Search results for " interleukin"

showing 10 items of 309 documents

Aggravated Atherosclerosis and Vascular Inflammation With Reduced Kidney Function Depend on Interleukin-17 Receptor A and Are Normalized by Inhibitio…

2018

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0301 basic medicinemedicine.medical_specialtylcsh:Diseases of the circulatory (Cardiovascular) systemIl17ra interleukin-17 receptor A (gene name)medicine.medical_treatmentInterleukin-17 receptormacrophage030204 cardiovascular system & hematologyLesionPRECLINICAL RESEARCH03 medical and health sciencesPCR polymerase chain reaction0302 clinical medicineInternal medicinemedicineMacrophageReceptorbusiness.industryCKD chronic kidney diseaseLDLr low-density lipoprotein receptorIL interleukinBlockadeEndothelial stem cell030104 developmental biologyEndocrinologyCytokinelcsh:RC666-701Interleukin 17medicine.symptomatherosclerosisCardiology and Cardiovascular Medicinebusinessinterleukin 17chronic kidney diseaseJACC: Basic to Translational Science
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Canakinumab as first-line biological therapy in Still’s disease and differences between the systemic and the chronic-articular courses: Real-life exp…

2022

ObjectiveInterleukin (IL)-1 inhibitors are largely employed in patients with Still’s disease; in cases with refractory arthritis, IL-6 inhibitors have shown to be effective on articular inflammatory involvement. The aim of the present study is to assess any difference in the effectiveness of the IL-1β antagonist canakinumab prescribed as first-line biologic agent between the systemic and the chronic-articular Still’s disease.MethodsData were drawn from the retrospective phase of the AutoInflammatory Disease Alliance (AIDA) international registry dedicated to Still’s disease. Patients with Still’s disease classified according to internationally accepted criteria (Yamaguchi criteria and/or Fa…

AOSD; adult onset Still’s disease; autoinflammatory diseases; biological therapy; interleukin-1; sJIA; systemic juvenile idiopathic arthritisadult onset Still’s diseaseAOSD adult onset Still’s disease autoinflammatory diseases biological therapy interleukin-1 sJIA systemic juvenile idiopathic arthritisSettore MED/38 - Pediatria Generale E Specialisticasystemic juvenile idiopathic arthritisbiological therapyAOSDGeneral Medicineautoinflammatory diseasesinterleukin-1sJIAFrontiers in Medicine
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Coronavirus Disease 2019–Associated Coagulopathy

2021

Patients with the severe form of coronavirus disease 2019 (COVID-19) have been frequently found to suffer from both arterial and venous thrombotic events due to the perpetuation of a hypercoagulable state. This phenomenon, termed COVID-19-associated coagulopathy (CC), is now considered a major component of the pathophysiology of this novel infectious disease, leading to widespread thrombosis. While at first, the vascular insults may be limited to the pulmonary microvasculature, as the disease progresses, systemic involvement occurs, culminating in distant organ thrombosis and multi-organ dysfunction syndrome. In this review article, we discuss recent insights into the pathophysiologic mecha…

ARDSPAI-1 Plasminogen Activator Inhibitor 1VTE venous thromboembolismDiseaseReview030204 cardiovascular system & hematologyCoronavirus Disease 20190302 clinical medicineCoagulopathy030212 general & internal medicineDIC disseminated intravascular coagulationDisseminated intravascular coagulationCOVID-19 Coronavirus disease 2019DVT deep vein thrombosisGeneral MedicineBlood Coagulation DisordersThrombosisICU intensive care unitTMA thrombotic microangiopathyDisease ProgressionCoronavirus Disease 2019 COVID-19 CoagulopathyVWF von Willebrand factormedicine.medical_specialtyThrombotic microangiopathyACE2 angiotensin-converting enzyme 2SARS-CoV-2 severe acute respiratory syndrome coronavirus 203 medical and health sciencesmedicineCoagulopathyHumansIntensive care medicineLY30 lysis at 30 minutesARDS acute respiratory distress syndromeHemostasisNO nitric oxideCoagulationbusiness.industrySARS-CoV-2COVID-19Thrombosismedicine.diseasetPA tissue plasminogen activatorReview articleIL interleukinCoronavirusVascular DisorderPE pulmonary embolismTF tissue factorbusinessCC COVID-associated coagulopathyMayo Clinic Proceedings
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Coexpression of IL-6 and soluble IL-6R causes nodular regenerative hyperplasia and adenomas of the liver

