Lei Shen
Associate Research ScientistAbout
Research
Publications
2026
Gut microbiota-derived cholic acid ameliorates lung inflammation in bronchopulmonary dysplasia through modulation of macrophage function
Zhao D, Gao C, Zhu D, Zheng X, Sun J, Liu C, Chen L, Shen L, Wang X, Zhang Y. Gut microbiota-derived cholic acid ameliorates lung inflammation in bronchopulmonary dysplasia through modulation of macrophage function. IScience 2026, 29: 115398. DOI: 10.1016/j.isci.2026.115398.Peer-Reviewed Original ResearchBronchopulmonary dysplasiaHIF-1aLung inflammationMacrophage functionNested case-control cohortGut bacterial generaGut microbiota-derived metabolitesRat BPD modelBronchopulmonary dysplasia infantsBronchopulmonary dysplasia patientsModulation of macrophage functionMicrobiota-derived metabolitesHIF-1a expressionSerum cholic acidRegulation of macrophage functionCholic acid supplementationCase-control cohortCholic acidPreterm controlsRNA-seqBacterial generaMass spectrometry analysisTranscriptional activityBPD modelMacrophage plasticityTCR-NF-κB signaling activates the SENP1-NR4A1 axis to fine-tune effector activation of CD8+ T cells
Jiang C, Yang Y, Tian J, Liang Z, Fan Q, Wang Q, Shen L, Wang S, He J, Cheng J. TCR-NF-κB signaling activates the SENP1-NR4A1 axis to fine-tune effector activation of CD8+ T cells. Cell Reports 2026, 45: 117102. PMID: 41831233, DOI: 10.1016/j.celrep.2026.117102.Peer-Reviewed Original ResearchConceptsT cell activationT cell receptorSENP1-mediated deSUMOylationT cellsCD8+ T cell-mediated immune responsesCD8+ T cell activationCD8+ T cell proliferationCD8+ T cell responsesActivation of CD8+ T cellsCD8+ T cellsCD8+ T cellsT cell-mediated immune responsesEffector activityT cell responsesT cell proliferationEarly occurrenceNuclear receptor NR4A1L. monocytogenes infectionNR4A1 activatorImmune activationImmune responseSENP1 deficiencyEffector gene expressionNR4A1Signaling pathwayObesity disrupts ILC2 metabolic and functional homeostasis by inhibiting mTORC1 signaling
Hu L, Wang D, Chen Y, Qiu J, Wang H, Zhang Y, Zhang M, Su X, Qiu J, Sun J, Shen L. Obesity disrupts ILC2 metabolic and functional homeostasis by inhibiting mTORC1 signaling. Cellular & Molecular Immunology 2026, 23: 301-314. PMID: 41593294, PMCID: PMC12948970, DOI: 10.1038/s41423-026-01389-9.Peer-Reviewed Original ResearchMeSH KeywordsAdipose TissueAnimalsHomeostasisHumansHypoxia-Inducible Factor 1, alpha SubunitImmunity, InnateInflammationInsulin ResistanceLymphocytesMaleMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLMice, KnockoutObesityPPAR gammaRegulatory-Associated Protein of mTORSignal TransductionConceptsMechanistic target of rapamycin complex 1Target of rapamycin complex 1Mechanistic targetCritical adaptor proteinMechanistic target of rapamycin complex 1 signalingRapamycin complex 1Adaptor proteinAdipose tissue homeostasisDeletion of RaptorObesity-associated insulin resistanceMitochondrial biogenesisRegulatory mechanismsTissue homeostasisGroup 2 innate lymphoid cellsType 2 cytokine productionFunctional homeostasisInsulin resistanceAdipose tissue inflammationHomeostasisObese miceImmunological homeostasisILC2 functionST2 expressionILC2sLymphoid cells
2025
mTORC1 signaling in group 2 innate lymphoid cells coordinates neuro-immune crosstalk in allergic lung inflammation
