Search results for "FOXP3"

showing 10 items of 140 documents

Enhanced production of CCL18 by tolerogenic dendritic cells is associated with inhibition of allergic airway reactivity

2012

Background IL-10–treated dendritic cells (DCs) have been shown to inhibit T-cell responses through induction of anergy and regulatory T cells in various model systems, including allergic inflammation, but the factors being involved in this inhibition are still unclear. Objective This study set out to analyze such factors produced or induced by IL-10–treated DCs by using gene expression profiling and to explore their function. Methods CD4 + T cells from allergic donors were stimulated with autologous monocyte-derived allergen-pulsed mature DCs or IL-10–treated DCs. After 24 hours, the transcriptional profile was analyzed by using Affymetrix technology. Results were validated by using quantit…

CD4-Positive T-LymphocytesChemokinemedicine.medical_treatmentImmunologyT-Lymphocytes RegulatoryAllergic inflammationMiceMice Inbred NODImmune ToleranceRespiratory HypersensitivitymedicineAnimalsHumansImmunology and AllergyCCL17dendritic cellsCells CulturedT(H)1/T(H)2 cellsMice KnockoutbiologyCCL18FOXP3regulationDendritic cellMicroarray AnalysisallergyCoculture TechniquesInterleukin-10Disease Models Animalhumanized miceCytokineChemokines CCImmunologyHumanized mousebiology.proteinChemokinesTranscriptomeJournal of Allergy and Clinical Immunology
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Regulatory T Cells Accumulate and Proliferate in the Ischemic Hemisphere for up to 30 Days after MCAO

2012

Local and peripheral immune responses are activated after ischemic stroke. In our present study, we investigated the temporal distribution, location, induction, and function of regulatory T cells (Tregs) and the possible involvement of microglia, macrophages, and dendritic cells after middle cerebral artery occlusion (MCAO). C57BL/6J and Foxp3EGFP transgenic mice were subjected to 30 minutes MCAO. On days 7, 14, and 30 after MCAO, Tregs and antigen presenting cells were analyzed using fluorescence activated cell sorting multicolor staining and immunohistochemistry. A strong accumulation of Tregs was observed on days 14 and 30 in the ischemic hemisphere accompanied by the elevated presence …

CD4-Positive T-LymphocytesGenetically modified mousePathologymedicine.medical_specialtyTime FactorsAntigen-Presenting CellsMice Transgenicchemical and pharmacologic phenomenaLymphocyte ActivationT-Lymphocytes RegulatoryNeuroprotectionFlow cytometryMice03 medical and health sciences0302 clinical medicineImmune systemGenes ReportermedicineAnimalsLymphocyte CountIL-2 receptorAntigen-presenting cellCell Proliferation030304 developmental biologyHomeodomain Proteins0303 health sciencesmedicine.diagnostic_testMicrogliabusiness.industryInterleukin-2 Receptor alpha SubunitFOXP3Forkhead Transcription FactorsInfarction Middle Cerebral Arteryhemic and immune systemsFlow CytometryImmunohistochemistryMice Inbred C57BLmedicine.anatomical_structureNeurology030220 oncology & carcinogenesisImmunologyOriginal ArticleNeurology (clinical)CorrigendumCardiology and Cardiovascular Medicinebusiness030217 neurology & neurosurgeryJournal of Cerebral Blood Flow & Metabolism
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Cutting Edge: TGF-β Induces a Regulatory Phenotype in CD4+CD25− T Cells through Foxp3 Induction and Down-Regulation of Smad7

2004

Abstract CD4+CD25+ regulatory cells are a subpopulation of T lymphocytes of thymic origin. However, recent data suggest an alternative commitment of regulatory T cells in the periphery, although the precise mechanism is unknown. In the present work, we demonstrate that TGF-β is able to induce Foxp3 expression and subsequently a regulatory phenotype in CD4+CD25− peripheral murine T cells. Similarly, TGF-β induced Foxp3 in human CD4+CD25− T cells. Moreover, we show that the inhibitory Smad7 protein that is normally induced by TGF-β and limits TGF-β signaling, is strongly down-regulated by Foxp3 at the transcriptional level. Foxp3-mediated down-regulation of Smad7 subsequently rendered CD4+CD2…

CD4-Positive T-LymphocytesImmunologyDown-Regulationchemical and pharmacologic phenomenaThymus GlandBiologyImmunophenotypingSmad7 ProteinMiceInterleukin 21Downregulation and upregulationT-Lymphocyte SubsetsTransforming Growth Factor betaTGF beta signaling pathwayAnimalsHumansImmunology and AllergyCytotoxic T cellIL-2 receptorCells CulturedZAP70FOXP3Cell DifferentiationForkhead Transcription FactorsReceptors Interleukin-2hemic and immune systemsPhenotypeCell biologyDNA-Binding ProteinsTrans-ActivatorsSpleenSignal TransductionThe Journal of Immunology
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Epicutaneous and Oral Low-Zone Tolerance Protects from Colitis in Mice