1998

Studies with tumor necrosis factor p55 receptor- and interleukin-6 (IL-6)-deficient mice have shown that IL-6 is required for hepatocyte proliferation and reconstitution of the liver mass after partial hepatectomy. The biological activities of IL-6 are potentiated when this cytokine binds soluble forms of its specific receptor subunit (sIL-6R) and the resulting complex interacts with the transmembrane signaling chain gp130. We show here that double transgenic mice expressing high levels of both human IL-6 and sIL-6R under the control of liver-specific promoters spontaneously develop nodules of hepatocellular hyperplasia around periportal spaces and present signs of sustained hepatocyte prol…

AdenomaSTAT3 Transcription FactorAdenomail-6; liver adenomas; nodular hyperplasia; soluble il-6rMice TransgenicBiologyGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins c-mycMiceMyeloproliferative Disordersil-6medicineAnimalsnodular hyperplasiaReceptorMolecular BiologyHyperplasialiver adenomasHaptoglobinsGeneral Immunology and MicrobiologyInterleukin-6General NeuroscienceLiver NeoplasmsHyperplasiaGlycoprotein 130medicine.diseaseReceptors Interleukin-6Liver regenerationLiver RegenerationDNA-Binding Proteinsmedicine.anatomical_structureGene Expression RegulationLiverSolubilityHepatocyteTrans-ActivatorsCancer researchEndothelium Vascularsoluble il-6rNodular regenerative hyperplasiaResearch ArticleThe EMBO Journal
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The transcription factor NFATc2 controls IL-6–dependent T cell activation in experimental colitis

2008

The nuclear factor of activated T cells (NFAT) family of transcription factors controls calcium signaling in T lymphocytes. In this study, we have identified a crucial regulatory role of the transcription factor NFATc2 in T cell–dependent experimental colitis. Similar to ulcerative colitis in humans, the expression of NFATc2 was up-regulated in oxazolone-induced chronic intestinal inflammation. Furthermore, NFATc2 deficiency suppressed colitis induced by oxazolone administration. This finding was associated with enhanced T cell apoptosis in the lamina propria and strikingly reduced production of IL-6, -13, and -17 by mucosal T lymphocytes. Further studies using knockout mice showed that IL-…

Adjuvants Immunologic; Animals; Humans; Interleukin-13; Interleukin-17; Interleukin-6; Lymphocyte Activation; Mice; Mice Inbred BALB C; Mice Knockout; Mice SCID; Models Biological; NFATC Transcription Factors; Oxazolone; T-LymphocytesT cellT-LymphocytesImmunologyMice SCIDBiologyLymphocyte ActivationInflammatory bowel diseaseModels BiologicalArticleOxazoloneTCIRG1chemistry.chemical_compoundMiceAdjuvants ImmunologicmedicineImmunology and AllergyCytotoxic T cellAnimalsHumansColitisMice KnockoutMice Inbred BALB CInterleukin-13NFATC Transcription FactorsInterleukin-6Interleukin-17OxazoloneArticlesmedicine.diseasemedicine.anatomical_structurechemistryImmunologyInterleukin 13Cancer researchInterleukin 17The Journal of Experimental Medicine
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Stat3 and Gfi-1 Transcription Factors Control Th17 Cell Immunosuppressive Activity via the Regulation of Ectonucleotidase Expression

2012

International audience; Although Th17 cells are known to promote tissue inflammation and autoimmunity, their role during cancer progression remains elusive. Here, we showed that in vitro Th17 cells generated with the cytokines IL-6 and TGF-β expressed CD39 and CD73 ectonucleotidases, leading to adenosine release and the subsequent suppression of CD4(+) and CD8(+) T cell effector functions. The IL-6-mediated activation of the transcription factor Stat3 and the TGF-β-driven downregulation of Gfi-1 transcription factor were both essential for the expression of ectonucleotidases during Th17 cell differentiation. Stat3 supported whereas Gfi-1 repressed CD39 and CD73 expression by binding to thei…

