Li Wen, MD, PhD
Professor of Medicine (Endocrinology)DownloadHi-Res Photo
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Endocrinology
Primary
Additional Titles
Director of Core Laboratory of Yale Center for Clinical Investigation (YCCI)
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Appointments
Endocrinology
Primary
Additional Titles
Director of Core Laboratory of Yale Center for Clinical Investigation (YCCI)
Contact Info
Appointments
Endocrinology
Primary
Additional Titles
Director of Core Laboratory of Yale Center for Clinical Investigation (YCCI)
Contact Info
About
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Titles
Professor of Medicine (Endocrinology)
Director of Core Laboratory of Yale Center for Clinical Investigation (YCCI)
Appointments
Endocrinology
ProfessorPrimary
Other Departments & Organizations
- All Institutions
- Diabetes Research Center
- Discovery to Cure Internship
- Endocrinology
- Fellowship Training
- Human and Translational Immunology Program
- Internal Medicine
Education & Training
- Postdoctoral Associate and Fellow
- Yale University (1997)
- PhD
- University of London (1992)
- MD
- Capital University of Medicine (1983)
Research
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Overview
Medical Research Interests
Antigen-Presenting Cells; Antigens, CD20; Autoimmune Diseases; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Diabetes Mellitus, Type 1; Hypersensitivity; Immune Tolerance; Immunity, Humoral; Immunity, Innate; Inflammasomes; Islets of Langerhans; Liver; Microbiota; Obesity; T-Lymphocytes, Regulatory; Toll-Like Receptors
ORCID
0000-0002-8805-2934
Research at a Glance
Yale Co-Authors
Frequent collaborators of Li Wen's published research.
Publications Timeline
A big-picture view of Li Wen's research output by year.
Research Interests
Research topics Li Wen is interested in exploring.
Ningwen Tai, PhD
Juan Huang
Jian Peng
Xin Yang, PhD
Youjia Hu, PhD
Jianlei Gu
147Publications
7,500Citations
Diabetes Mellitus, Type 1
CD8-Positive T-Lymphocytes
CD4-Positive T-Lymphocytes
Islets of Langerhans
Autoimmune Diseases
Immune Tolerance
Publications
2026
IL17-deficient NOD mice are protected from autoimmune diabetes due to decreased antigen presentation and T cell activation
Pearson J, Li Y, Huang J, Peng J, Wong F, Wen L. IL17-deficient NOD mice are protected from autoimmune diabetes due to decreased antigen presentation and T cell activation. Frontiers In Immunology 2026, 16: 1728313. PMID: 41613137, PMCID: PMC12850519, DOI: 10.3389/fimmu.2025.1728313.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsConceptsCD8+ T cellsType 1 diabetesNOD miceT cellsIL-17Autoimmune diabetesAntigen presentationAutoantigen-specific T-cell responseType 3 innate lymphoid cellsSusceptibility to type 1 diabetesDevelopment of type 1 diabetesExogenous IL-17Type 1 diabetes developmentAdoptive transfer studiesIL-17 blockadeIL-17 deficiencyRegulatory T cellsT cell responsesIL-12/IL-23T cell activationDevelopment of autoimmunityInsulin-producing beta cellsNon-immune cellsEpithelial cell functionProinflammatory cytokine secretion
2025
Is the NOD mouse a good model for type 1 diabetes?
