Search results for "t-lymphocytes"

showing 10 items of 1380 documents

Cutting Edge: Trans-Signaling via the Soluble IL-6R Abrogates the Induction of FoxP3 in Naive CD4+CD25− T Cells

2007

Abstract Chronic inflammatory diseases may develop when regulatory T cells (Tregs) fail to control the balance between tolerance and immunity. Alternatively, activated immune cells might prevent the induction or activation of Tregs in such diseases. In this study, we demonstrate that trans-signaling into T cells via the soluble IL-6 receptor completely abrogates the de novo induction of adaptive Tregs. Mechanistically, IL-6 trans-signaling augmented the expression of the TGF-β signaling inhibitor SMAD7. Consequently, SMAD7 overexpression in T cells using newly created transgenic mice rendered CD4+CD25− T cells resistant to the induction of FoxP3. Finally, IL-6 trans-signaling inhibited Treg…

Regulatory T cellImmunologyMice Transgenicchemical and pharmacologic phenomenaMice SCIDBiologyT-Lymphocytes RegulatoryAutoimmune DiseasesSmad7 ProteinMiceInterleukin 21Immune systemTransforming Growth Factor betaImmunitymedicineAnimalsHumansImmunology and AllergyCytotoxic T cellIL-2 receptorInflammationMice Inbred BALB CInterleukin-6ZAP70FOXP3Forkhead Transcription FactorsColitisReceptors Interleukin-6Cell biologyDisease Models Animalmedicine.anatomical_structureGene Expression RegulationChronic DiseaseImmunologySignal TransductionThe Journal of Immunology
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Large scale preparation of human MHC class II+ integrin beta(1)+ Tregs.

2010

Abstract The human CD4 + CD25 + FoxP3 + regulatory T cell population (Tregs) contains both MHC class II + and MHC class II − cells. MHC class II + Tregs belong to the integrin α 4 β 1 + subpopulation and exclusively execute contact-dependent suppressive activity. Here we present a method optimized for isolation of these MHC class II expressing Tregs from large leukaphereses products using magnetic microbeads that achieves a reproducible purity of more than 90% and enables the use of this small-sized Treg population in pre-clinical application and basic research.

Regulatory T cellImmunologyPopulationIntegrinchemical and pharmacologic phenomenaIntegrin alpha4beta1T-Lymphocytes RegulatoryT-Lymphocyte SubsetsmedicineImmune ToleranceImmunology and AllergyHumansIL-2 receptorLeukapheresiseducationCells CulturedMHC class IIeducation.field_of_studybiologyImmunomagnetic SeparationHistocompatibility Antigens Class IIInterleukin-2 Receptor alpha SubunitFOXP3hemic and immune systemsForkhead Transcription FactorsT lymphocyteMHC restrictionFlow CytometryCell biologyHigh-Throughput Screening Assaysmedicine.anatomical_structureImmunologyCD4 Antigensbiology.proteinJournal of immunological methods
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Tumor cells convert immature myeloid dendritic cells into TGF-β–secreting cells inducing CD4+CD25+ regulatory T cell proliferation

2005

The mechanisms through which regulatory T cells accumulate in lymphoid organs of tumor-bearing hosts remain elusive. Our experiments indicate that the accumulation of CD4+CD25+ regulatory T cells (T reg cells) expressing FoxP3 and exhibiting immunosuppressive function originates from the proliferation of naturally occurring CD25+ T cells and requires signaling through transforming growth factor (TGF)–β receptor II. During tumor progression, a subset of dendritic cells (DCs) exhibiting a myeloid immature phenotype is recruited to draining lymph nodes. This DC subset selectively promotes the proliferation of T reg cells in a TGF-β–dependent manner in mice and rats. Tumor cells are necessary a…

