2025
Hypercholesterolemia-induced LXR signaling in smooth muscle cells contributes to vascular lesion remodeling and visceral function
Zhang H, de Urturi D, Fernández-Tussy P, Huang Y, Jovin D, Zhang X, Huang S, Lek M, da Silva Catarino J, Sternak M, Citrin K, Swirski F, Gustafsson J, Greif D, Esplugues E, Biwer L, Suárez Y, Fernández-Hernando C. Hypercholesterolemia-induced LXR signaling in smooth muscle cells contributes to vascular lesion remodeling and visceral function. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2417512122. PMID: 40035761, PMCID: PMC11912459, DOI: 10.1073/pnas.2417512122.Peer-Reviewed Original ResearchConceptsVascular smooth muscle cellsSmooth muscle cellsLiver X receptorLesion remodelingMuscle cellsVascular functionArterial media layerContribution of lipid metabolismPhenotypic switchingRegulate vascular toneMonocyte-derived macrophagesLipid metabolismPhenotypic switching of vascular smooth muscle cellsSwitching of vascular smooth muscle cellsNecrotic core areaRegulate vascular functionFoam cell populationVisceral myopathyBladder remodelingAortic atheromaFibrous cap thicknessRemodeling in vivoLipid malabsorptionVascular toneAbundant cell type
2017
TH17 cells express ST2 and are controlled by the alarmin IL-33 in the small intestine
Pascual-Reguant A, 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 ResearchConceptsPro-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 ResearchConceptsIL-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
2011
miR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling
Dávalos A, Goedeke L, Smibert P, RamÃrez CM, Warrier NP, Andreo U, Cirera-Salinas D, Rayner K, Suresh U, Pastor-Pareja JC, Esplugues E, Fisher EA, Penalva LO, Moore KJ, Suárez Y, Lai EC, Fernández-Hernando C. miR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling. Proceedings Of The National Academy Of Sciences Of The United States Of America 2011, 108: 9232-9237. PMID: 21576456, PMCID: PMC3107310, DOI: 10.1073/pnas.1102281108.Peer-Reviewed Original ResearchConceptsFatty acid metabolismFatty acid oxidationMiR-33aInsulin receptor substrate 2Sirtuin 6Acid metabolismInsulin-signaling pathwayIntronic microRNAsSterol regulatory element-binding protein 2Acid oxidationHost genesKey enzymeHepatic cell linesMetabolic syndromeCarnitine palmitoyltransferase 1AMetabolic pathwaysSubstrate 2Cellular imbalanceProtein 2Cholesterol homeostasisGenesCell linesLevels of HDLPathwayMetabolism resultsTh17 Cells Express Interleukin-10 Receptor and Are Controlled by Foxp3− and Foxp3+ Regulatory CD4+ T Cells in an Interleukin-10-Dependent Manner
Huber S, Gagliani N, Esplugues E, O'Connor W, Huber FJ, Chaudhry A, Kamanaka M, Kobayashi Y, Booth CJ, Rudensky AY, Roncarolo MG, Battaglia M, Flavell RA. Th17 Cells Express Interleukin-10 Receptor and Are Controlled by Foxp3− and Foxp3+ Regulatory CD4+ T Cells in an Interleukin-10-Dependent Manner. Immunity 2011, 34: 554-565. PMID: 21511184, PMCID: PMC3113617, DOI: 10.1016/j.immuni.2011.01.020.Peer-Reviewed Original ResearchConceptsIL-10 signalingT cellsIL-10-dependent mannerIL-10-producing cellsIL-17A-producing CD4T cell-specific blockadeT helper 17 (Th17) cellsHelper 17 cellsIL-10 treatmentChronic inflammatory diseaseInterleukin-10 receptorRegulatory CD4Intestinal inflammationRegulatory cellsInflammatory diseasesExtracellular microorganismsReceptor αCell frequencySmall intestineHost defenseCD4Selective increaseDirect signalingVivoCells
2005
The Adaptor Protein 3BP2 Binds Human CD244 and Links this Receptor to Vav Signaling, ERK Activation, and NK Cell Killing
Saborit-Villarroya I, Del Valle J, Romero X, Esplugues E, Lauzurica P, Engel P, MartÃn M. The Adaptor Protein 3BP2 Binds Human CD244 and Links this Receptor to Vav Signaling, ERK Activation, and NK Cell Killing. The Journal Of Immunology 2005, 175: 4226-4235. PMID: 16177062, DOI: 10.4049/jimmunol.175.7.4226.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsAntigens, CDCell Line, TumorCoculture TechniquesCytotoxicity, ImmunologicExtracellular Signal-Regulated MAP KinasesHumansInterferon-gammaKiller Cells, NaturalLigandsMembrane GlycoproteinsMicePhosphorylationReceptors, ImmunologicSignal TransductionSignaling Lymphocytic Activation Molecule FamilyYeastsConceptsERK activationSrc homology 2 domainThree-hybrid analysisDisease gene productCell surface proteinsLymphocytic activation molecule-associated proteinSAP recruitmentAdaptor proteinConsensus motifGene productsAdaptor 3BP2CD150 familySurface proteinsSAP associationPhysical interactionProteinCellular activationPhosphorylationCell killingMyeloid cellsMotifCellsActivationBindingPresent evidence
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