Search results for " Interleukin-2"

showing 10 items of 63 documents

Circulating interleukin (IL)-8, IL-2R, IL-12, and IL-15 levels are independently prognostic in primary myelofibrosis: a comprehensive cytokine profil…

2011

Purpose Abnormal cytokine expression accompanies myelofibrosis and might be a therapeutic target for Janus-associated kinase (JAK) inhibitor drugs. This study describes the spectrum of plasma cytokine abnormalities in primary myelofibrosis (PMF) and examines their phenotypic correlates and prognostic significance. Patients and Methods Patients included in this study were required to have archived plasma, bone marrow biopsy, and cytogenetic information available at the time of first referral to the Mayo Clinic. Multiplex biometric sandwich immunoassay was used to measure plasma levels of 30 cytokines. Results In total, 127 PMF patients were studied; comparison with normal controls (n = 35) r…

MaleCancer Researchmedicine.medical_treatmentBiopsyKaplan-Meier EstimateRisk FactorsMedicineMacrophage inflammatory proteinAged 80 and overInterleukin-15Janus kinase 2biologyInterleukinBone Marrow ExaminationMiddle AgedPrognosisInterleukin-12Up-RegulationCytokinePhenotypeOncologyInterleukin 15Cytogenetic AnalysisFemalemedicine.drugAdultGenotypeMinnesotaProtein Array AnalysisEnzyme-Linked Immunosorbent AssayRisk AssessmentPredictive Value of TestsBiomarkers TumorHumansMyelofibrosisInterferon alfaAgedProportional Hazards ModelsChi-Square Distributionbusiness.industryInterleukin-8Receptors Interleukin-2Janus Kinase 2medicine.diseasePacritinibPrimary MyelofibrosisCase-Control StudiesImmunologyMutationbiology.proteinbusinessJournal of clinical oncology : official journal of the American Society of Clinical Oncology
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An anti-interleukin-2 receptor drug attenuates T- helper 1 lymphocytes-mediated inflammation in an acute model of endotoxin-induced uveitis.

2014

The aim of the present study was to evaluate the anti-inflammatory efficacy of Daclizumab, an anti-interleukin-2 receptor drug, in an experimental uveitis model upon a subcutaneous injection of lipopolysaccharide into Lewis rats, a valuable model for ocular acute inflammatory processes. The integrity of the blood-aqueous barrier was assessed 24 h after endotoxin-induced uveitis by evaluating two parameters: cell count and protein concentration in aqueous humors. The histopathology of all the ocular structures (cornea, lens, sclera, choroid, retina, uvea, and anterior and posterior chambers) was also considered. Enzyme-linked immunosorbent assays of the aqueous humor samples were performed t…

MaleChemokineAnatomy and PhysiologyDaclizumabmedicine.medical_treatmentlcsh:MedicineBiochemistryRedox SignalingOxidative DamageDaclizumabImmune PhysiologyMolecular Cell BiologyBasic Cancer ResearchSignaling in Cellular ProcessesInterferon gammalcsh:ScienceMultidisciplinarybiologyT CellsOxygen MetabolismCytokinemedicine.anatomical_structureOncologyAcute DiseaseCytokinesMedicineImmunotherapymedicine.symptomUveitismedicine.drugResearch ArticleSignal TransductionInterleukin 2Cell PhysiologyImmune CellsImmunologyInflammationAntibodies Monoclonal HumanizedSignaling PathwaysUveitisOcular SystemmedicineAnimalsBiologyInflammationbusiness.industrylcsh:RImmunityReceptors Interleukin-2UveaTh1 Cellsmedicine.diseaseeye diseasesEndotoxinsDisease Models AnimalMetabolismRats Inbred LewImmune SystemImmunoglobulin GImmunologybiology.proteinlcsh:Qsense organsMolecular NeurosciencebusinessNeurosciencePLoS ONE
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MiR-146b-5p regulates IL-23 receptor complex expression in chronic lymphocytic leukemia cells

2022

Abstract Chronic lymphocytic leukemia (CLL) cells express the interleukin-23 receptor (IL-23R) chain, but the expression of the complementary IL-12Rβ1 chain requires cell stimulation via surface CD40 molecules (and not via the B-cell receptor [BCR]). This stimulation induces the expression of a heterodimeric functional IL-23R complex and the secretion of IL-23, initiating an autocrine loop that drives leukemic cell expansion. Based on the observation in 224 untreated Binet stage A patients that the cases with the lowest miR-146b-5p concentrations had the shortest time to first treatment (TTFT), we hypothesized that miR-146b-5p could negatively regulate IL-12Rβ1 side chain expression and clo…

MiceMicroRNAsCD40 LigandAnimalsReceptors Antigen B-CellChronic lymphocytic leukemia interleukin-23 receptor (IL-23R) MiR-146bSettore MED/05 - Patologia ClinicaRNA MessengerHematologySettore MED/08 - Anatomia PatologicaInterleukin-23Leukemia Lymphocytic Chronic B-CellBlood Advances
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Interleukin-2 receptor gene expression by bronchoalveolar lavage lymphocytes in pulmonary sarcoidosis.

