Search results for "Cytokines"

showing 10 items of 845 documents

Inflammatory Characteristics of Monocytes from Pediatric Patients with Tuberous Sclerosis.

2015

Objective  Therapeutic options for the tuberous sclerosis complex (TSC) syndrome showed varying outcomes. Malfunctional tsc1 / tsc2 genes leave mTOR uninhibited, a positive downstream modulator of the innate proinflammatory immune system, which has not yet been described in pediatric patients with TSC. Methods  Using polymerase chain reaction (PCR) gene expression levels of monocytes after cultivation with lipopolysaccharide (LPS) or with LPS + mTOR inhibitor rapamycin, patients with TSC ( n  = 16) were compared with healthy subjects ( n  = 20). Results  Compared with monocytes from healthy controls, LPS showed a more prominent gene expression pattern in patients with TSC (CCL24, CXCL10, IL…

Lipopolysaccharidescongenital hereditary and neonatal diseases and abnormalitiesLipopolysaccharideGene ExpressionMonocytesProinflammatory cytokinechemistry.chemical_compoundTuberous sclerosisTuberous SclerosisGene expressionmedicineCXCL10HumansChildInflammationSirolimusbusiness.industryTOR Serine-Threonine KinasesInfant NewbornInfantGeneral Medicinemedicine.diseasemedicine.anatomical_structureCross-Sectional StudieschemistryChild PreschoolPediatrics Perinatology and Child HealthImmunologyCytokinesNeurology (clinical)TSC1TSC2Inflammation MediatorsbusinessCCL24Immunosuppressive AgentsNeuropediatrics
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Tissue inhibitor of metalloproteinases-2 (TIMP-2) in rat liver cells is increased by lipopolysaccharide and prostaglandin E2

1995

AbstractTo explore the functional role of TIMP-2 in liver, we determined TIMP-2 mRNA levels in primary rat hepatocytes and in total rat liver. Rat hepatocytes constitutively express TIMP-2 mRNA at a low level. Incubation with dexamethasone, prostaglandin E2 and a combination of inflammatory cytokines leads to an up-regulation of TIMP-2 mRNA. In rats in vivo we found a dramatic increase of TIMP-2 expression after intraperitoneal injection of lipopolysaccharide. Compared to our previous findings on TIMP-1 we conclude that TIMP-2 mRNA expression is regulated in a distinct and partially opposite manner. Over-production of TIMP-2 could inhibit the activity of metalloproteinases and thus lead to …

Lipopolysaccharidesmedicine.medical_specialtyLipopolysaccharidemedicine.medical_treatmentInflammatory mediatorIntraperitoneal injectionBiophysicsTissue inhibitor of metalloproteinaseMatrix metalloproteinaseBiochemistryDexamethasoneDinoprostoneCell LineProinflammatory cytokineMicechemistry.chemical_compoundStructural BiologyFibrosisIn vivoInternal medicineGeneticsmedicineAnimalsHumansRNA MessengerProstaglandin E2Molecular BiologyCells CulturedTissue Inhibitor of Metalloproteinase-2ChemistryMetalloendopeptidasesProteinsExtracellular matrixCell BiologyTissue inhibitor of metalloproteinasemedicine.diseaseFibrosisRatsEndocrinologyGene Expression RegulationLiverProtein BiosynthesisCytokinesRat hepatocytemedicine.drug
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Immune-inflammatory and metabolic effects of high dose furosemide plus hypertonic saline solution (HSS) treatment in cirrhotic subjects with refracto…

2016

Introduction Patients with chronic liver diseases are usually thin as a result of hypermetabolism and malnutrition expressed by reduced levels of leptin and impairment of other adyponectins such as visfatin. Aims We evaluated the metabolic and inflammatory effects of intravenous high-dose furosemide plus hypertonic saline solutions (HSS) compared with repeated paracentesis and a standard oral diuretic schedule, in patients with cirrhosis and refractory ascites. Methods 59 consecutive cirrhotic patients with refractory ascites unresponsive to outpatient treatment. Enrolled subjects were randomized to treatment with intravenous infusion of furosemide (125-250mg⁄bid) plus small volumes of HSS …