Wang D, Hu L, Chen J, Qiu J, Chen Y, Zhang M, Zhao L, Su X, Sun J, Qiu J, Tang W, Zhou W, Shen L. mTORC1 signaling in group 2 innate lymphoid cells coordinates neuro-immune crosstalk in allergic lung inflammation. Nature Communications 2025, 17: 62. PMID: 41318705, PMCID: PMC12769748, DOI: 10.1038/s41467-025-66683-y.Peer-Reviewed Original ResearchConceptsGroup 2 innate lymphoid cellsMechanistic target of rapamycin complex 1Neuromedin U receptor 1Neuro-immune crosstalkAllergic lung inflammationILC2 cellsAllergic asthmaILC2 activationLung inflammationLymphoid cellsNeuromedin UPharmacological inhibitionGenetic ablationTissue-derived stimuliType 2 inflammationIL-13 productionTarget of rapamycin complex 1Mechanistic target of rapamycin complex 1 signalingMechanistic targetInhibition of mechanistic target of rapamycin complex 1Ablation of RaptorRapamycin complex 1ILC2sIL-5Allergic inflammationMetabolic heterogeneity in adipose resident immunocytes and its link to type 2 diabetes via response to catabolism defects
Huang S, Chen X, Yuan Y, Yuan Y, Shen L, Wang H, Tang W, Bi Y, Wu T. Metabolic heterogeneity in adipose resident immunocytes and its link to type 2 diabetes via response to catabolism defects. Genomics 2025, 117: 111152. PMID: 41207448, DOI: 10.1016/j.ygeno.2025.111152.Peer-Reviewed Original ResearchConceptsType 2 diabetesResident immunocytesMetabolic heterogeneityCatabolic defectMetabolic perturbationsMetabolic patternsImmune cell functionResident immune cellsVisceral adipose tissueImmune cellsResponse to metabolic perturbationsMetabolic factorsMetabolic defectsAdipose dysfunctionMetabolic diseasesAdipose tissueCell functionDiverse responsesImpaired capacityAdiposeImmunocytesImmunogenic heterogeneityDiverse functionsMetabolic reductionMetabolic activityJawbone mesenchymal stromal cells attenuate acute inflammation via hematopoietic niche reinforcement
Wang X, Chen Q, Sun J, Huang Z, Zhang Z, Lu T, Huang X, Sun S, Liu Y, Pan H, Mei L, Cooper P, Dai Q, Shen L, Jiang L. Jawbone mesenchymal stromal cells attenuate acute inflammation via hematopoietic niche reinforcement. Frontiers In Bioengineering And Biotechnology 2025, 13: 1596143. PMID: 40861852, PMCID: PMC12375904, DOI: 10.3389/fbioe.2025.1596143.Peer-Reviewed Original ResearchHematopoietic stem cellsHematopoietic stem cell differentiationMesenchymal stem cellsMultilineage differentiation potentialCo-culture systemSystemic inflammationB cellsImmunoregulatory functionsTherapeutic efficacySingle-cell sequencingCommitment of hematopoietic stem cellsInfected miceMouse modelTissue immunofluorescenceLineage commitment of hematopoietic stem cellsInfection modelStem cellsMultilineage potentialDifferentiation potentialB cell generationBone marrow microenvironmentLineage commitmentBone marrow nicheAdipogenic differentiation assaysCo-CultureLKB1 regulates ILC3 postnatal development and effector function through metabolic programming
Zhang H, Zhao L, Zhang Q, Hu L, Su X, Sun J, Shen L. LKB1 regulates ILC3 postnatal development and effector function through metabolic programming. Frontiers In Immunology 2025, 16: 1587256. PMID: 40539052, PMCID: PMC12176730, DOI: 10.3389/fimmu.2025.1587256.Peer-Reviewed Original ResearchMeSH KeywordsAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesAnimalsCitrobacter rodentiumEnterobacteriaceae InfectionsImmunity, InnateInterleukin-22InterleukinsIntestinal MucosaIntestinesLymphocytesMetabolic ReprogrammingMiceMice, Inbred C57BLMice, KnockoutProtein Serine-Threonine KinasesConceptsLiver