Wong F, Pearson J, Wen L. Is the NOD mouse a good model for type 1 diabetes? Diabetologia 2025, 69: 3-19. PMID: 41206392, PMCID: PMC12686005, DOI: 10.1007/s00125-025-06579-0.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsPdgfrα deficiency in islet β-cells up-regulates apoptosis of beta-cells and disturbs glucose metabolism in B6 mice
Zhang L, Xing Y, Wang P, Gu J, Peng J, Huang J, Pearson J, Hu Y, Zhao H, Wong F, Wen L. Pdgfrα deficiency in islet β-cells up-regulates apoptosis of beta-cells and disturbs glucose metabolism in B6 mice. Frontiers In Endocrinology 2025, 16: 1630979. PMID: 41234234, PMCID: PMC12605365, DOI: 10.3389/fendo.2025.1630979.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsConceptsB cell apoptosisB cell functionApoptosis of beta-cellsAminoacyl-tRNA synthetasesB cellsGlucose metabolismType 2 diabetesExpression of Gadd45bB cell-specificB cell survivalPI3K pathwayInsulin contentApoptotic pathwayInsulin biosynthesisHigh-fat diet conditionsDownstream effectorsSignaling pathwayIslet B-cell functionB-cell dysfunctionBeta-cellsATF5 expressionK pathwayB cell proliferationDevelopment of type 2 diabetesApoptosisToll-like receptors in B cells and obesity
Wang P, Hou C, Wong F, Wen L. Toll-like receptors in B cells and obesity. Trends In Molecular Medicine 2025, 31: 1114-1123. PMID: 40527636, DOI: 10.1016/j.molmed.2025.05.005.Peer-Reviewed Original ResearchCitationsAltmetricConceptsToll-like receptorsPathogen-associated molecular patternsB cellsDendritic cellsFunction of Toll-like receptorsActivation of dendritic cellsActivation of TLR signalingExcessive adipose tissue accumulationSignaling mechanisms of Toll-like receptorsT cell differentiationAdipose tissue accumulationContext of obesityMechanisms of Toll-like receptorsChronic inflammationInflammatory activityAdaptive immunityImmune responseMetabolic dysregulationTLR signalingImmune functionObesityTissue accumulationMetabolic diseasesMolecular patternsSignaling mechanismsExtracellular vesicles as precision therapeutics for psychiatric conditions: targeting interactions among neuronal, glial, and immune networks
Kawiková I, Špička V, Lai J, Askenase P, Wen L, Kejík Z, Jakubek M, Valeš K, Španiel F. Extracellular vesicles as precision therapeutics for psychiatric conditions: targeting interactions among neuronal, glial, and immune networks. Frontiers In Immunology 2025, 16: 1454306. PMID: 40264776, PMCID: PMC12011847, DOI: 10.3389/fimmu.2025.1454306.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsDevelopment of immune therapiesEVs-based therapyIatrogenic immune deficienciesRobust preclinical dataExploitation of extracellular vesiclesPsychiatric diseasesDiagnostic biomarker panelExtracellular vesiclesRecipient cell functionsImmune therapyImmune deficiencyPatient subsetsPreclinical dataFluid abnormalitiesBiomarker panelEV administrationImmune systemIntercellular communicationPrecision therapeuticsTherapyTherapeutic toolCell functionRegulatory approvalPsychiatric conditionsBrain regionsGut Microbiota Modulation by Inulin Improves Metabolism and Ovarian Function in Polycystic Ovary Syndrome
Geng L, Yang X, Sun J, Ran X, Zhou D, Ye M, Wen L, Wang R, Chen M. Gut Microbiota Modulation by Inulin Improves Metabolism and Ovarian Function in Polycystic Ovary Syndrome. Advanced Science 2025, 12: 2412558. PMID: 40192074, PMCID: PMC12120758, DOI: 10.1002/advs.202412558.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsCo-abundance groupsGut microbiotaFecal microbiota transplantationGut microbiota regulationEffects of inulinGut microbiota modulationModulating gut microbiotaAntibiotic-treated miceLipopolysaccharide-binding proteinPolycystic ovary syndromeBifidobacterium speciesMicrobiota regulationMicrobiota modulationPCOS miceBiosynthesis capacityFecal SCFA contentInulin treatmentSCFA contentMicrobiota transplantationMicrobiotaLipid accumulationGutProtective effect of inulinGlucolipid metabolismPCOS cohort
2024
Perinatal Hypoxia and Immune System Activation in Schizophrenia Pathogenesis: Critical Considerations During COVID-19 Pandemic.