Liver CirrhosisMaleLeptinCirrhosisPhysiologyPeptide Hormonesmedicine.medical_treatmentdiureticlcsh:MedicineVisfatinPathology and Laboratory MedicineFurosemide; Hypertonic Saline Solution; TNF-alpha; IL-1beta; IL-6; ANP; BNP; Visfatin; Leptin; cirrhosis; refractory ascites; paracentesis; diureticBiochemistryGastroenterology0302 clinical medicineRecurrenceFurosemideImmune PhysiologyMedicine and Health SciencesParacentesisDiureticslcsh:ScienceImmune ResponseSalineHypertonicInnate Immune SystemMultidisciplinarymedicine.diagnostic_testLiver DiseasesPhysicsLeptinrefractory asciteAscitesClassical MechanicsFurosemideHematologyMiddle AgedBody FluidsBloodTreatment OutcomeCirrhosis030220 oncology & carcinogenesisPhysical SciencesHypermetabolismCytokinesAdministration IntravenousFemale030211 gastroenterology & hepatologyAnatomyInflammation MediatorsANPResearch ArticleTNF-alphamedicine.drugparacentesimedicine.medical_specialtyInflammatory DiseasesImmunologyGastroenterology and HepatologyBlood Plasma03 medical and health sciencesSigns and SymptomsDiagnostic MedicineOsmotic PressureInternal medicinePressuremedicineTonicityHumansAgedInflammationSaline Solution HypertonicIL-6business.industrylcsh:RBiology and Life SciencesMolecular DevelopmentIL-1betamedicine.diseaseHormonesHypertonic salineEndocrinologyImmune Systemlcsh:QHypertonic Saline SolutionDiureticbusinessBiomarkersDevelopmental BiologyBNPcirrhosi
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IL-10 down-regulates T cell activation by antigen-presenting liver sinusoidal endothelial cells through decreased antigen uptake via the mannose rece…

1998

SUMMARYOur study demonstrates that antigen-presenting liver sinusoidal endothelial cells (LSEC) induce production of interferon-gamma (IFN-γ) from cloned Th1 CD4+ T cells. We show that LSEC used the mannose receptor for antigen uptake, which further strengthened the role of LSEC as antigen-presenting cell (APC) population in the liver. The ability of LSEC to activate cloned CD4+ T cells antigen-specifically was down-regulated by exogenous prostaglandin E2 (PGE2) and by IL-10. We identify two separate mechanisms by which IL-10 down-regulated T cell activation through LSEC. IL-10 decreased the constitutive surface expression of MHC class II as well as of the accessory molecules CD80 and CD86 …

Liver cytologyT cellT-LymphocytesImmunologyAntigen presentationAntigen-Presenting CellsDown-RegulationReceptors Cell SurfaceBiologyLymphocyte ActivationDinoprostoneMiceAntigenAntigens CDmedicineImmunology and AllergyAnimalsLectins C-TypeCD86Antigen PresentationMice Inbred BALB CMembrane GlycoproteinsHistocompatibility Antigens Class IIOriginal ArticlesInterleukin-10Interleukin 10medicine.anatomical_structureMannose-Binding LectinsLiverImmunologyB7-1 AntigenCytokinesFemaleB7-2 AntigenEndothelium VascularMannoseCD80Mannose receptorMannose ReceptorClinical and experimental immunology
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Activation of the PD-1 Pathway Contributes to Immune Escape in EGFR-Driven Lung Tumors

2013

Abstract The success in lung cancer therapy with programmed death (PD)-1 blockade suggests that immune escape mechanisms contribute to lung tumor pathogenesis. We identified a correlation between EGF receptor (EGFR) pathway activation and a signature of immunosuppression manifested by upregulation of PD-1, PD-L1, CTL antigen-4 (CTLA-4), and multiple tumor-promoting inflammatory cytokines. We observed decreased CTLs and increased markers of T-cell exhaustion in mouse models of EGFR-driven lung cancer. PD-1 antibody blockade improved the survival of mice with EGFR-driven adenocarcinomas by enhancing effector T-cell function and lowering the levels of tumor-promoting cytokines. Expression of m…