Adoptive cell transferMESH : Transcription FactorsCellular differentiationMESH: Th17 CellsT-LymphocytesCellMESH : Promoter Regions GeneticMESH : RNA Small InterferingMESH: Mice KnockoutMice0302 clinical medicineTransforming Growth Factor betaMESH: RNA Small InterferingMESH : STAT3 Transcription FactorImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyEctonucleotidaseMESH: AnimalsRNA Small InterferingSTAT3MESH: Lymphocytes Tumor-InfiltratingPromoter Regions GeneticMESH: Antigens CD5'-NucleotidaseRegulation of gene expressionMice Knockout0303 health sciencesMESH : Gene Expression RegulationApyraseMESH: STAT3 Transcription FactorMESH: Transcription FactorsMESH: Gene Expression RegulationMESH : Mice TransgenicCell biologyMESH : Lymphocytes Tumor-InfiltratingDNA-Binding ProteinsMESH : ApyraseInfectious Diseasesmedicine.anatomical_structure[SDV.IMM]Life Sciences [q-bio]/ImmunologyMESH : DNA-Binding ProteinsMESH: ApyraseSTAT3 Transcription Factor[SDV.IMM] Life Sciences [q-bio]/ImmunologyMESH : Interleukin-6MESH: Mice TransgenicT cellImmunologyMice TransgenicMESH : Mice Inbred C57BLBiology03 medical and health sciencesLymphocytes Tumor-InfiltratingMESH: Mice Inbred C57BLAntigens CDMESH: Promoter Regions GeneticMESH : 5'-NucleotidaseMESH : MicemedicineMESH : Antigens CDMESH : Th17 CellsAnimalsTranscription factorMESH: MiceMESH: Transforming Growth Factor beta030304 developmental biologyMESH : T-LymphocytesBinding SitesInterleukin-6MESH: Interleukin-6Mice Inbred C57BLMESH: T-LymphocytesMESH : Transforming Growth Factor betaMESH: Binding SitesGene Expression Regulationbiology.proteinMESH : Mice KnockoutTh17 CellsMESH : AnimalsMESH: 5'-NucleotidaseMESH: DNA-Binding ProteinsMESH : Binding Sites030215 immunologyTranscription FactorsImmunity
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Interferon-Beta Therapy of Multiple Sclerosis Patients Improves the Responsiveness of T Cells for Immune Suppression by Regulatory T Cells

2015

Multiple sclerosis (MS) is an inflammatory autoimmune disease characterized by imbalanced immune regulatory networks, and MS patient-derived T effector cells are inefficiently suppressed through regulatory T cells (Treg), a phenomenon known as Treg resistance. In the current study we investigated T cell function in MS patients before and after interferon-beta therapy. We compared cytokine profile, responsiveness for Treg-mediated suppression ex vivo and evaluated reactivity of T cells in vivo using a humanized mouse model. We found that CD4+ and CD8+ T cells of therapy-naive MS patients were resistant to Treg-mediated suppression. Treg resistance is associated with an augmented IL-6 product…

AdultAdolescentdiagnosisReceptor expressionT cellchemical and pharmacologic phenomenaMice SCIDAntibodies Monoclonal Humanizedmultiple sclerosisT-Lymphocytes RegulatoryCatalysisArticleInorganic ChemistryTCIRG1lcsh:ChemistryInterleukin 21Young AdultImmune systemCytotoxic T cellMedicineAnimalsHumansIL-2 receptorPhysical and Theoretical ChemistryMolecular BiologyT effector cellslcsh:QH301-705.5SpectroscopyImmunosuppression TherapyInflammationtherapybusiness.industryOrganic Chemistryimmune regulationGeneral MedicineInterferon-betaMiddle AgedReceptors Interleukin-6Computer Science ApplicationsTregmedicine.anatomical_structureAnimals Newbornlcsh:Biology (General)lcsh:QD1-999ImmunologyLeukocytes MononuclearbusinessCD8International Journal of Molecular Sciences
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Study of T-cell activation in Type I diabetic patients and pre-Type I diabetic subjects by cytometric analysis: Antigen expression defectin vitro

