Enric Esplugues, PhD
Associate Research ScientistDownloadHi-Res Photo
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Comparative Medicine
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Associate Research Scientist
Biography
Enric Esplugues studied Biology (Biomedicine) at the University of Barcelona. From 1998 to 2003, he performed his PhD with Prof. Pilar Lauzurica at the Department of Cell Biology, Physiology and Immunology at the University of Barcelona. He did his postdoctoral training with Prof. Richard Flavell at Yale School of Medicine (2005-2008). He was Associate Research Scientist at the Immunobiology Department from 2008 to 2011. Then, Enric started his laboratory as an Assistant Professor of Medicine in the Immunology Institute at the Icahn School of Medicine at Mount Sinai (New York). He is currently a Research Scientist in the Immunobiology Department at Yale School of Medicine.
Appointments
Comparative Medicine
Associate Research ScientistPrimary
Other Departments & Organizations
Education & Training
- Postdoc
- Yale School of Medicine (2008)
- PhD
- University of Barcelona (2003)
Research
Overview
Medical Research Interests
Autoimmune Diseases; Autoimmunity; Immune System Diseases
Public Health Interests
Cancer; Nutrition
Research at a Glance
Yale Co-Authors
Frequent collaborators of Enric Esplugues's published research.
Publications Timeline
A big-picture view of Enric Esplugues's research output by year.
Research Interests
Research topics Enric Esplugues is interested in exploring.
Yajaira Suarez, PhD
Carlos Fernandez-Hernando, PhD
Joseph Craft, MD
Hanming Zhang, PhD
Akiko Iwasaki, PhD
Daniel Greif, MD
38Publications
4,959Citations
Autoimmunity
Autoimmune Diseases
Immune System Diseases
Publications
2024
Abstract 129: Hypercholesterolemia-induced Lxr Signaling In Smc Contributes To Atherosclerotic Lesion Remodeling And Regulates Vascular And Visceral Smc Function
Zhang H, Biwer L, de Urturi D, Fernandez-Tussy P, Jovin D, Huang Y, Zhang X, Esplugues E, Greif D, Suarez Y, Fernandez-Hernando C. Abstract 129: Hypercholesterolemia-induced Lxr Signaling In Smc Contributes To Atherosclerotic Lesion Remodeling And Regulates Vascular And Visceral Smc Function. Arteriosclerosis Thrombosis And Vascular Biology 2024, 44: a129-a129. DOI: 10.1161/atvb.44.suppl_1.129.Peer-Reviewed Original ResearchConceptsLiver X receptorTranscription factorsVascular smooth muscle cellsRegulation of lipid metabolismLXR signalingB geneScRNA-seqFate decisionsSignaling eventsSMC functionGene expressionActivation of liver X receptorCell statesLesion remodelingCharacterized miceLipid metabolismLineage tracingPhenotypic switchingX receptorReduced fibrous cap thicknessTranscriptionFeatures of plaque instabilitySmooth muscle cellsLipid absorptionProgression of atherosclerosisFatty acid binding protein 5 suppression attenuates obesity-induced hepatocellular carcinoma by promoting ferroptosis and intratumoral immune rewiring
Sun J, Esplugues E, Bort A, Cardelo M, Ruz-Maldonado I, Fernández-Tussy P, Wong C, Wang H, Ojima I, Kaczocha M, Perry R, Suárez Y, Fernández-Hernando C. Fatty acid binding protein 5 suppression attenuates obesity-induced hepatocellular carcinoma by promoting ferroptosis and intratumoral immune rewiring. Nature Metabolism 2024, 6: 741-763. PMID: 38664583, DOI: 10.1038/s42255-024-01019-6.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsFatty acid binding protein 5Tumor-associated macrophagesHepatocellular carcinomaImmunosuppressive phenotype of tumor-associated macrophagesIncreased CD8+ T cell activationCD8+ T cell activationPhenotype of tumor-associated macrophagesPro-inflammatory tumor microenvironmentCo-stimulatory molecules CD80T cell activationHepatocellular carcinoma burdenTransformation of hepatocytesBinding protein 5Potential therapeutic approachImmunosuppressive phenotypeTumor microenvironmentFerroptosis-induced cell deathMale miceEnhanced ferroptosisTherapeutic approachesPharmacological inhibitionGenetic ablationIncreased expressionSingle-cell atlasAnalysis of transformed cellsDynamic metabolism of endothelial triglycerides protects against atherosclerosis in mice