Regulatory T cellImmunologychemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryArticleMiceInterleukin 21Transforming Growth Factor betaCell Line TumorNeoplasmsmedicineAnimalsImmunology and AllergyCytotoxic T cellIL-2 receptorAntigen-presenting cellCell ProliferationDNA PrimersInterleukin 3Reverse Transcriptase Polymerase Chain ReactionCell DifferentiationForkhead Transcription FactorsRats Inbred Strainshemic and immune systemsDendritic CellsNatural killer T cellImmunohistochemistryMolecular biologyRatsCell biologymedicine.anatomical_structureBromodeoxyuridineInterleukin 12Receptors Transforming Growth Factor betaSignal TransductionJournal of Experimental Medicine
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Immunopathology of leishmaniasis: an update.

2007

Leishmaniasis represents a severe, increasing, public health problem. The perspective of its control is highly dependent on research progress, on therapeutic manipulations of the immune system, and on vaccine development. There is a correlation between the clinical outcome of Leishmania infection and the cytokine response profile. While a protective immune response against Leishmania has been clearly identified to be related to the influence of a type-1 response and IFN-γ production, the precise role of T helper (TH) 2 cytokines in non-healing infections requires further exploration. IL-4 and IL-13 (TH2 cytokines) can promote disease progression in cutaneous leishmaniasis, whereas IL-4 woul…

Regulatory T cellImmunopathology; LeishmaniasisengT-LymphocytesImmunologyApoptosisImmunopathology03 medical and health sciences0302 clinical medicineImmune systemCutaneous leishmaniasisImmunopathologyLeishmaniasisengmedicineImmunology and AllergyAnimalsHumansLeishmaniasisPharmacologybiologybusiness.industryLeishmaniasismedicine.diseaseLeishmaniabiology.organism_classificationmedicine.anatomical_structureVisceral leishmaniasis030220 oncology & carcinogenesisImmunologybusinessCD8030215 immunologyInternational journal of immunopathology and pharmacology
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DRB1*0401-restricted human T cell clone specific for the major proinsulin73-90 epitope expresses a down-regulatory T helper 2 phenotype.

2006

Recently, we have identified proinsulin (P-Ins) 73-90 as an immunodominant T cell epitope of HLA-DRB1*0401 (DR4) subjects with β-islet cell autoimmunity and of HLA-DR4/CD4 double-transgenic mice immunized with human P-Ins. We have compared the fine specificities of one human CD4 T cell clone and two mouse T cell hybridoma clones recognizing this epitope, and, although these three clones all recognized the same core region (LALEGSLQK), there were major differences in how they interacted with the peptide (p)/HLA complex, reflecting the fact that human P-Ins is a foreign antigen in the mouse and an autoantigen in the type 1 diabetes patient. The human T cell clone was forkhead transcription f…

Regulatory T cellT cellT-LymphocytesMolecular Sequence DataClone (cell biology)Mice TransgenicHuman leukocyte antigenBiologyEpitopeEpitopesMiceAntigenT-Lymphocyte SubsetsmedicineCytotoxic T cellAnimalsHumansAmino Acid SequenceAmino AcidsMultidisciplinaryFOXP3Forkhead Transcription FactorsHLA-DR AntigensBiological SciencesMolecular biologyPeptide Fragmentsmedicine.anatomical_structurePhenotypeHLA-DRB1 ChainsProinsulinProceedings of the National Academy of Sciences of the United States of America
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The ubiquitin-specific protease USP8 is critical for the development and homeostasis of T cells

2015

The modification of proteins by ubiquitin has a major role in cells of the immune system and is counteracted by various deubiquitinating enzymes (DUBs) with poorly defined functions. Here we identified the ubiquitin-specific protease USP8 as a regulatory component of the T cell antigen receptor (TCR) signalosome that interacted with the adaptor Gads and the regulatory molecule 14-3-3β. Caspase-dependent processing of USP8 occurred after stimulation of the TCR. T cell-specific deletion of USP8 in mice revealed that USP8 was essential for thymocyte maturation and upregulation of the gene encoding the cytokine receptor IL-7Rα mediated by the transcription factor Foxo1. Mice with T cell-specifi…