Lung NeoplasmsT-LymphocytesT cellProgrammed Cell Death 1 ReceptorMice TransgenicLymphocyte ActivationB7-H1 AntigenArticleCell LineProinflammatory cytokineMiceCarcinoma Non-Small-Cell LungTumor MicroenvironmentmedicineAnimalsHumansCytotoxic T cellEpidermal growth factor receptorLung cancerEGFR inhibitorsTumor microenvironmentbiologyOncogenesmedicine.diseaseErbB ReceptorsGene Expression Regulation NeoplasticMice Inbred C57BLmedicine.anatomical_structureOncologyTumor EscapeImmunologyCancer researchbiology.proteinCytokinesTumor EscapeSignal TransductionCancer Discovery
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Deficient cytokine response of human allergen-specific T lymphocytes from humanized SCID mice and reconstitution by professional antigen-presenting c…

2000

Abstract Background: Hu-PBL-SCID mice generated by the transfer of PBMCs from atopic individuals may provide a physiologic in vivo model for investigating human responses to allergens and potential approaches toward immunotherapy. Objective: This study was undertaken to investigate the functional activity and cytokine profile of human allergen-reactive T lymphocytes isolated from hu-PBL-SCID mice. Methods: PBMCs from allergic individuals were coinjected with allergen into SCID mice. Human lymphocyte migration and phenotype were established by reverse transcription–PCR and immunohistochemistry, IgE levels in sera were determined, and the frequency of allergen-reactive cytokine-producing T ly…

Lymphoid Tissuemedicine.medical_treatmentT-LymphocytesImmunologyAntigen-Presenting CellsMice SCIDBiologyImmunoglobulin EEpitopesMiceImmune systemTh2 CellsCell MovementmedicineImmunology and AllergyAnimalsHumansInterferon gammaRNA MessengerAntigen-presenting cellInterleukin 5Cells CulturedT lymphocyteImmunotherapyAllergensImmunoglobulin ECytokineImmunologyAntibody Formationbiology.proteinCytokinesPeritoneumSpleenmedicine.drugThe Journal of allergy and clinical immunology
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Emerging drugs for the treatment of vitiligo.

2020

Introduction: Vitiligo is a relatively common autoimmune depigmenting disorder of the skin. There has been a great advance in understanding the pathological basis, which has led to the development and utilization of various new molecules in treating vitiligo. This review aims at a comprehensively describing the treatments available and the emerging treatment aspects and the scope for future developments.Areas covered: This study comprehensively summarizes the current concepts in the pathogenesis of vitiligo with special focus on the cytokine and signaling pathways, which are the targets for newer drugs. JAK kinase signaling pathways and the cytokines involved are the focus of vitiligo treat…

MAP Kinase Signaling SystemAdministration TopicalVitiligoAdministration OralVitiligoBiologicsBioinformatics030226 pharmacology & pharmacy03 medical and health scienceschemistry.chemical_compound0302 clinical medicineClinical Trials Phase II as TopicLocalized vitiligoMedicineHumansJanus Kinase InhibitorsPharmacology (medical)skin and connective tissue diseasesRandomized Controlled Trials as TopicPharmacologytreatmentintegumentary systembusiness.industrymedicine.diseaseCombined Modality TherapyJAK inhibitorchemistryClinical Trials Phase III as Topic030220 oncology & carcinogenesisCytokinesAfamelanotideDermatologic AgentsbusinessJanus kinaseBiologics; JAK inhibitor; treatment; vitiligoExpert opinion on emerging drugs
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The stimulation of arginine transport by TNFα in human endothelial cells depends on NF-κB activation

2004

In human saphenous vein endothelial cells (HSVECs), tumor necrosis factor-alpha (TNFalpha) and bacterial lipopolysaccharide (LPS), but neither interferon gamma (IFNgamma) nor interleukin 1beta (IL-1beta), stimulate arginine transport. The effects of TNFalpha and LPS are due solely to the enhancement of system y+ activity, whereas system y+L is substantially unaffected. TNFalpha causes an increased expression of SLC7A2/CAT-2B gene while SLC7A1/CAT-1 expression is not altered by the cytokine. The suppression of PKC-dependent transduction pathways, obtained with the inhibitor chelerytrhine, the inhibitor peptide of PKCzeta isoform, or chronic exposure to phorbol esters, does not prevent TNFalp…

