Search results for "l2"

showing 10 items of 413 documents

Dual therapy with peg-interferon and ribavirin in thalassemia major patients with chronic HCV infection: Is there still an indication?

2016

Background: Iron overload and hepatitis C virus (HCV) infection together can lead to chronic liver damage in thalassemia major (TM) patients. Aims: We investigated viral, genetic, and disease factors influencing sustained virological response (SVR) after peg-interferon and ribavirin therapy in TM patients with HCV infection. Methods: We analyzed 230 TM patients with HCV infection (mean age 36.0 ± 6.3 years; 59.1% genotype 1; 32.2% genotype 2; 3.4% genotype 3; and 5.3% genotype 4; 28.7% carried CC allele of rs12979860 in IL28B locus; 79.6% had chronic hepatitis and 20.4% cirrhosis; 63.5% naive and 36.5% previously treated with interferon alone) treated in 14 Italian centers. Results: By mul…

Liver Cirrhosis0301 basic medicineMaleCirrhosisThalassemiaHepacivirusCirrhosis; Hepatitis C virus; IL28B polymorphisms; Iron liver overload; Peg-interferon; Ribavirin; Sustained virological response; Thalassemia major; Adult; Antiviral Agents; Drug Therapy Combination; Female; Heart Diseases; Hepacivirus; Hepatitis C Chronic; Humans; Interferon-alpha; Interleukins; Italy; Liver Cirrhosis; Logistic Models; Male; Multivariate Analysis; Polymorphism Single Nucleotide; Retrospective Studies; Ribavirin; Treatment Outcome; Viral Load; beta-Thalassemiamedicine.disease_causeGastroenterologychemistry.chemical_compound0302 clinical medicineRetrospective StudieThalassemia majorMultivariate AnalysiGastroenterologyBeta thalassemiaHepatitis CViral LoadSustained virological responseHeart DiseaseTreatment OutcomeItaly030211 gastroenterology & hepatologyDrug Therapy CombinationFemaleViral loadHumanAdultmedicine.medical_specialtyHeart DiseasesLogistic ModelHepatitis C virusLiver CirrhosiAlpha interferonIL28B polymorphismAntiviral AgentsPolymorphism Single Nucleotide03 medical and health sciencesIron liver overloadInternal medicineRibavirinmedicineHumansRetrospective StudiesAntiviral AgentCirrhosiHepaciviruPeg-interferonHepatologybusiness.industryInterleukinsRibavirinbeta-ThalassemiaInterferon-alphaHepatitis C ChronicInterleukinmedicine.diseaseLogistic Models030104 developmental biologychemistryMultivariate AnalysisImmunologyInterferonsbusinessHepatitis C viru
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Dendritic cells in liver injury and fibrosis: shortcomings and promises.

2013

SummaryThe phenotype and function of liver dendritic cells (LDCs) are poorly understood. This Snapshot summarizes our current knowledge on LDCs in the healthy and injured liver, and their role in fibrosis progression and reversal. It also draws attention to various pitfalls in the current experimental design and conclusions based on available data.

Liver CirrhosisLiver dendritic cellsPlasmacytoid dendritic cellBiologyCCL2MiceFMS-like tyrosine kinase 3 ligandFibrosismedicineAnimalsHumansAntigen-presenting cellLiver injuryHepatologyFlt3LDendritic Cellsmedicine.diseaseCD11c-DTRDisease Models Animalmedicine.anatomical_structurePhenotypeLiverImmunologyHepatic stellate cellDisease ProgressionBone marrowToleranceJournal of hepatology
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Loss of p53 Attenuates the Contribution of IL-6 Deletion on Suppressed Tumor Progression and Extended Survival in Kras-Driven Murine Lung Cancer

2013

Interleukin-6 (IL-6) is involved in lung cancer tumorigenesis, tumor progression, metastasis, and drug resistance. Previous studies show that blockade of IL-6 signaling can inhibit tumor growth and increase drug sensitivity in mouse models. Clinical trials in non-small cell lung cancer (NSCLC) reveal that IL-6 targeted therapy relieves NSCLC-related anemia and cachexia, although other clinical effects require further study. We crossed IL-6(-/-) mice with Kras(G12D) mutant mice, which develop lung tumors after activation of mutant Kras(G12D), to investigate whether IL-6 inhibition contributes to tumor progression and survival time in vivo. Kras(G12D); IL-6(-/-) mice exhibited increased tumor…

