Models, AnimalFemaleHumansMaleMiceMiddle AgedNeuroimagingPhenotypeRatsStress, PsychologicalYoung AdultConceptsIntermediate phenotypesCore symptoms of depressionAmplitude of low-frequency fluctuationNeuroimaging patternsSubtypes of depressionCore depressive symptomsExpression of risk genesDiverse clinical populationsSymptoms of depressionRodent modelsAssociated with depressionLow-frequency fluctuationsStress-related changesDepression subtypesCore symptomsCross-species validationPsychiatric disordersNeuropsychiatric disordersDepressive symptomsBehavioral manifestationsStress modelDepression cohortClinical populationsSensorimotor regionsAnhedoniaAnti-Syndecan 2 Antibody Treatment Reduces Edema Formation and Inflammation of Murine Laser-Induced CNV.
Corti F, Locri F, Plastino F, Perrotta P, Zsebo K, Ristori E, Yin X, Song E, André H, Simons M. Anti-Syndecan 2 Antibody Treatment Reduces Edema Formation and Inflammation of Murine Laser-Induced CNV. Translational Vision Science & Technology 2025, 14: 10. PMID: 39792057, PMCID: PMC11730891, DOI: 10.1167/tvst.14.1.10.Peer-Reviewed Original ResearchConceptsAge-related macular degenerationLaser-induced choroidal neovascularizationAnti-VEGF therapyTransendothelial electrical resistanceVEGF-A activityChoroidal neovascularizationIntravitreal injectionRetinal lesionsLong-term anti-VEGF therapyMurine laser-induced choroidal neovascularizationNeovascular age-related macular degenerationWet age-related macular degenerationAlteration of visual acuityIntravitreal anti-VEGF therapySide effectsLocal intravitreal injectionReduced edema formationSuppression of edemaRelated side effectsPermeability in vitroEndothelial cell junctionsNeovascular AMDVisual acuityAssessed in vitroMacular degenerationThe etiology and prevention of early‐stage tau pathology in higher cortical circuits: Insights from aging rhesus macaques
Datta D, Arnsten A. The etiology and prevention of early‐stage tau pathology in higher cortical circuits: Insights from aging rhesus macaques. Alzheimer's & Dementia 2025, 21: e14477. PMID: 39776253, PMCID: PMC11848412, DOI: 10.1002/alz.14477.Peer-Reviewed Original ResearchMeSH KeywordsAgingAlzheimer DiseaseAmyloid beta-PeptidesAnimalsCerebral CortexDisease Models, AnimalHumansMacaca mulattaPhosphorylationtau ProteinsConceptsAged macaquesAged rhesus macaquesP-tauTau hyperphosphorylationCortical circuitsAmyloid-beta generationSoluble phosphorylated tauCognitive deficitsAged monkeysSoluble hyperphosphorylated tauSporadic Alzheimer's diseaseAssociation cortexEarly-stage pathologyRhesus macaquesIncreased ABCalcium dysregulationCalcium regulationToxic to neuronsHyperphosphorylated tauAmyloid-betaCortexInflammatory signalingP-tau217 levelsTau pathologyPhosphorylated tau
2024
Efficacy of GABA aminotransferase inactivator OV329 in models of neuropathic and inflammatory pain without tolerance or addiction
Wirt J, Ferreira L, Jesus C, Woodward T, Oliva I, Xu Z, Crystal J, Pepin R, Silverman R, Hohmann A. Efficacy of GABA aminotransferase inactivator OV329 in models of neuropathic and inflammatory pain without tolerance or addiction. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 122: e2318833121. PMID: 39793055, PMCID: PMC11725897, DOI: 10.1073/pnas.2318833121.Peer-Reviewed Original ResearchConceptsComplete Freund's adjuvantInflammatory painMechanical hypersensitivityAntinociceptive efficacyGlutamate levelsInjection of complete Freund's adjuvantConditioned place preference assayPaclitaxel-induced mechanical hypersensitivitySpinal site of actionSide effectsEnhancement of GABAergic transmissionChemotherapeutic agent paclitaxelPaclitaxel-induced increaseCompared to morphineLumbar spinal cordIncreased endogenous GABA levelsReduced glutamate levelsNeuropathic nociceptionSite of actionGABAergic transmissionAnalgesic strategiesPathological painGABAergic inhibitionSpinal sitesAbuse liabilityHeterogeneous Cardiac-Derived and Neural Crest–Derived Aortic Smooth Muscle Cells Exhibit Similar Transcriptional Changes After TGFβ Signaling Disruption
Ren P, Jiang B, Hassab A, Li G, Li W, Assi R, Tellides G. Heterogeneous Cardiac-Derived and Neural Crest–Derived Aortic Smooth Muscle Cells Exhibit Similar Transcriptional Changes After TGFβ Signaling Disruption. Arteriosclerosis Thrombosis And Vascular Biology 2024, 45: 260-276. PMID: 39697172, DOI: 10.1161/atvbaha.124.321706.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaAortic AneurysmCell LineageDisease Models, AnimalGene Expression ProfilingHomeobox Protein Nkx-2.5HumansMaleMarfan SyndromeMiceMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MuscleMyosin Heavy ChainsNeural CrestPhenotypeReceptor, Transforming Growth Factor-beta Type IIReceptors, Transforming Growth Factor betaSignal TransductionSingle-Cell AnalysisTranscription, GeneticTranscriptomeTransforming Growth Factor betaWnt1 ProteinConceptsSmooth muscle cell clustersSmooth muscle cellsAortic smooth muscle cellsNeural crest-derived smooth muscle cellsCardiac derivativesMurine aortic smooth muscle cellsNeural crest originReceptor deletionAortic rootAdult miceNeural crest progenitorsNKX2-5Proximal aortaTranscriptional changesMouse modelTGFB signalingMuscle cellsConditional deletionAdult human aortaEmbryological originIncreased expressionAnalyzed single-cell transcriptomesTGFB receptorsBasal stateAortic homeostasisRenal Angptl4 is a key fibrogenic molecule in progressive diabetic kidney disease