1993

In Type I diabetes the observation of a decreased release of interleukin-2 (IL-2) and soluble IL-2 receptors by means of stimulated lymphocytes in vitro indicates that a primary immunoregulatory defect may be involved. To confirm this hypothesis we investigated the T-cell activation trend, evaluating the surface expression of IL-2 receptor (CD25), transferrin (CD71), HLA class II (DR), and CD69 phenotypes after in vitro stimulation with phytohemagglutinin (PHA; 1 and 10 micrograms/ml) and concanavalin A (12.5 micrograms/ml) in six newly diagnosed Type I diabetics and six islet cell- and insulin autoantibody-positive first-degree relatives. As controls were studied six long-standing Type I d…

AdultAntigens Differentiation T-LymphocyteCD4-Positive T-LymphocytesMaleInterleukin 2medicine.medical_specialtyTime FactorsAdolescentCD3 ComplexCD8 AntigensT-Lymphocytesmedicine.medical_treatmentT cellImmunologyTransferrin receptorBiologyLymphocyte ActivationAntigenAntigens CDInternal medicineDiabetes mellitusReceptors TransferrinmedicineHumansImmunology and AllergyLectins C-TypeIL-2 receptorPhytohemagglutininsReceptorInsulinReceptors Interleukin-2HLA-DR Antigensmedicine.diseaseAntigens Differentiation B-LymphocyteKineticsDiabetes Mellitus Type 1Endocrinologymedicine.anatomical_structureInterleukin-2Femalemedicine.drugJournal of Clinical Immunology
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Early administration of an immunomodulator and induction of remission in insulin-dependent diabetes mellitus

1990

A clinical trial was undertaken to determine whether intensive thymopentin administration enhances remission of insulin-dependent diabetes (IDDM) during the first year after diagnosis. Dosage with insulin was minimized with target control of blood glucose levels less than or equal to 7.8 mmol/l before meals. Remission was defined as a prolonged period after IDDM onset (not less than 3 months) characterized by a non-insulin-receiving (NIR) state in which target metabolic control was reached without administration of insulin and with a valid C-peptide response, evaluated after standard breakfast. Sixteen IDDM patients aged 12-31 years, recruited within 2 weeks of initiation of insulin therapy…

AdultBlood Glucosemedicine.medical_specialtyAdolescentmedicine.medical_treatmentImmunologyGastroenterologyInternal medicineDiabetes mellitusmedicineHumansInsulinImmunology and AllergyThymopentinChildGlycemicImmunity CellularC-Peptidebusiness.industryInsulinRemission InductionHemoglobin AReceptors Interleukin-2medicine.diseaseClinical trialTiterDiabetes Mellitus Type 1EndocrinologyChild PreschoolInsulin dependent diabetesMetabolic control analysisThymopentinbusinessmedicine.drugJournal of Autoimmunity
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Hematologic effects of recombinant human granulocyte colony-stimulating factor in patients with malignancy.

1989

Abstract The effect of recombinant human granulocyte colony-stimulating factor (G-CSF) on hematologic parameters was evaluated in a phase I clinical study in 18 patients with advanced malignancy. G-CSF was administered once daily as a 30-minute infusion for 14 days; three patients each were treated at increasing dose levels of 1, 3, 10, 30, and 60 micrograms kg-1 day-1. A transient decrease in neutrophil and monocyte counts was observed immediately after the G-CSF infusion, followed by a dose-dependent increase of up to 15-fold. G-CSF-induced neutrophils exhibited an increased O2- radical production, and serum levels of enzymes related to granulocyte turnover, including lysozyme and elastas…

AdultBlood Plateletsmedicine.medical_specialtySide effectImmunologyAntineoplastic AgentsPlatelet Membrane GlycoproteinsGranulocyteMalignancyBiochemistryLeukocyte CountColony-Stimulating FactorsSuperoxidesInternal medicineGranulocyte Colony-Stimulating FactormedicineHumansPlateletBone painAgedbusiness.industryPlatelet CountMonocyteElastaseReceptors Interleukin-2Cell BiologyHematologyMiddle Agedmedicine.diseaseRecombinant ProteinsGranulocyte colony-stimulating factorHematopoiesisEndocrinologymedicine.anatomical_structureImmunologyDrug Evaluationmedicine.symptombusinessBlood
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