Boutagy N, Gamez-Mendez A, Fowler J, Zhang H, Chaube B, Esplugues E, Kuo A, Lee S, Horikami D, Zhang J, Citrin K, Singh A, Coon B, Lee M, Suarez Y, Fernandez-Hernando C, Sessa W. Dynamic metabolism of endothelial triglycerides protects against atherosclerosis in mice. Journal Of Clinical Investigation 2024, 134: e170453. PMID: 38175710, PMCID: PMC10866653, DOI: 10.1172/jci170453.Peer-Reviewed Original ResearchCitationsAltmetric
2023
SARS-CoV-2-encoded small RNAs are able to repress the host expression of SERINC5 to facilitate viral replication
Meseguer S, Rubio M, Lainez B, Pérez-Benavente B, Pérez-Moraga R, Romera-Giner S, García-García F, Martinez-Macias O, Cremades A, Iborra F, Candelas-Rivera O, Almazan F, Esplugues E. SARS-CoV-2-encoded small RNAs are able to repress the host expression of SERINC5 to facilitate viral replication. Frontiers In Microbiology 2023, 14: 1066493. PMID: 36876111, PMCID: PMC9978209, DOI: 10.3389/fmicb.2023.1066493.Peer-Reviewed Original ResearchCitationsAltmetricConceptsViral infectionSARS-CoV-2 viral infectionSARS-CoV-2 infectionCOVID-19 patientsMitochondrial antiviral signaling proteinInnate immunity factorsInnate immune responseVero E6 cellsSARS-CoV-2Viral proteinsImmune responseE6 cellsTherapeutic potentialViral replicationInfectionVero E6Immunity factorsSmall viral RNAsCertain virusesProtein 5SERINC5 expressionViral RNAHost expressionDifferent virusesVirus
2020
The induction and function of the anti-inflammatory fate of TH17 cells
Xu H, Agalioti T, Zhao J, Steglich B, Wahib R, Vesely MCA, Bielecki P, Bailis W, Jackson R, Perez D, Izbicki J, Licona-Limón P, Kaartinen V, Geginat J, Esplugues E, Tolosa E, Huber S, Flavell RA, Gagliani N. The induction and function of the anti-inflammatory fate of TH17 cells. Nature Communications 2020, 11: 3334. PMID: 32620760, PMCID: PMC7335205, DOI: 10.1038/s41467-020-17097-5.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and Concepts
2019
Effector TH17 Cells Give Rise to Long-Lived TRM Cells that Are Essential for an Immediate Response against Bacterial Infection
Vesely M, Pallis P, Bielecki P, Low JS, Zhao J, Harman CCD, Kroehling L, Jackson R, Bailis W, Licona-Limón P, Xu H, Iijima N, Pillai PS, Kaplan DH, Weaver CT, Kluger Y, Kowalczyk MS, Iwasaki A, Pereira JP, Esplugues E, Gagliani N, Flavell RA. Effector TH17 Cells Give Rise to Long-Lived TRM Cells that Are Essential for an Immediate Response against Bacterial Infection. Cell 2019, 178: 1176-1188.e15. PMID: 31442406, PMCID: PMC7057720, DOI: 10.1016/j.cell.2019.07.032.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsCD4 TTissue-resident memory T cellsBacterial infectionsResident memory T cellsFunction of airwayLife-long protectionEffector memory TMemory T cellsTh17 cellsTRM cellsΓδ TEffector cellsMemory TBacterial clearanceT cellsIL-7Adaptive immunityMouse modelMemory responsesVaccine designHost defenseLymphatic endothelial cellsDepletion studiesEndothelial cellsCellular origin
2018
Microbiota-driven interleukin-17-producing cells and eosinophils synergize to accelerate multiple myeloma progression
Calcinotto A, Brevi A, Chesi M, Ferrarese R, Garcia Perez L, Grioni M, Kumar S, Garbitt VM, Sharik ME, Henderson KJ, Tonon G, Tomura M, Miwa Y, Esplugues E, Flavell RA, Huber S, Canducci F, Rajkumar VS, Bergsagel PL, Bellone M. Microbiota-driven interleukin-17-producing cells and eosinophils synergize to accelerate multiple myeloma progression. Nature Communications 2018, 9: 4832. PMID: 30510245, PMCID: PMC6277390, DOI: 10.1038/s41467-018-07305-8.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsIL-17Multiple myelomaTh17 cellsDisease progressionBone marrowInterleukin-17-producing cellsFaster disease progressionMultiple myeloma progressionExtramucosal tumorsMM patientsAvailable therapiesIL-17RAIL-5Myeloma progressionPlasma cellsGut microbiotaCommensal bacteriaInnate immunityIntestinal microbesMurine plasma cellsPrevotella heparinolyticaEosinophilsMiceProgressionSTAT3 phosphorylation