kinase B1Intestinal immune homeostasisEffector functionsPostnatal developmentImmune homeostasisFlow cytometryGroup 3 innate lymphoid cellsMetabolic regulationIntestinal immunityLKB1 deficiencyIL-22 productionLKB1-deficient miceConditional knockout miceIntestinal inflammatory responsePotential therapeutic implicationsImpaired cell metabolismILC3 numbersIntestinal ILC3sLymphoid cellsILC3 functionCytokine productionILC3sKnockout miceMitochondrial massILC3 activationT-bet+ILC3 in peripheral blood is increased in the ankylosing spondylitis with high disease activity
Liu Y, Shen Y, Ding H, He D, Cheng P, Wu X, Xiang Z, Shen L, Bian Y, Zhu Q. T-bet+ILC3 in peripheral blood is increased in the ankylosing spondylitis with high disease activity. Heliyon 2025, 11: e41678. PMID: 39866450, PMCID: PMC11757778, DOI: 10.1016/j.heliyon.2025.e41678.Peer-Reviewed Original ResearchInnate lymphoid cellsHigh disease activityErythrocyte sedimentation rateDisease Activity ScoreAS patientsDisease activityPeripheral bloodT-betAnkylosing SpondylitisSystemic inflammationC reactive protein (CRP) levelPlasma levelsActivity scoreDistribution of ILC subsetsLuminex liquid suspension chipPlasma levels of IL-17AT-box transcription factor 21Levels of IL-17AInflammatory processAS Disease Activity ScoreInnate lymphoid cell subsetsLow disease activityChronic autoimmune diseaseDisease severity scoresTranscription factor 21
2024
Osteopetrosis-like disorders induced by osteoblast-specific retinoic acid signaling inhibition in mice
Sun S, Liu Y, Sun J, Zan B, Cui Y, Jin A, Xu H, Huang X, Zhu Y, Yang Y, Gao X, Lu T, Wang X, Liu J, Mei L, Shen L, Dai Q, Jiang L. Osteopetrosis-like disorders induced by osteoblast-specific retinoic acid signaling inhibition in mice. Bone Research 2024, 12: 61. PMID: 39419968, PMCID: PMC11487257, DOI: 10.1038/s41413-024-00353-5.Peer-Reviewed Original ResearchConceptsBone marrowFlow cytometry of peripheral bloodMutant miceFlow cytometryImmune systemRetinoic acidRetinoic acid signalingMarrow cavityB lymphocyte differentiationImmune system dysfunctionPoor bone qualityMetabolite of vitamin AOsteoimmunological mechanismsInfective complicationsThin cortical boneImmune dysfunctionCell autonomous mannerPeripheral bloodHematopoietic progenitorsBone healthCell crosstalkBone densityHematopoietic developmentHuman osteopetrosisMouse modelSirtuin 6 inhibits group 3 innate lymphoid cell function and gut immunity by suppressing IL-22 production
Su X, Zhao L, Zhang H, Wang D, Sun J, Shen L. Sirtuin 6 inhibits group 3 innate lymphoid cell function and gut immunity by suppressing IL-22 production. Frontiers In Immunology 2024, 15: 1402834. PMID: 39253083, PMCID: PMC11381250, DOI: 10.3389/fimmu.2024.1402834.Peer-Reviewed Original ResearchCitrobacter rodentium infectionIL-22 productionSirtuin 6Regulating gut immune responsesNicotinamide adenine dinucleotide (NAD+)-dependent deacetylaseDextran sodium sulfate-induced colitis modelIntestinal epithelial cell differentiationGroup 3 innate lymphoid cellsDextran sodium sulfate-induced colitisEpithelial cell differentiationGut immune responseFlow cytometryEpigenetic regulationIncreased IL-22 productionCell-intrinsic mannerDependent deacetylaseIntestinal ILC3sCell numberIntestinal inflammatory responseLymphoid cell functionGut defenseConditional knockout miceGut immunityIL-22 expressionHost defense
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