1989

Current concepts of the immunopathogenesis of sarcoidosis favor a central role of activated, interleukin-2 (IL-2) producing helper T-cells at sites of inflammation. Normally, activated T-cells release IL-2 and express IL-2 receptors (IL-2R). IL-2R+ cells, however, are not uniformly found in patients with clinically active disease. To determine whether the lack of IL-2R+ cells is caused by a dysregulation of the IL-2R gene or by the mode of T-cell activation in pulmonary sarcoidosis, we quantified IL-2 and IL-2R m-RNA transcripts, IL-2 release, and IL-2R surface protein in peripheral blood lymphocytes of patients with sarcoidosis and normal control subjects before and after in vitro stimulat…

Pulmonary and Respiratory MedicineInterleukin 2AdultLung DiseasesPathologymedicine.medical_specialtySarcoidosisLymphocyteT-LymphocytesInflammationLymphocyte ActivationIn vivomedicineHumansRNA MessengerReceptorLungmedicine.diagnostic_testbusiness.industryReceptors Interleukin-2medicine.diseasemedicine.anatomical_structureBronchoalveolar lavageGene Expression RegulationImmunologyInterleukin-2Sarcoidosismedicine.symptombusinessBronchoalveolar Lavage Fluidmedicine.drugThe American review of respiratory disease
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Lung-restricted activation of the alveolar macrophage/monocyte system in pulmonary sarcoidosis.

1992

An activation of T-cells that is restricted to the lung has been demonstrated in pulmonary sarcoidosis. The role of blood monocytes (MO) and alveolar macrophages (AM) in this concept of compartmentalized inflammation has not yet been evaluated. In order to elucidate this question, we measured the release of tumor necrosis factor alpha (TNF alpha) and interleukin-1 (IL-1) by peripheral blood mononuclear cells (PBMNC) and AM in 43 patients with sarcoidosis (32 with active, 11 with inactive disease) without therapy and correlated the spontaneous monokine release to parameters of the T-cell alveolitis and the course of the disease. TNF alpha as well as IL-1 were spontaneously released by AM of …

Pulmonary and Respiratory MedicineInterleukin 2Lung Diseasesmedicine.medical_specialtyTime FactorsSarcoidosisLung Diseases/metabolism610 MedizinInflammationSarcoidosis/metabolismLymphocyte ActivationMacrophages Alveolar/secretionPeripheral blood mononuclear cellMonocytesInterleukin-1/secretionInternal medicineMacrophages AlveolarmedicineMacrophageHumansddc:610Receptors Interleukin-2/metabolismTumor Necrosis Factor-alpha/secretionbusiness.industryTumor Necrosis Factor-alphaMonocyteLeukocytes Mononuclear/secretionMonocytes/immunologyReceptors Interleukin-2Macrophage ActivationMonokinemedicine.anatomical_structureEndocrinologyImmunologyAlveolar macrophageLeukocytes MononuclearInterleukin-2Tumor necrosis factor alphamedicine.symptomInterleukin-2/secretionbusinessmedicine.drugInterleukin-1The American review of respiratory disease
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Rho prevents apoptosis through Bcl-2 expression: Implications for interleukin-2 receptor signal transduction

1997

Here we describe a Rho-mediated apoptosis suppression pathway driven by Bcl-2 expression in the interleukin (IL)-4- or IL-2-dependent murine T cell line TS1 alpha beta. IL-2, but not IL-4, induces Bcl-2 expression through RhoA activation which is inhibited by the specific Rho family inhibitor, Clostridium difficile Toxin B, as well as by a dominant negative RhoA mutant. Using transient transfections of RhoA mutants tagged with the vesicular stomatitis virus glycoprotein, we show that a constitutively active RhoA mutant induces Bcl-2 expression and prevents apoptosis upon IL-4 withdrawal. Finally, we have identified the signaling pathway involved together with RhoA in Bcl-2 induction and sho…

RHOAImmunologyDown-RegulationClostridium difficile toxin AApoptosisClostridium difficile toxin BTransfectionCell LineMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundGTP-Binding ProteinsAnimalsHumansImmunology and AllergyPhosphatidylinositolProtein kinase AProtein Kinase CbiologyKinaseInterleukinReceptors Interleukin-2Molecular biologyCell biologyProto-Oncogene Proteins c-bcl-2chemistrybiology.proteinInterleukin-2Signal transductionrhoA GTP-Binding ProteinSignal TransductionEuropean Journal of Immunology
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Intermolecular Cystine-Bonding of Murine Interleukin 2 Indicates that Ligand Dimerization is Important for the Formation of the High-Affinity Recepto…