Regulatory T cellT-LymphocytesImmunologyReceptors Antigen T-Cell610 Medicine & healthBiologyCD8-Positive T-LymphocytesJurkat cellsJurkat CellsMiceddc:570EndopeptidasesmedicineImmunology and AllergyAnimalsHomeostasisHumans10239 Institute of Laboratory Animal ScienceIL-2 receptorAdaptor Proteins Signal Transducing2403 ImmunologyReceptors Interleukin-7ThymocytesEndosomal Sorting Complexes Required for TransportForkhead Box Protein O1ZAP70T-cell receptorCD28Cell DifferentiationForkhead Transcription FactorsColitisCell biologyThymocytemedicine.anatomical_structure2723 Immunology and Allergy570 Life sciences; biology590 Animals (Zoology)Ubiquitin ThiolesteraseCD8
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Mast cells counteract regulatory T-cell suppression through interleukin-6 and OX40/OX40L axis toward Th17-cell differentiation

2009

Abstract The development of inflammatory diseases implies inactivation of regulatory T (Treg) cells through mechanisms that still are largely unknown. Here we showed that mast cells (MCs), an early source of inflammatory mediators, are able to counteract Treg inhibition over effector T cells. To gain insight into the molecules involved in their interplay, we set up an in vitro system in which all 3 cellular components were put in contact. Reversal of Treg suppression required T cell–derived interleukin-6 (IL-6) and the OX40/OX40L axis. In the presence of activated MCs, concomitant abundance of IL-6 and paucity of Th1/Th2 cytokines skewed Tregs and effector T cells into IL-17–producing T cel…

Regulatory T cellmedicine.medical_treatmentCellular differentiationImmunologyPriming (immunology)chemical and pharmacologic phenomenaMice TransgenicMast cell; T regulatory cell; Immune responseBiologyLymphocyte ActivationT-Lymphocytes RegulatoryBiochemistryImmune toleranceMiceMice CongenicmedicineImmune ToleranceMast CellT regulatory cellImmune responseCells CulturedCell ProliferationAnimalInterleukin-6Experimental autoimmune encephalomyelitisInterleukin-17hemic and immune systemsCell DifferentiationT lymphocyteT-Lymphocytes Helper-InducerHematologyCell BiologyReceptors OX40medicine.diseaseCell biologyMice Inbred C57BLmedicine.anatomical_structureCytokineImmunologyAnimals; Cell Differentiation; Cell Proliferation; Cells Cultured; Immune Tolerance; Interleukin-17; Interleukin-6; Lymphocyte Activation; Mast Cells; Membrane Glycoproteins; Mice; Mice Congenic; Mice Inbred C57BL; Mice Transgenic; Receptors OX40; Signal Transduction; T-Lymphocytes Helper-Inducer; T-Lymphocytes Regulatory; Tumor Necrosis Factors; Hematology; Biochemistry; Cell Biology; ImmunologyInterleukin 17Membrane GlycoproteinTumor Necrosis FactorSignal Transduction
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Proliferative activity in stenotic human aortocoronary bypass grafts

2002

Abstract Background: Aortocoronary bypass graft disease is responsible for long-term failure of autologous vein grafts. The analyses of proliferation and cell type characterisation in human bypass grafts harvested during re-do surgery make it possible to investigate the cellular processes leading to bypass graft failure. Methods: 30 stenotic vein grafts and 25 control veins were explantated during re-do heart surgery procedures. The total area and cell count of the neointima, media and adventitia were calculated computer-assisted. Actively proliferating cells were identified using antibody to Ki-67 and positive cells were determined by double-label immunocytochemistry with SMC α-actin, CD 3…