Lung Neoplasmsmedicine.medical_treatmentlcsh:Medicinemedicine.disease_causeMetastasisTargeted therapyMice0302 clinical medicineCarcinoma Non-Small-Cell LungNeoplasm MetastasisPhosphorylationlcsh:Science0303 health sciencesMultidisciplinary3. Good healthGene Expression Regulation Neoplastic030220 oncology & carcinogenesisDisease ProgressionKRASResearch ArticleSignal TransductionSTAT3 Transcription FactorMice TransgenicBiologyProto-Oncogene Proteins p21(ras)03 medical and health sciencesFLOXmedicineAnimalsHumansLung cancerneoplasms030304 developmental biologyChemokine CCL20Interleukin-6Tumor Necrosis Factor-alphalcsh:RCancermedicine.diseaseSurvival Analysisdigestive system diseasesrespiratory tract diseasesDisease Models AnimalTumor progressionMutationCancer researchChemokine CCL19lcsh:QTumor Suppressor Protein p53CarcinogenesisPLoS ONE
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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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Extracellular Vesicles From Liver Progenitor Cells Downregulates Fibroblast Metabolic Activity and Increase the Expression of Immune-Response Related…

2021

Extracellular vesicles (EVs) mediate cell-to-cell crosstalk whose content can induce changes in acceptor cells and their microenvironment. MLP29 cells are mouse liver progenitor cells that release EVs loaded with signaling cues that could affect cell fate. In the current work, we incubated 3T3-L1 mouse fibroblasts with MLP29-derived EVs, and then analyzed changes by proteomics and transcriptomics. Results showed a general downregulation of protein and transcript expression related to proliferative and metabolic routes dependent on TGF-beta. We also observed an increase in the ERBB2 interacting protein (ERBIN) and Cxcl2, together with an induction of ribosome biogenesis and interferon-relate…

MLP29ChemistryMLP29 cell crosstalk exosomes extracellular vesicles (EVs) fibroblast immune responseCell BiologyexosomesCell fate determinationcell crosstalkMicrovesiclesfibroblastimmune responseCell biologyCell and Developmental BiologyCXCL2Crosstalk (biology)Immune systemmedicine.anatomical_structurelcsh:Biology (General)Downregulation and upregulationmedicineProgenitor cellextracellular vesicles (EVs)Fibroblastlcsh:QH301-705.5Original ResearchDevelopmental Biology
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Intraperitoneal administration of the anti-IL-23 antibody prevents the establishment of intestinal nematodes in mice

2018

AbstractPrevious studies have established that an increased Th-9 response creates a hostile environment for nematode parasites. Given that IL-23, a cytokine required for maintenance of the IL-17–secreting phenotype, has inhibitory effects on IL-9 production, we hypothesized that reducing circulating IL-23 by treatment with anti-IL-23 antibodies would reduce the establishment and development of parasitic intestinal nematodes. In this study, we show that animals treated with anti-IL-23 monoclonal antibodies showed a drastic reduction in the number of mouse pinworms (Aspiculuris tetraptera) recovered from the intestine (p < 0.001) at 23 days post-infection compared to the untreated animals.…

Male0301 basic medicineChemokinemedicine.drug_classmedicine.medical_treatmentlcsh:MedicineMonoclonal antibodyInterleukin-23Inflammatory bowel diseaseArticleParasite LoadMice03 medical and health sciencesInterleukin 23medicineAnimalsNematode Infectionslcsh:ScienceMice Inbred ICRMultidisciplinarybiologyInterleukinslcsh:RAntibodies Monoclonalmedicine.diseasebiology.organism_classificationIntestinesCCL20030104 developmental biologyNematodeCytokineImmunologybiology.proteinlcsh:QAntibodyInjections Intraperitoneal
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SETD7 mediates spinal microgliosis and neuropathic pain in a rat model of peripheral nerve injury

2019

Abstract Gene transcription regulation is critical for the development of spinal microgliosis and neuropathic pain after peripheral nerve injury. Using a model of chronic constriction injury (CCI) of the sciatic nerve, this study characterized the role of SET domain containing lysine methyltransferase 7 (SETD7) which monomethylates histone H3 lysine 4 (H3K4me1), a marker for active gene transcription. SETD7 protein expression in the spinal dorsal horn ipsilateral to nerve lesion was increased from one day to 14 days after CCI, concomitantly with the expression of inflammatory genes, Ccl2, Il-6 and Il-1β. The CCI-induced SETD7 expression was predominantly localized to microglia, as demonstra…

Male0301 basic medicineSpinal Cord Dorsal HornPathologymedicine.medical_specialtyImmunologyCCL2MicrogliosisRats Sprague-Dawley03 medical and health sciencesBehavioral Neuroscience0302 clinical medicinePeripheral Nerve InjuriesGanglia SpinalmedicineAnimalsGene knockdownMicrogliaEndocrine and Autonomic Systemsbusiness.industryHistone-Lysine N-MethyltransferaseNerve injurySciatic NerveSpineRats030104 developmental biologymedicine.anatomical_structureSpinal CordHyperalgesiaNeuropathic painPeripheral nerve injuryNeuralgiaFemaleMicrogliaSciatic nervemedicine.symptombusiness030217 neurology & neurosurgeryBrain, Behavior, and Immunity
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Combination of KIR 2DL2 and HLA-C1 (Asn 80) confers susceptibility to type 1 diabetes in Latvians.