Srivastava S, Zhou H, Shenoi R, Morris M, Lainez-Mas B, Goedeke L, Rajendran B, Setia O, Aryal B, Kanasaki K, Koya D, Inoki K, Dardik A, Bell T, Fernández-Hernando C, Shulman G, Goodwin J. Renal Angptl4 is a key fibrogenic molecule in progressive diabetic kidney disease. Science Advances 2024, 10: eadn6068. PMID: 39630889, PMCID: PMC11616692, DOI: 10.1126/sciadv.adn6068.Peer-Reviewed Original ResearchConceptsAngiopoietin-like 4Diabetic kidney diseaseIntegrin B1Fibrogenic moleculesMutant miceSTING pathway activationIncreased fatty acid oxidationProgressive diabetic kidney diseaseDiabetic kidneyKidney diseaseReduced epithelial-to-mesenchymal transitionEpithelial-to-mesenchymal transitionFatty acid oxidationExpression of pro-inflammatory cytokinesTargeted pharmacological therapiesGene expressionMitochondrial damageEndothelial-to-mesenchymal transitionPro-inflammatory cytokinesPathway activationPharmacological therapyControl miceIntegrinAcid oxidationFibrogenic phenotypeIntrathecal lactate dehydrogenase A inhibitors FX11 and oxamate alleviate chronic constriction injury-induced nociceptive sensitization through neuroinflammation and angiogenesis
Cheng H, Chen N, Chen W, Wu Z, Sun Y, Teng W, Su F, Sung C, Wen Z. Intrathecal lactate dehydrogenase A inhibitors FX11 and oxamate alleviate chronic constriction injury-induced nociceptive sensitization through neuroinflammation and angiogenesis. The Journal Of Headache And Pain 2024, 25: 207. PMID: 39587478, PMCID: PMC11590346, DOI: 10.1186/s10194-024-01916-x.Peer-Reviewed Original ResearchConceptsLactate dehydrogenase ANeuropathic painNociceptive sensitizationLDHA inhibitorsTreat neuropathic painType of painUpregulation of glycolysisCCI-induced neuroinflammationCentral nervous systemBackgroundNeuropathic painNeuropathic ratsSpinal roleNociceptive behaviorBlood vessel growthImmunohistochemical analysisControl inflammationPainEffective treatmentConclusionIn conclusionHIF-1aCellular mechanismsNervous systemTherapeutic targetVessel growthWestern blottingMonoclonal antibodies that block Roundabout 1 and 2 signaling target pathological ocular neovascularization through myeloid cells
Geraldo L, Xu Y, Mouthon G, Furtado J, Leser F, Blazer L, Adams J, Zhang S, Zheng L, Song E, Robinson M, Thomas J, Sidhu S, Eichmann A. Monoclonal antibodies that block Roundabout 1 and 2 signaling target pathological ocular neovascularization through myeloid cells. Science Translational Medicine 2024, 16: eadn8388. PMID: 39565875, PMCID: PMC11822886, DOI: 10.1126/scitranslmed.adn8388.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalCorneal NeovascularizationDisease Models, AnimalHumansIntercellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLMyeloid CellsNeovascularization, PathologicNerve Tissue ProteinsReceptors, ImmunologicRetinaRetinal NeovascularizationSignal TransductionConceptsOxygen-induced retinopathyPathological ocular neovascularizationCorneal neovascularizationMyeloid cellsOcular neovascularizationHeterogeneous population of myeloid cellsBlood-retina barrier integrityPopulation of myeloid cellsActivation of myeloid cellsMonoclonal antibodiesOcular neovascular diseasesBlinding eye diseaseHuman monoclonal antibodyExtracellular domainMouse model in vivoModel in vivoMAb treatmentMyeloid populationsOIR retinasNeovascular diseasesVision lossEye diseaseSlit-RoboSlit-Robo signalingBlocking antibodiesMouse Models Enable the Functional Investigation of Tertiary Lymphoid Structures in Cancer
Jeevanandam A, Yin Z, Connolly K, Joshi N. Mouse Models Enable the Functional Investigation of Tertiary Lymphoid Structures in Cancer. Methods In Molecular Biology 2024, 2864: 57-76. PMID: 39527217, DOI: 10.1007/978-1-0716-4184-2_4.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDisease Models, AnimalHumansLungMiceNeoplasmsTertiary Lymphoid StructuresTumor MicroenvironmentConceptsTertiary lymphoid structuresTertiary lymphoid structure formationSecondary lymphoid organsLymphoid structuresMurine modelFeatures of tertiary lymphoid structuresFunction of tertiary lymphoid structuresMouse modelPersistent inflammatory stimulationAssociated with positive clinical outcomesTissue-specific regulatory mechanismsPositive clinical outcomesPrognostic significanceClinical outcomesGut environmentNonlymphoid tissuesLymphoid aggregatesLymphoid organsMouse lungCancer patientsGenetic sequencesInflammatory stimulationRegulatory mechanismsTherapeutic modulationClinical efforts
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply