Search results for "Interleukin-2 Receptor alpha Subunit"

showing 10 items of 33 documents

Interferon-α Suppresses cAMP to Disarm Human Regulatory T Cells

2013

Abstract IFN-α is an antineoplastic agent in the treatment of several solid and hematologic malignancies that exerts strong immune- and autoimmune-stimulating activity. However, the mechanisms of immune activation by IFN-α remain incompletely understood, particularly with regard to CD4+CD25highFoxp+ regulatory T cells (Treg). Here, we show that IFN-α deactivates the suppressive function of human Treg by downregulating their intracellular cAMP level. IFN-α–mediated Treg inactivation increased CD4+ effector T-cell activation and natural killer cell tumor cytotoxicity. Mechanistically, repression of cAMP in Treg was caused by IFN-α–induced MAP–ERK kinase (MEK)/extracellular signal-regulated ki…

MAPK/ERK pathwayCancer Researchmedicine.medical_treatmentGraft vs Host DiseaseAutoimmunitychemical and pharmacologic phenomenaBiologyLymphocyte ActivationT-Lymphocytes RegulatoryNatural killer cellMiceImmune systemDownregulation and upregulationT-Lymphocyte SubsetsCyclic AMPmedicineAnimalsHumansIL-2 receptorPhosphorylationExtracellular Signal-Regulated MAP KinasesCells CulturedMitogen-Activated Protein Kinase KinasesInterleukin-2 Receptor alpha SubunitInterferon-alphaFOXP3hemic and immune systemsDNA-Binding ProteinsKiller Cells NaturalSTAT Transcription Factorsmedicine.anatomical_structureCytokineOncologyHumanized mouseImmunologyCancer researchCancer Research
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P38 MAP Kinase Signaling Is Required for the Conversion of CD4+CD25− T Cells into iTreg

2008

CD4+CD25+ regulatory T cells (Treg) are important mediators of immune tolerance. A subset of Treg can be generated in the periphery by TGF-beta dependent conversion of conventional CD4+CD25− T cells into induced Treg (iTreg). In chronic viral infection or malignancy, such induced iTreg, which limit the depletion of aberrant or infected cells, may be of pathogenic relevance. To identify potential targets for therapeutic intervention, we investigated the TGF-beta signaling in Treg. In contrast to conventional CD4+ T cells, Treg exhibited marked activation of the p38 MAP kinase pathway. Inhibition of p38 MAP kinase activity prevented the TGF-beta-dependent conversion of CD4+CD25− T cells into …

MAPK/ERK pathwayp38 mitogen-activated protein kinasesImmunologyBlotting WesternImmunology/Immunomodulationlcsh:MedicineImmunology/Autoimmunitychemical and pharmacologic phenomenaBiologyT-Lymphocytes Regulatoryp38 Mitogen-Activated Protein KinasesImmune toleranceImmunology/Leukocyte Signaling and Gene ExpressionMiceAnimalsIL-2 receptorlcsh:ScienceMultidisciplinarylcsh:RInterleukin-2 Receptor alpha SubunitFOXP3hemic and immune systemsFlow CytometryCell biologyMitogen-activated protein kinaseCD4 Antigensbiology.proteinPhosphorylationlcsh:QSignal transductionResearch ArticleSignal TransductionPLoS ONE
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Inflammatory activation and endothelial dysfunction markers in patients with permanent atrial fibrillation: A cross-sectional study

2020

In recent years a growing body of evidence supported the role of inflammation in the initiation, maintenance and outcome of atrial fibrillation (AF). Nevertheless, despite a large amount of information, whether AF or the underlying structural heart disease (SHD) is the cause of the inflammatory process is still under debate. We, therefore, sought to determine if the inflammatory process reflect an underlying disease or the arrhythmia 'per se'. We evaluated plasma levels of soluble Interleukin 2 Receptor Alpha (sIL-2Rα), TNF-α and IL-18 in 100 consecutive patients with permanent AF, (43 with a SHD and 57 without a SHD) compared to 121 age and sex-matched controls which had normal sinus rhyth…

MaleAgingmedicine.medical_specialtyHeart diseaseAlpha (ethology)InflammationDiseaseSystemic inflammationendothelial dysfunctionInternal medicineAtrial FibrillationmedicineHumansEndothelial dysfunctionReactive hyperemiaAgedAged 80 and overInflammationTumor Necrosis Factor-alphabusiness.industryInterleukin-18Interleukin-2 Receptor alpha SubunitAtrial fibrillationAtrial fibrillation Cytokines Endothelial dysfunction Inflammation Structural heart diseaseCell BiologyMiddle Agedmedicine.diseasestructural heart diseasecytokinesCross-Sectional StudiesLogistic ModelsROC CurveCase-Control StudiesCardiologyFemaleEndothelium Vascularmedicine.symptombusinessBiomarkersResearch Paper
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Loss of histone macroH2A1 in hepatocellular carcinoma cells promotes paracrine-mediated chemoresistance and CD4