2008

Summary Killer immunoglobulin-like receptors (KIRs) are known to modulate natural killer (NK) and NK T-cell function by interacting with human leucocyte antigen (HLA) class I ligands on target cells. The aim of our study was to investigate the influence of KIR2D genes with their HLA-C ligands in susceptibility to type 1 diabetes. A total of 98 type 1 diabetes patients and 70 healthy subjects from Latvia were typed for KIR genes and HLA-C ligands using polymerase chain reaction-based genotyping. The HLA C1+/C2+ combination was positively, and C1–/C2+ combination was negatively, associated with type 1 diabetes. Stratification analysis of KIR/HLA-C ligand combinations showed 2DL2+/C1+, 2DL3+/C…

MaleAdolescentGenotypeImmunologyHuman leukocyte antigenHLA-C AntigensBiologyWhite Peoplelaw.inventionImmune systemGene FrequencylawGeneticsmedicineHumansGenetic Predisposition to DiseaseReceptorChildMolecular BiologyGenotypingGeneGenetics (clinical)Polymerase chain reactionType 1 diabetesInfant NewbornInfantGeneral Medicinemedicine.diseaseLatviaDiabetes Mellitus Type 1Child PreschoolReceptors KIR2DL2ImmunologyFemaleFunction (biology)International journal of immunogenetics
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Angiotensin II-Induced Mononuclear Leukocyte Interactions with Arteriolar and Venular Endothelium Are Mediated by the Release of Different CC Chemoki…

2006

Abstract Angiotensin II (Ang-II) is associated with atherogenesis and arterial subendothelial mononuclear leukocyte infiltration. We have demonstrated that Ang-II causes the initial attachment of mononuclear cells to the arteriolar endothelium. We now report on the contribution of CC chemokines to this response. Intraperitoneal administration of 1 nM Ang-II induced MCP-1, RANTES, and MIP-1α generation, maximal at 4 h, followed by mononuclear leukocyte recruitment at 8 and 24 h. Using intravital microscopy within the rat mesenteric microcirculation 4 h after exposure to 1 nM Ang-II, arteriolar mononuclear cell adhesion was 80–90% inhibited by pretreatment with Met-RANTES, a CCR1 and CCR5 ant…

MaleCCR1EndotheliumImmunologyVascular Cell Adhesion Molecule-1Peripheral blood mononuclear cellUmbilical CordRats Sprague-DawleyLeukocyte CountCell MovementCell AdhesionLeukocytesmedicineAnimalsHumansImmunology and AllergyEndotheliumChemokine CCL5Cells CulturedChemokine CCL2Angiotensin II receptor type 1Chemokine CCL26business.industryAngiotensin IIMonocyteEpithelial Cellsmedicine.diseaseAngiotensin IIMolecular biologyRatsP-Selectinmedicine.anatomical_structureChemokines CCImmunologycardiovascular systembusinessInfiltration (medical)Intravital microscopyThe Journal of Immunology
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Control of Cell Migration and Inflammatory Mediators Production by CORM-2 in Osteoarthritic Synoviocytes

2011

Background Osteoarthritis (OA) is the most widespread degenerative joint disease. Inflamed synovial cells contribute to the release of inflammatory and catabolic mediators during OA leading to destruction of articular tissues. We have shown previously that CO-releasing molecules exert anti-inflammatory effects in animal models and OA chondrocytes. We have studied the ability of CORM-2 to modify the migration of human OA synoviocytes and the production of chemokines and other mediators sustaining inflammatory and catabolic processes in the OA joint. Methodology/Principal Findings OA synoviocytes were stimulated with interleukin(IL)-1β in the absence or presence of CORM-2. Migration assay was…

MaleChemokineAnatomy and PhysiologyInterleukin-1betalcsh:MedicineGene ExpressionMatrix metalloproteinaseBiochemistryCell MovementDrug Discoverylcsh:ScienceMusculoskeletal SystemCells CulturedChemokine CCL2MultidisciplinarybiologyReverse Transcriptase Polymerase Chain ReactionSynovial MembraneNF-kappa BInterleukinCell migrationmedicine.anatomical_structureMedicineFemaleMatrix Metalloproteinase 3Inflammation MediatorsMatrix Metalloproteinase 1Mitogen-Activated Protein KinasesResearch ArticleCell PhysiologyBlotting WesternRheumatologySynovitisOsteoarthritisOrganometallic CompoundsmedicineHumansInterleukin 8BiologyAgedCell ProliferationChemokine CCL20lcsh:RInterleukin-8medicine.diseaseTranscription Factor AP-1CCL20Oxidative StressSmall MoleculesImmunologyCancer researchbiology.proteinlcsh:QSynovial membraneHeme Oxygenase-1PLoS ONE
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