MAPK/ERK pathwayLipopolysaccharidesmedicine.medical_specialtyUmbilical VeinsTime FactorsCAT transporterArginineTranscription Geneticp38 mitogen-activated protein kinasesmedicine.medical_treatmentBiophysicsPharmacologyBiologyArgininePolymerase Chain Reactionp38 Mitogen-Activated Protein KinasesBiochemistryInterferon-gammaInternal medicineCationsmedicineTNFαHumansInterferon gammaRNA MessengerCationic Amino Acid Transporter 2Cells CulturedProtein Kinase CArginine transportReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaNF-kappa BBiological TransportCell BiologyCytokineEndocrinologySLC7 geneAmino Acid Transport Systems BasicCytokinesTumor necrosis factor alphaEndothelium VascularSignal transductionMitogen-Activated Protein KinasesPeptidesmedicine.drugInterleukin-1Signal TransductionNFκBBiochimica et Biophysica Acta (BBA) - Biomembranes
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Evaluation of the Role of Candida albicans Agglutinin-Like Sequence (Als) Proteins in Human Oral Epithelial Cell Interactions

2012

The fungus C. albicans uses adhesins to interact with human epithelial surfaces in the processes of colonization and pathogenesis. The C. albicans ALS (agglutinin-like sequence) gene family encodes eight large cell-surface glycoproteins (Als1-Als7 and Als9) that have adhesive function. This study utilized C. albicans Δals mutant strains to investigate the role of the Als family in oral epithelial cell adhesion and damage, cytokine induction and activation of a MAPK-based (MKP1/c-Fos) signaling pathway that discriminates between yeast and hyphae. Of the eight Δals mutants tested, only the Δals3 strain showed significant reductions in oral epithelial cell adhesion and damage, and cytokine pro…

MAPK/ERK pathwaySciencemedicine.medical_treatmentImmunologyBlotting WesternMycologyMicrobiologyFungal ProteinsMolecular Cell BiologymedicineGeneticsHumansPhosphorylationCandida albicansCell damageBiologyMultidisciplinarybiologyQRImmunityMouth MucosaDual Specificity Phosphatase 1Epithelial Cellsbiology.organism_classificationmedicine.diseaseCorpus albicansSignaling CascadesCell biologyBacterial adhesinCytokineImmune SystemMedicineCytokinesSignal transductionCellular TypesCandidalysinCell Adhesion MoleculesProto-Oncogene Proteins c-fosResearch ArticleDevelopmental BiologySignal Transduction
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Candida albicans Yeast and Hyphae are Discriminated by MAPK Signaling in Vaginal Epithelial Cells

2011

We previously reported that a bi-phasic innate immune MAPK response, constituting activation of the mitogen-activated protein kinase (MAPK) phosphatase MKP1 and c-Fos transcription factor, discriminates between the yeast and hyphal forms of Candida albicans in oral epithelial cells (ECs). Since the vast majority of mucosal Candida infections are vaginal, we sought to determine whether a similar bi-phasic MAPK-based immune response was activated by C. albicans in vaginal ECs. Here, we demonstrate that vaginal ECs orchestrate an innate response to C. albicans via NF-κB and MAPK signaling pathways. However, unlike in oral ECs, the first MAPK response, defined by c-Jun transcription factor acti…

MAPK/ERK pathwaylcsh:MedicineYeast and Fungal ModelsPathogenesisSignal transductionMolecular cell biologyCandida albicansGranulocyte Colony-Stimulating FactorCandida albicanslcsh:ScienceImmune Response0303 health sciencesMultidisciplinarybiologyCandidiasisNF-kappa BSignaling cascadesObstetrics and GynecologyCorpus albicansInnate ImmunityHost-Pathogen InteractionInfectious DiseasesVaginaCytokinesMedicineFemaleSignal transductionCandidalysinResearch ArticleMAPK signaling cascadesMAP Kinase Signaling SystemUrologyImmunologySexually Transmitted DiseasesHyphaeMycologyMicrobiologyMicrobiologyImmune Activation03 medical and health sciencesModel OrganismsHumansTranscription factorBiology030304 developmental biologyInnate immune systemChemokine CCL20030306 microbiologyGenitourinary InfectionsInterleukin-6lcsh:RImmunityFungiMouth MucosaImmune DefenseEpithelial Cellsbiology.organism_classificationImmunity InnateCCL20Immune Systemlcsh:QClinical ImmunologyPLoS ONE
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