1992

Interleukin 2 is thought to be active as a monomeric protein. As the nonessential Cys-140 of murine interleukin 2 (mIL2) is located in the hydrophobic interface of the amphiphilic F domain it was successfully used to stabilize hydrophobic amino acid contacts between two mIL2 cores yielding biologically active cystine-bonded dimeric mIL2. (3H) thymidine incorporation assays with intermolecular cystine-bonded or monomeric mIL2 revealed almost identical median effective concentrations (EC50) and high-affinity dissociation constants (Kdh), respectively. Comparative binding and internalization assays suggest that one cystine-bonded dimeric or two monomeric mIL2 molecules bind to the high-affinit…

Receptor complexStereochemistryMolecular Sequence DataClinical BiochemistrySuccinimidesLigandsCell LineMicechemistry.chemical_compoundEndocrinologyAnimalsAmino Acid SequenceReceptorPeptide sequencechemistry.chemical_classificationMolecular massLigandReceptors Interleukin-2Cell BiologyAmino acidDissociation constantKineticsCross-Linking ReagentsMonomerchemistryBiochemistryCystineInterleukin-2Cell DivisionGrowth Factors
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T cell avidity determines the level of CTL activation

2004

To investigate the influence of avidity on T cell activation in vitro and in vivo, we analyzed T cells from St40 and St42 mice, which express the same transgenic TCR specific for an E1a-derived epitope of adenovirus type 5 with different expression levels and therefore different avidities. Splenocytes from both strains showed comparable cytolytic activities and required identical peptide concentrations for efficient target cell lysis and up-regulation of activation markers. However, the kinetics of CD25 up-regulation were strikingly different: whereas the majority of the high-avidity St42 T cells up-regulated the IL-2Ralpha chain within a few hours, low-avidity St40 T cells expressed only 5…

T cellImmunologyReceptors Antigen T-CellMice Transgenicchemical and pharmacologic phenomenaStreptamerBiologyLymphocyte ActivationAdenoviridaeMiceInterleukin 21medicineAnimalsImmunology and AllergyCytotoxic T cellIL-2 receptorAntigen-presenting cellCells CulturedCD28Receptors Interleukin-2Natural killer T cellAdoptive TransferMolecular biologymedicine.anatomical_structureCytokinesImmunizationBiomarkersCell DivisionSpleenT-Lymphocytes CytotoxicEuropean Journal of Immunology
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Infectious Tolerance

2002

Regulatory CD4(+)CD25(+) T cells (Treg) are mandatory for maintaining immunologic self-tolerance. We demonstrate that the cell-cell contact-mediated suppression of conventional CD4(+) T cells by human CD25(+) Treg cells is fixation resistant, independent from membrane-bound TGF-beta but requires activation and protein synthesis of CD25(+) Treg cells. Coactivation of CD25(+) Treg cells with Treg cell-depleted CD4(+) T cells results in anergized CD4(+) T cells that in turn inhibit the activation of conventional, freshly isolated CD4(+) T helper (Th) cells. This infectious suppressive activity, transferred from CD25(+) Treg cells via cell contact, is cell contact-independent and partially medi…

TGF-βCD4-Positive T-Lymphocyteshuman regulatory T cellsT-LymphocytesImmunologyCellchemical and pharmacologic phenomenaIn Vitro TechniquesLymphocyte ActivationT-Lymphocytes RegulatoryImmune toleranceInterleukin 21AntigenTransforming Growth Factor betaCD4+CD25+ T cellsCell AdhesionImmune TolerancemedicineHumansImmunology and AllergyCytotoxic T cellIL-2 receptorbiologyBrief Definitive ReportModels ImmunologicalReceptors Interleukin-2hemic and immune systemsT-Lymphocytes Helper-InducerTransforming growth factor betainfectious tolerancemedicine.anatomical_structureT cell inhibitionImmunologyCancer researchbiology.proteinTransforming growth factorJournal of Experimental Medicine
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Perpetual proliferation of LYT-1 cells requires repetitive signals for IL-2 receptor induction by antigen-presenting cells.

1984

Abstract T cell lines with specificity for bovine insulin and ovalbumin were maintained by serial stimulation with antigen presented on irradiated syngeneic spleen cells, alternating 3 days later with subculture in IL-2 containing medium (CM). When the cultures were repetitively split in CM, with concomitant dilution of antigen-presenting cells, a gradual loss of proliferative capacity of the cells in the presence of CM was observed. Absorption studies revealed a 20-fold reduction of IL-2 receptors on the surface of T blasts assayed 12 days after antigenic stimulation as compared with day 5 blasts. This decrement in the number of IL-2 acceptor sites reflected an actual decrease in cell surf…

Time FactorsCell divisionOvalbuminT cellT-LymphocytesImmunologyReceptors Antigen T-CellLymphocyte ActivationAbsorptionCell LineMiceAntigenmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorAntigensReceptors ImmunologicReceptorAntigen-presenting cellCD40biologyReceptors Interleukin-2HematologyMolecular biologymedicine.anatomical_structureImmunologybiology.proteinInterleukin-2SpleenImmunobiology
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