2019

Rationale: Loss of histone macroH2A1 induces appearance of cancer stem cells (CSCs)-like cells in hepatocellular carcinoma (HCC). How CSCs interact with the tumor microenvironment and the adaptive immune system is unclear. Methods: We screened aggressive human HCC for macroH2A1 and CD44 CSC marker expression. We also knocked down (KD) macroH2A1 in HCC cells, and performed integrated transcriptomic and secretomic analyses. Results: Human HCC showed low macroH2A1 and high CD44 expression compared to control tissues. MacroH2A1 KD CSC-like cells transferred paracrinally their chemoresistant properties to parental HCC cells. MacroH2A1 KD conditioned media transcriptionally reprogrammed parental …

MaleCarcinoma HepatocellularT-Lymphocytes RegulatoryHistonesadaptive immune systemCell Line TumorParacrine CommunicationTumor MicroenvironmentHumansMetabolomicschemoresistance.neoplasmsLiver Neoplasmshistone macroH2A1Interleukin-2 Receptor alpha SubunitForkhead Transcription Factorshepatocellular carcinomaMiddle Ageddigestive system diseasesGene Expression Regulation NeoplasticHyaluronan ReceptorsDrug Resistance NeoplasmGene Knockdown TechniquesNeoplastic Stem CellsGlycolysisResearch PaperTheranostics
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Epigenetic Control of the foxp3 Locus in Regulatory T Cells

2007

Compelling evidence suggests that the transcription factor Foxp3 acts as a master switch governing the development and function of CD4+ regulatory T cells (Tregs). However, whether transcriptional control of Foxp3 expression itself contributes to the development of a stable Treg lineage has thus far not been investigated. We here identified an evolutionarily conserved region within the foxp3 locus upstream of exon-1 possessing transcriptional activity. Bisulphite sequencing and chromatin immunoprecipitation revealed complete demethylation of CpG motifs as well as histone modifications within the conserved region in ex vivo isolated Foxp3+CD25+CD4+ Tregs, but not in naïve CD25−CD4+ T cells. …

MaleQH301-705.5Bisulfite sequencingImmunologyMolecular Sequence Datachemical and pharmacologic phenomenaCell SeparationThymus GlandBiologyT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticMiceTranscriptional regulationAnimalsEpigeneticsBiology (General)Regulation of gene expressionMice Inbred BALB CGeneral Immunology and MicrobiologyBase SequenceGeneral NeuroscienceInterleukin-2 Receptor alpha SubunitFOXP3Homo (human)hemic and immune systemsForkhead Transcription FactorsDNA MethylationFlow CytometryMolecular biologyMus (mouse)Cell biologyIn VitroDNA demethylationGene Expression RegulationDNA methylationCpG IslandsGeneral Agricultural and Biological SciencesChromatin immunoprecipitationResearch ArticlePLoS Biology
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Docosahexaenoic acid reduces suppressive and migratory functions of CD4CD25 regulatory T-cells

2009

Immunological tolerance is one of the fundamental aspects of the immune system. The CD4(+)CD25(+) regulatory T (Treg) cells have emerged as key players in the development of tolerance to self and foreign antigens. However, little is known about the endogenous factors and mechanisms controlling their suppressive capacity on immune response. In this study, we observed that docosahexaenoic acid (DHA), an n-3 polyunsaturated fatty acid, diminished, in a dose-dependent manner, the capacity of Treg cells to inhibit the CD4(+)CD25(-) effector T-cell proliferation. DHA not only reduced the migration of Treg cells toward chemokines but also downregulated the mRNA expression of CCR-4 and CXCR-4 in Tr…

MaleReceptors CXCR4Chemokineextracellular signal-regulated kinase 1/2Receptors CCR4Docosahexaenoic Acidschemical and pharmacologic phenomenaQD415-436T-Lymphocytes RegulatoryBiochemistryMicehistone desacetylase 7EndocrinologyImmune systemAntigenAntigens CDCell MovementTransforming Growth Factor betaAnimalsCTLA-4 AntigenRNA MessengerIL-2 receptorCells CulturedCell ProliferationDose-Response Relationship DrugbiologySmad7Reverse Transcriptase Polymerase Chain ReactionInterleukin-2 Receptor alpha SubunitFOXP3Forkhead Transcription Factorshemic and immune systemsCell BiologyTransforming growth factor betaInterleukin-10Cell biologyMice Inbred C57BLInterleukin 10Docosahexaenoic acidImmunologybiology.proteinResearch ArticleJournal of Lipid Research
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Increased immunosuppressive function of CD4(+)CD25(+)Foxp3(+)GITR+ T regulatory cells from NFATc2((-/-)) mice controls allergen-induced experimental …