2016

Tolerance to environmental antigens that encounter the organism at interfaces like skin or gut prevents deleterious systemic immune responses. The aim of this study was to analyze whether and how low doses of haptens, by entry through the skin or gastrointestinal tract, affect the outcome of the predominantly Th1/Th17-mediated 2,4,6-trinitro-benzenesulfonic acid-induced colitis, which mimics an autoimmune bowl disease in man. Epicutaneous and oral applications of low doses of the allergen resulted in the induction of low-zone tolerance (LZT) and protected from colitis development, demonstrated by a significantly reduced inflammatory response of the gut in vivo. In line with this observation…

CD4-Positive T-LymphocytesMale0301 basic medicineAdoptive cell transferT cellAdministration Oralchemical and pharmacologic phenomenaDermatologyAdministration CutaneousDermatitis ContactT-Lymphocytes RegulatoryBiochemistryImmune toleranceMice03 medical and health sciences0302 clinical medicineImmune systemAntigenImmune TolerancemedicineAnimalsHumansIL-2 receptorColitisMolecular Biologybusiness.industryInterleukin-2 Receptor alpha SubunitFOXP3Cell BiologyAllergensColitismedicine.diseaseAdoptive TransferInterleukin-10Disease Models Animal030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisImmunologyFemalebusinessJournal of Investigative Dermatology
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Protein kinase CK2 enables regulatory T cells to suppress excessive TH2 responses in vivo

2014

The quality of the adaptive immune response depends on the differentiation of distinct CD4(+) helper T cell subsets, and the magnitude of an immune response is controlled by CD4(+)Foxp3(+) regulatory T cells (Treg cells). However, how a tissue- and cell type-specific suppressor program of Treg cells is mechanistically orchestrated has remained largely unexplored. Through the use of Treg cell-specific gene targeting, we found that the suppression of allergic immune responses in the lungs mediated by T helper type 2 (TH2) cells was dependent on the activity of the protein kinase CK2. Genetic ablation of the β-subunit of CK2 specifically in Treg cells resulted in the proliferation of a hithert…

CD4-Positive T-LymphocytesMaleT cellImmunologyMice TransgenicReceptors Cell Surfacechemical and pharmacologic phenomenaCell Growth ProcessesT-Lymphocytes RegulatoryCell LineMiceTh2 CellsImmune systemHypersensitivitymedicineAnimalsHumansImmunology and AllergyIL-2 receptorCasein Kinase IIMice Inbred BALB CChemistryPeripheral toleranceFOXP3Cell DifferentiationForkhead Transcription FactorsDendritic CellsAcquired immune systemCell biologyMice Inbred C57BLmedicine.anatomical_structureCell cultureInterferon Regulatory FactorsImmunologyLeukocytes MononuclearIRF4Nature Immunology
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Local blockade of IL-6R signaling induces lung CD4+ T cell apoptosis in a murine model of asthma via regulatory T cells.

2007

We previously reported high levels of the soluble form of the IL-6R (sIL-6R) in the airways of asthmatic subjects. Here, we analyzed the IL-6R effects on Th2 cell survival in the lung by locally antagonizing sIL-6R-mediated trans-signaling with a designer fusion protein (gp130-Fc) as well as IL-6R signaling with an antibody against the gp80 unit of the IL-6R (alphaIL-6R) in a murine model of asthma after ovalbumin peptide (OVA) sensitization and challenge. Blockade of the sIL-6R led to a significant decrease in inflammatory cells by an apoptosis-independent mechanism. In contrast, local treatment with alphaIL-6R antibodies that also block signaling via the membrane-bound IL-6R (mIL-6R) led …

CD4-Positive T-LymphocytesSTAT3 Transcription FactorOvalbuminT cellRecombinant Fusion ProteinsImmunologyGene ExpressionApoptosisBiologyT-Lymphocytes RegulatoryAntibodiesInterleukin 21MicemedicineCytokine Receptor gp130Immunology and AllergyCytotoxic T cellAnimalsIL-2 receptorPhosphorylationLungMice Inbred BALB CInterleukin-6FOXP3Forkhead Transcription FactorsGeneral MedicineT lymphocyterespiratory systemReceptors Interleukin-6AsthmaCoculture TechniquesImmunoglobulin Fc FragmentsDisease Models Animalmedicine.anatomical_structureApoptosisImmunologyCancer researchFemaleImmunizationSignal transductionBronchoalveolar Lavage FluidSignal TransductionInternational immunology
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miR-155 inhibition sensitizes CD4+ Th cells for TREG mediated suppression.