2017
Intestinal type 1 regulatory T cells migrate to periphery to suppress diabetogenic T cells and prevent diabetes development
Yu H, Gagliani N, Ishigame H, Huber S, Zhu S, Esplugues E, Herold KC, Wen L, Flavell RA. Intestinal type 1 regulatory T cells migrate to periphery to suppress diabetogenic T cells and prevent diabetes development. Proceedings Of The National Academy Of Sciences Of The United States Of America 2017, 114: 10443-10448. PMID: 28894001, PMCID: PMC5625908, DOI: 10.1073/pnas.1705599114.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAdoptive TransferAnimalsCell- and Tissue-Based TherapyCell DifferentiationCell MovementCell ProliferationDiabetes Mellitus, Type 1DysbiosisFemaleGastrointestinal MicrobiomeImmune ToleranceInterleukin-10IntestinesMiceMice, Inbred NODMice, KnockoutReceptors, CCR4Receptors, CCR5Receptors, CCR7T-Lymphocytes, RegulatoryConceptsRegulatory T cellsTr1 cellsT cellsIL-10-producing type 1 regulatory T cellsType 1 regulatory T cellsAntigen-specific Tr1 cellsGut-associated lymphoid tissueDouble reporter miceDiabetogenic T cellsEffector T cellsDevelopment of diabetesT cells migrateIL-10 signalingType 1 diabetes managementIL-10R.NOD miceIL-10Diabetes incidenceDiabetes developmentAutoimmune diseasesTCR transgenicTh1 cellsLymphoid tissueChemokine receptorsPreclinical modelsTH17 cells express ST2 and are controlled by the alarmin IL-33 in the small intestine
Pascual-Reguant A, Bayat Sarmadi J, Baumann C, Noster R, Cirera-Salinas D, Curato C, Pelczar P, Huber S, Zielinski CE, Löhning M, Hauser AE, Esplugues E. TH17 cells express ST2 and are controlled by the alarmin IL-33 in the small intestine. Mucosal Immunology 2017, 10: 1431-1442. PMID: 28198366, DOI: 10.1038/mi.2017.5.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsPro-inflammatory TH17 cellsIntestinal epithelial cellsTh17 cellsSmall intestineIL-33IL-33/ST2 axisPro-inflammatory T cellsAlarmin IL-33Alarmin interleukin-33IL-33 receptorPro-inflammatory cytokinesAbsence of ST2Beneficial host responseIL-10Interleukin-33Autoimmune diseasesTissue inflammationInflammatory responseImmunosuppressive propertiesT cellsImmune responseInflamed tissuesHost responseImmune systemRegulatory phenotypeIL-10 Receptor Signaling Is Essential for TR1 Cell Function In Vivo
Brockmann L, Gagliani N, Steglich B, Giannou AD, Kempski J, Pelczar P, Geffken M, Mfarrej B, Huber F, Herkel J, Wan YY, Esplugues E, Battaglia M, Krebs CF, Flavell RA, Huber S. IL-10 Receptor Signaling Is Essential for TR1 Cell Function In Vivo. The Journal Of Immunology 2017, 198: 1130-1141. PMID: 28003377, PMCID: PMC5263184, DOI: 10.4049/jimmunol.1601045.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsIL-10 receptor signalingCell regulatory activityIL-10Receptor signalingIL-10 receptor expressionRegulatory type 1 (Tr1) cellsInflammatory bowel disease modelCell therapyInflammatory bowel diseaseIL-10 productionIL-10 receptorMurine inflammatory bowel disease modelT-cell therapyType 1 cellsBowel diseaseCell-based therapiesIL-10RαClinical trialsReceptor expressionIntestinal homeostasisSuppressive activityReporter miceTransgenic miceTherapyRegulatory activity
Academic Achievements & Community Involvement
honor CCFA Senior Award
National AwardCrohn's & Colitis Foundation of AmericaDetails07/01/2014United Stateshonor Ramon Margalef Award
International AwardUniversity of BarcelonaDetails05/23/2005Spain
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