2012

The expansion of effector T cells is tightly controlled by transcription factors like nuclear factor of activated T cells (NFAT) family members that mediate early intracellular responses to T cell receptor-mediated signals. In this study we show that, after allergen challenge, NFATc2((-/-)) mice had augmented number of functionally intact CD4(+)CD25(++)GITR(++) T regulatory (T regs) cells in the lung. Anti-GITR antibody treatment inhibited T regulatory cell function and enhanced the number of activated lung CD4(+) T cells associated with increased IL-2 and pSTAT-5 in the airways of NFATc2((-/-)) mice in experimental allergic asthma. This agonistic treatment led to increased inflammation in …

NFATC2T cellImmunologyInflammationBiologyT-Lymphocytes RegulatoryInterleukin 21MiceTh2 CellsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyAnimalsIL-2 receptorLungImmunosuppression TherapyMice KnockoutNFATC Transcription FactorsInterleukin-2 Receptor alpha SubunitFOXP3NFATForkhead Transcription FactorsHematologyAllergensAsthmarespiratory tract diseasesDisease Models Animalmedicine.anatomical_structureImmunologyCD4 Antigensbiology.proteinCytokinesTh17 CellsFemalemedicine.symptomAntibodySpleenImmunobiology
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Crosstalk of regulatory T cells and tolerogenic dendritic cells prevents contact allergy in subjects with low zone tolerance

2012

Background Allergic contact dermatitis is one of the most common occupational diseases. A main protective mechanism in those who do not develop allergic contact dermatitis is tolerance induction by repeated exposure to low doses of contact allergen, which is termed low zone tolerance (LZT). The mechanisms that determine the tolerance induction in subjects with LZT are still elusive. Objective We performed analysis of the role of CD4 + CD25 + forkhead box protein 3 (FOXP3)–positive regulatory T (Treg) cells and dendritic cells (DCs) in mice with LZT. Methods Mechanisms of tolerance induction were analyzed in a murine model of LZT by using FOXP3 and IL-10 reporter mice, as well as mice that a…

Receptors CCR7Adoptive cell transferImmunologyMice Transgenicchemical and pharmacologic phenomenaCell CommunicationBiologyLymphocyte ActivationT-Lymphocytes RegulatoryMiceImmune ToleranceAnimalsImmunology and AllergyIL-2 receptorInterleukin-2 Receptor alpha SubunitFOXP3Forkhead Transcription Factorshemic and immune systemsDendritic CellsDendritic cellCD11c AntigenInterleukin-10Tolerance inductionInterleukin 10CTLA-4Dermatitis Allergic ContactImmunologyCD8Journal of Allergy and Clinical 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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Interleukin-7 matures suppressive CD127(+) forkhead box P3 (FoxP3)(+) T cells into CD127(-) CD25(high) FoxP3(+) regulatory T cells.

2011

We have identified a novel interleukin (IL)-7-responsive T cell population [forkhead box P3 (FoxP3(+) ) CD4(+) CD25(+) CD127(+) ] that is comparably functionally suppressive to conventional FoxP3(+) CD4(+) CD25(+) regulatory T cells (T(regs) ). Although IL-2 is the most critical cytokine for thymic development of FoxP3(+) T(regs) , in the periphery other cytokines can be compensatory. CD25(+) CD127(+) T cells treated with IL-7 phenotypically 'matured' into the known 'classical' FoxP3(+) CD4(+) CD25(high) CD127(-) FoxP3(+) T(regs) . In freshly isolated splenocytes, the highest level of FoxP3 expression was found in CD127(+) CD25(+) T cells when compared with CD127(-) CD25(+) or CD127(+) CD25…

Translational StudiesT cellImmunologyActive Transport Cell Nucleuschemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryInterleukin-7 Receptor alpha SubunitInterleukin 21MiceAntigenAntigens CDT-Lymphocyte SubsetsmedicineImmunology and AllergyCytotoxic T cellAnimalsCTLA-4 AntigenIL-2 receptorInterleukin-7 receptorCells CulturedCell NucleusMice Inbred BALB CInterleukin-7autoimmunityInterleukin-2 Receptor alpha SubunitFOXP3virus diseaseshemic and immune systemsCell DifferentiationForkhead Transcription FactorsT lymphocyteMice Inbred C57BLmedicine.anatomical_structureGene Expression RegulationImmunologyLeukocyte Common AntigensFoxP3 TregClinical and experimental immunology
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