2009

BackgroundIn humans and mice naturally occurring CD4(+)CD25(+) regulatory T cells (nTregs) are a thymus-derived subset of T cells, crucial for the maintenance of peripheral tolerance by controlling not only potentially autoreactive T cells but virtually all cells of the adaptive and innate immune system. Recent work using Dicer-deficient mice irrevocably demonstrated the importance of miRNAs for nTreg cell-mediated tolerance.Principal findingsDNA-Microarray analyses of human as well as murine conventional CD4(+) Th cells and nTregs revealed a strong up-regulation of mature miR-155 (microRNA-155) upon activation in both populations. Studying miR-155 expression in FoxP3-deficient scurfy mice …

CD4-Positive T-LymphocytesScienceImmunology/ImmunomodulationBiologyModels BiologicalT-Lymphocytes RegulatoryImmune tolerancemiR-155MiceDownregulation and upregulationImmune ToleranceAnimalsHumansIL-2 receptorOligonucleotide Array Sequence AnalysisMultidisciplinaryInnate immune systemGenetics and Genomics/Functional GenomicsQInterleukin-2 Receptor alpha SubunitRPeripheral toleranceFOXP3Forkhead Transcription FactorsTransfectionImmunity InnateCell biologyUp-RegulationKineticsMicroRNAsImmunologyImmunology/Immune ResponseMedicineGenetics and Genomics/Genetics of the Immune SystemResearch ArticlePLoS ONE
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A CD40/CD40L feedback loop drives the breakdown of CD8+T-cell tolerance following depletion of suppressive CD4+T cells

2014

Dendritic cells (DCs) are the key APCs not only for the priming of naive T cells, but also for the induction and maintenance of peripheral T-cell tolerance. We have recently shown that cognate interactions between Foxp3(+) Tregs and steady-state DCs are crucial to maintain the tolerogenic potential of DCs. Using DIETER mice, which allow the induction of antigen presentation selectively on DCs without altering their maturation status, we show here that breakdown of CD8(+) T-cell tolerance, which ensues after depletion of suppressive CD4(+) T cells, is driven by a positive feedback loop in which autoreactive CD8(+) T cells activate DCs via CD40. These data identify ligation of CD40 on DCs as …

CD40ImmunologyAntigen presentationPriming (immunology)Peripheral toleranceFOXP3chemical and pharmacologic phenomenahemic and immune systemsBiologyImmune toleranceImmunologybiology.proteinImmunology and AllergyCytotoxic T cellAntigen-presenting cellEuropean Journal of Immunology
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Functionally Altered GPI-Anchor Negative Treg Following Alemtuzumab-Based T-Cell Depletion Are Associated with Acute Gvhd.

2012

Abstract Abstract 3059 Introduction: The monoclonal anti-CD52antibody Alemtuzumab is frequently used for T-cell depletion (TCD) in the context of allogeneic hematopoietic stem cell transplantation (HSCT) to prevent graft versus host disease (GVHD). We previously demonstrated the long term persistence of functionally impaired glycosylphosphatidylinositol (GPI)-anchor negative effector T-cells in patients receiving high dose (100mg) Alemtuzumab in combination with a dose reduced conditioning regimen (Fludarabin + Melpahlan) (Meyer, Wagner et al. BMT 2010). Despite of Alemtuzumab-mediated TCD, half of our patients developed acute GVHD. Since regulatory T cells (Treg) play a major role for cont…

CD52business.industrymedicine.medical_treatmentImmunologyFOXP3hemic and immune systemschemical and pharmacologic phenomenaContext (language use)Cell BiologyHematologyHematopoietic stem cell transplantationmedicine.diseaseBiochemistryGraft-versus-host diseaseimmune system diseasesImmunologymedicineAlemtuzumabIL-2 receptorInterleukin-7 receptorbusinessmedicine.drugBlood
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Interleukin-30 feeds breast cancer stem cells via CXCL10 and IL23 autocrine loops and shapes immune contexture and host outcome

2021

BackgroundBreast cancer (BC) progression to metastatic disease is the leading cause of death in women worldwide. Metastasis is driven by cancer stem cells (CSCs) and signals from their microenvironment. Interleukin (IL) 30 promotes BC progression, and its expression correlates with disease recurrence and mortality. Whether it acts by regulating BCSCs is unknown and could have significant therapeutic implications.MethodsHuman (h) and murine (m) BCSCs were tested for their production of and response to IL30 by using flow cytometry, confocal microscopy, proliferation and sphere-formation assays, and PCR array. Immunocompetent mice were used to investigate the role of BCSC-derived IL30 on tumor…

Cancer Research2434ImmunologyTriple Negative Breast NeoplasmsBiologyInterleukin-23Paracrine signallingMiceCancer stem cellCell Line Tumorbreast neoplasmsImmunology and Allergytumor microenvironmentAnimalsHumans1506Autocrine signallingRC254-282PharmacologyTumor microenvironmentbreast neoplasms cytokines tumor microenvironmentInterleukinsInnate lymphoid cellNeoplasms. Tumors. Oncology. Including cancer and carcinogensFOXP3Basic Tumor ImmunologyDendritic cellcytokinesChemokine CXCL10Autocrine CommunicationOncologyKLF4Cancer researchNeoplastic Stem CellsMolecular MedicineFemaleJournal for Immunotherapy of Cancer
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