2010
CD69 limits early inflammatory diseases associated with immune response to Listeria monocytogenes infection
Vega‐Ramos J, Alari‐Pahissa E, del Valle J, Carrasco‐Marín E, Esplugues E, Borràs M, Martínez‐A C, Lauzurica P. CD69 limits early inflammatory diseases associated with immune response to Listeria monocytogenes infection. Immunology And Cell Biology 2010, 88: 707-715. PMID: 20440294, DOI: 10.1038/icb.2010.62.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDAntigens, Differentiation, T-LymphocyteApoptosisDendritic CellsDNA-Binding ProteinsImmunity, InnateInflammationInterferon Type IInterferon-gammaLectins, C-TypeListeriosisLiverMacrophages, PeritonealMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutSpleenT-LymphocytesTransforming Growth Factor beta1ConceptsListeria monocytogenes infectionMonocytogenes infectionT cellsLM-specific T cellsEarly inflammatory diseaseInfection-induced immunopathologyPotent inflammatory responseBone marrow-derived macrophagesMarrow-derived macrophagesWild-type controlsDendritic cellsTh1 cytokinesImmune pathologyLM infectionInflammatory diseasesInflammatory responseImmune responseLymphocyte apoptosisHost protectionSpleen damageDay 1CD69Mouse infectionCell activationIFN enhancement
2006
CD69 targeting differentially affects the course of collagen-induced arthritis
Sancho D, Gómez M, del Hoyo G, Lamana A, Esplugues E, Lauzurica P, Martinez-A C, Sánchez-Madrid F. CD69 targeting differentially affects the course of collagen-induced arthritis. Journal Of Leukocyte Biology 2006, 80: 1233-1241. PMID: 16921025, DOI: 10.1189/jlb.1205749.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsAntibodies, MonoclonalAntigens, CDAntigens, Differentiation, T-LymphocyteArthritis, ExperimentalCell ProliferationCollagen Type IIImmunoglobulin GInflammationInterferon-gammaLectins, C-TypeLymphocyte DepletionMiceMice, Inbred BALB CMice, Inbred DBAMice, KnockoutT-LymphocytesConceptsCollagen-induced arthritisCII-specific T cellsLymphocyte proliferative responsesChronic inflammatory diseaseActivation of leukocytesWild-type animalsInflammation correlatesAdoptive transferDBA/1 miceProinflammatory cytokinesInflammatory diseasesInflammatory fociCD69 expressionCD69 mAbT cellsImmune responseIFN-gammaInflammatory sitesProliferative responseCD69Type II collagenArthritisDecreased productionDiseaseMice
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, Martín 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 evidenceInduction of tumor NK-cell immunity by anti-CD69 antibody therapy
Esplugues E, Vega-Ramos J, Cartoixà D, Vazquez BN, Salaet I, Engel P, Lauzurica P. Induction of tumor NK-cell immunity by anti-CD69 antibody therapy. Blood 2005, 105: 4399-4406. PMID: 15692061, DOI: 10.1182/blood-2004-10-3854.Peer-Reviewed Original ResearchConceptsAntitumor responseNK cell cytolytic activityMonoclonal antibodiesCD69 monoclonal antibodiesNK cell immunityNK cytotoxic activityInterferon-gamma productionTGF-beta productionActivation marker CD69Production of cytokinesInnate immune systemReceptor-independent mannerNK cellsAntibody therapyLung metastasesCD69 expressionTherapeutic administrationCD69 mAbImmune responseCytolytic activityGamma productionImmune systemTumor growthTumor primingCD69
2003
CD69 downregulates autoimmune reactivity through active transforming growth factor-β production in collagen-induced arthritis
Sancho D, Gómez M, Viedma F, Esplugues E, Gordón-Alonso M, García-López MA, de la Fuente H, Martínez-A C, Lauzurica P, Sánchez-Madrid F. CD69 downregulates autoimmune reactivity through active transforming growth factor-β production in collagen-induced arthritis. Journal Of Clinical Investigation 2003, 112: 872-882. PMID: 12975472, PMCID: PMC193672, DOI: 10.1172/jci19112.Peer-Reviewed Original ResearchConceptsCollagen-induced arthritisCD69-/- miceAutoimmune reactivitySeverity of CIAProinflammatory cytokine mRNA levelsB cell immune responsesProinflammatory cytokines IL-1betaCD69-deficient miceRole of CD69Cell immune responsesCytokine mRNA levelsCytokines IL-1betaActivation of leukocytesTGF-beta1 productionNegative cell linesSplenocyte subsetsProinflammatory mediatorsBeta antibodyIL-1betaInflammatory fociLocal injectionSynovial leukocytesImmune responseCIA severityInflammatory sitesEnhanced Antitumor Immunity in Mice Deficient in CD69
Esplugues E, Sancho D, Vega-Ramos J, Martínez-A C, Syrbe U, Hamann A, Engel P, Sánchez-Madrid F, Lauzurica P. Enhanced Antitumor Immunity in Mice Deficient in CD69. Journal Of Experimental Medicine 2003, 197: 1093-1106. PMID: 12732655, PMCID: PMC2193974, DOI: 10.1084/jem.20021337.Peer-Reviewed Original ResearchConceptsAnti-tumor responseCD69-/- miceEnhanced anti-tumor responseWT miceMHC class I- tumorsT cell productionTGF-beta productionChemokine MCP-1Wild-type miceTGF-beta regulationLocal lymphocytesAntitumor immunityVivo blockadeNK cellsAntibody treatmentI tumorsMCP-1CD69 expressionLymphocyte apoptosisMice DeficientTherapy of tumorsTumor growthCD69MiceVivo role
2001
CD84 Functions as a Homophilic Adhesion Molecule and Enhances IFN-γ Secretion: Adhesion Is Mediated by Ig-Like Domain 1
Martin M, Romero X, de la Fuente M, Tovar V, Zapater N, Esplugues E, Pizcueta P, Bosch J, Engel P. CD84 Functions as a Homophilic Adhesion Molecule and Enhances IFN-γ Secretion: Adhesion Is Mediated by Ig-Like Domain 1. The Journal Of Immunology 2001, 167: 3668-3676. PMID: 11564780, DOI: 10.4049/jimmunol.167.7.3668.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalAntigens, CDBinding, CompetitiveCell AdhesionCell Adhesion MoleculesCells, CulturedChildChild, PreschoolCOS CellsHumansImmunoglobulinsInterferon-gammaLymphocyte ActivationMembrane GlycoproteinsMiceProtein Structure, TertiarySignaling Lymphocytic Activation Molecule FamilyThymus GlandT-LymphocytesTumor Cells, CulturedConceptsFusion proteinExtracellular domainSoluble Ig fusion proteinDomain 1Homophilic adhesion moleculeFirst extracellular domainLymphoproliferative disease geneReceptor-ligand interactionsIg-like domains 1Cytoplasmic tailProtein 1ADisease genesCell surface moleculesHuman CD84Ligand-receptor recognitionCD2 familyMature T cellsCD84Own ligandConcurrent ligationMouse chimerasReceptor recognitionIg fusion proteinProteinCell maturation