ReoperationNeointimaCell typemedicine.medical_specialtyPathologyProliferation indexT-LymphocytesImmunocytochemistryCellCell CountBypass graftsMuscle Smooth VascularPathology and Forensic MedicineAntigens CDAdventitiaInternal medicineHumansMedicineSaphenous VeinCoronary Artery Bypassbiologybusiness.industryMacrophagesGraft SurvivalGraft Occlusion VascularGeneral MedicineImmunohistochemistryActinsKi-67 Antigenmedicine.anatomical_structurecardiovascular systembiology.proteinCardiologyAntibodyCardiology and Cardiovascular MedicinebusinessBiomarkersCell DivisionCardiovascular Pathology
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Neuroinflammation by cytotoxic T-lymphocytes impairs retrograde axonal transport in an oligodendrocyte mutant mouse.

2012

Mice overexpressing proteolipid protein (PLP) develop a leukodystrophy-like disease involving cytotoxic, CD8+ T-lymphocytes. Here we show that these cytotoxic T-lymphocytes perturb retrograde axonal transport. Using fluorogold stereotactically injected into the colliculus superior, we found that PLP overexpression in oligodendrocytes led to significantly reduced retrograde axonal transport in retina ganglion cell axons. We also observed an accumulation of mitochondria in the juxtaparanodal axonal swellings, indicative for a disturbed axonal transport. PLP overexpression in the absence of T-lymphocytes rescued retrograde axonal transport defects and abolished axonal swellings. Bone marrow tr…

Retinal Ganglion CellsProteolipid protein 1MouseCD8-Positive T-LymphocytesGranzymesMyelinMiceBone Marrow TransplantationNeuronsddc:616MultidisciplinarybiologyQRNeurodegenerative DiseasesAnimal ModelsCell biologyOligodendrogliamedicine.anatomical_structureNeurologyMedicineResearch ArticleHeterozygoteMultiple SclerosisProteolipidsScienceImmunologyMice Transgenicchemical and pharmacologic phenomenaAutoimmune DiseasesModel OrganismsmedicineAnimalsBiologyNeuroinflammationInflammationImmunityDemyelinating DisordersOligodendrocyteAxonsGranzyme BPerforinGranzymenervous systemImmune SystemImmunologyMutationAxoplasmic transportbiology.proteinClinical ImmunologyMolecular NeuroscienceT-Lymphocytes CytotoxicNeurosciencePLoS ONE
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Bacterial and viral infections and related inflammatory responses in chronic obstructive pulmonary disease

2021

Abstract In chronic obstructive pulmonary disease (COPD) patients, bacterial and viral infections play a relevant role in worsening lung function and, therefore, favour disease progression. The inflammatory response to lung infections may become a specific indication of the bacterial and viral infections. We here review data on the bacterial–viral infections and related airways and lung parenchyma inflammation in stable and exacerbated COPD, focussing our attention on the prevalent molecular pathways in these different clinical conditions. The roles of macrophages, autophagy and NETosis are also briefly discussed in the context of lung infections in COPD. Controlling their combined response…

Review ArticleNK cells030204 cardiovascular system & hematologyAdaptive Immunitymedicine.disease_causeAutoimmunityPulmonary Disease Chronic Obstructive0302 clinical medicineNETosiPulmonary Medicine030212 general & internal medicineLungRespiratory Tract InfectionsT-lymphocytesCOPDB cellpyroptosisautoimmunityPyroptosisNETosisGeneral Medicinerespiratory systemAcquired immune systemmacrophagesmedicine.anatomical_structureautoimmunity; autophagy; B cells; dendritic cells; disability; ILCs; macrophages; NETosis; NK cells; outcome; pyroptosis; T-lymphocytesDisease Progressionoutcomemedicine.symptomSignal Transductionautophagydendritic cellILCsContext (language use)Inflammationmacrophage03 medical and health sciencesImmune systemmedicineHumansNK celldendritic cellsB cellsLungbusiness.industrymedicine.diseaseImmunity Innaterespiratory tract diseasespyroptosiILCdisabilityImmunologybusiness
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