Kawikova I, Hakenova K, Lebedeva M, Kleteckova L, Jakob L, Spicka V, Wen L, Spaniel F, Vales K. Perinatal Hypoxia and Immune System Activation in Schizophrenia Pathogenesis: Critical Considerations During COVID-19 Pandemic. Physiological Research 2024, 73: s615-s639. PMID: 39589306, PMCID: PMC11627263, DOI: 10.33549/physiolres.935501.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsPerinatal hypoxiaPerinatal factorsMaternal immune activationImmune system activationDevelopment of experimental modelsInteraction of genetic backgroundAssociated with hypoxiaNeurodevelopmental disordersMaternal infectionObstetric complicationsSchizophrenia pathogenesisImmune activationMetabolic disturbancesTherapeutic strategiesPerinatal periodSchizophrenia etiologyDisorganized thoughtsExperimental modelSchizophreniaSystem activityEmotional bluntingHypoxiaChronic stressGenetic backgroundCognitive impairmentRegulatory CD4+ T cells redirected against pathogenic CD8+ T cells protect NOD mice from development of autoimmune diabetes
Kakabadse D, Chen D, Fishman S, Weinstein-Marom H, Davies J, Wen L, Gross G, Wong F. Regulatory CD4+ T cells redirected against pathogenic CD8+ T cells protect NOD mice from development of autoimmune diabetes. Frontiers In Immunology 2024, 15: 1463971. PMID: 39351219, PMCID: PMC11439686, DOI: 10.3389/fimmu.2024.1463971.Peer-Reviewed Original ResearchCitationsAltmetricConceptsCD8+ T cellsCD4+ T cellsAntigen-specific CD8+ T cellsDevelopment of autoimmune diabetesRegulatory T cellsCo-transfer experimentsT cellsNOD miceAutoimmune diabetesAntigen-specific CD4+ T cellsRegulatory CD4+ T cellsAntigen-specific cytotoxic CD8Pathogenic CD8+ T cellsPre-diabetic NOD micePolyclonal CD4+ T cellsDevelopment of type 1 diabetesSuppresses autoimmune diabetesAntigen-specific CD4Expression of Foxp3Young NOD miceT cell-T cellMarkers in vitroType 1 diabetesAdoptive transferTreg cellsBile acid-gut microbiota imbalance in cholestasis and its long-term effect in mice
Yang X, Xu Y, Li J, Ran X, Gu Z, Song L, Zhang L, Wen L, Ji G, Wang R. Bile acid-gut microbiota imbalance in cholestasis and its long-term effect in mice. MSystems 2024, 9: e00127-24. PMID: 38934542, PMCID: PMC11265269, DOI: 10.1128/msystems.00127-24.Peer-Reviewed Original ResearchCitationsConceptsGut microbiotaGut microbiota dysbiosisDysregulated gut microbiotaGut microbiota transplantationGerm-free miceVirulence factorsSmall intestinal bacteriaBile acid homeostasisMicrobiota dysbiosisDecreased diversityMicrobiota imbalanceMicrobiotaMouse model of cholestasisBile acidsMouse modelIntestinal bacteriaAcid homeostasisMicrobiota transplantationClinical management of patientsGutHepatic bile acidsLong-term effectsPre-clinical findingsModel of cholestasisManagement of patientsGut microbiota from B-cell-specific TLR9-deficient NOD mice promote IL-10+ Breg cells and protect against T1D
Yang X, Huang J, Peng J, Wang P, Wong F, Wang R, Wang D, Wen L. Gut microbiota from B-cell-specific TLR9-deficient NOD mice promote IL-10+ Breg cells and protect against T1D. Frontiers In Immunology 2024, 15: 1413177. PMID: 38903498, PMCID: PMC11187306, DOI: 10.3389/fimmu.2024.1413177.Peer-Reviewed Original ResearchCitationsAltmetricConceptsGut microbiotaGerm-free miceToll-like receptor 9Increased gut permeabilityIntestinal microbiotaGut permeabilityT1D developmentGut microbiota compositionFecal samplesTransferred to germ-free miceGut barrier integrityBreg cell differentiationMicrobiota influenceMucin degradationMicrobiota compositionBreg cellsAltered microbiotaMicrobiota impactMicrobiotaGene expressionImmune regulationDevelopment of T1DCell differentiationGutNOD mice
Academic Achievements & Community Involvement
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- September 16, 2024
Treating Obesity with Gut Microbiota
- August 14, 2024
A Link Between the Immune System and Obesity
- December 07, 2022
New Professors in Department of Internal Medicine (December 2022)
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