Search results for " chemokine"

showing 10 items of 79 documents

The Transcription Factor Promyelocytic Leukemia Zinc Finger Protein Is Associated With Expression of Liver‐Homing Receptors on Human Blood CD56bright…

2020

The transcription factor promyelocytic leukemia zinc finger protein (PLZF) is involved in the development of natural killer (NK) cells and innate lymphoid cells, including liver‐resident NK cells in mice. In human NK cells, the role of PLZF in liver residency is still unknown. Expression of PLZF in matched human peripheral blood‐ and liver‐derived NK cells and the association of PLZF expression with surface molecules and transcription factors relevant for tissue residency were investigated using multiparameter flow cytometry and assessing single‐cell messenger RNA (mRNA) levels. Intrahepatic cluster of differentiation (CD)56bright NK cells expressed significantly higher levels of PLZF than …

[SDV.IMM] Life Sciences [q-bio]/ImmunologyPopulationCellC-C chemokine receptor type 6Biology03 medical and health sciences0302 clinical medicinemedicinelcsh:RC799-869ReceptoreducationTranscription factor030304 developmental biology0303 health sciencesMessenger RNAeducation.field_of_studyHepatologyCluster of differentiationInnate lymphoid cellOriginal ArticlesSISTM3. Good healthmedicine.anatomical_structureCancer research[SDV.IMM]Life Sciences [q-bio]/ImmunologyOriginal Articlelcsh:Diseases of the digestive system. Gastroenterology030215 immunologyHepatology Communications
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A T cell-specific deletion of HDAC1 protects against experimental autoimmune encephalomyelitis.

2017

Multiple sclerosis (MS) is a human neurodegenerative disease characterized by the invasion of autoreactive T cells from the periphery into the CNS. Application of pan-histone deacetylase inhibitors (HDACi) ameliorates experimental autoimmune encephalomyelitis (EAE), an animal model for MS, suggesting that HDACi might be a potential therapeutic strategy for MS. However, the function of individual HDAC members in the pathogenesis of EAE is not known. In this study we report that mice with a T cell-specific deletion of HDAC1 (using the Cd4-Cre deleter strain; HDAC1-cKO) were completely resistant to EAE despite the ability of HDAC1cKO CD4+ T cells to differentiate into Th17 cells. RNA sequencin…

0301 basic medicineReceptors CCR6Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisReceptors CCR4T cellImmunologyCCR4Histone Deacetylase 1C-C chemokine receptor type 6Biologymedicine.disease_causeAutoimmunity03 medical and health sciencesChemokine receptorMice0302 clinical medicineCell MovementmedicineImmunology and AllergyAnimalsHumansCells CulturedMice KnockoutChimeraMultiple sclerosisExperimental autoimmune encephalomyelitisGene targetingmedicine.diseaseMolecular biologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureSTAT1 Transcription FactorCancer researchTh17 Cells030215 immunologyJournal of autoimmunity
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CC chemokine receptor 5 polymorphism in Italian patients with Beḩet's disease

2012

OBJECTIVE: To evaluate the potential role of CC chemokine receptor 5 (CCR5)Δ32 polymorphism in the susceptibility to and clinical expression of Behcet's disease (BD) in a cohort of Italian patients. METHODS: One hundred and ninety-six consecutive Italian patients satisfying the ISG criteria for BD were followed up for 8 years, and 180 healthy age- and sex-matched blood donors were molecularly genotyped for the CCR5Δ32 polymorphism. A standard microlymphocytotoxicity technique was used to serotype HLA-B51. The patients were subgrouped on the basis of the presence or absence of clinical manifestations. RESULTS: The distribution of the CCR5Δ32 genotype differed between BD patients and controls…

AdultMalemedicine.medical_specialtyHeterozygoteReceptors CCR5Behcet's disease CCR5 polymorphismBehcet's diseaseGastroenterologyRheumatologyGeneticGene FrequencyInternal medicineGenotypeReceptorsMedicineHumansPharmacology (medical)Genetic Predisposition to DiseaseAllelePolymorphismAllele frequencyPolymorphism Geneticbusiness.industryBehcet SyndromeHomozygoteCase-control studyOdds ratiomedicine.diseaseBeḩet's disease; CC chemokine receptor 5 Δ32 olymorphism; Chemokines; Disease manifestations; Adult; Behcet Syndrome; Case-Control Studies; Female; Gene Frequency; Genetic Predisposition to Disease; HLA-B Antigens; Heterozygote; Homozygote; Humans; Italy; Male; Polymorphism Genetic; Receptors CCR5; Rheumatology; Pharmacology (medical)Adult; Behcet Syndrome; Case-Control Studies; Female; Gene Frequency; Genetic Predisposition to Disease; HLA-B Antigens; Heterozygote; Homozygote; Humans; Italy; Male; Polymorphism Genetic; Receptors CCR5ItalyHLA-B AntigensCase-Control StudiesImmunologyCohortFemalebusinessCC chemokine receptorsCCR5
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Double Negative (IgG+IgD-CD27-) B Cells are Increased in a Cohort of Moderate-Severe Alzheimer’s Disease Patients and Show a Pro-Inflammatory Traffic…

2014

Alzheimer's disease (AD) is a progressive, irreversible, and debilitating disease for which no effective preventive or disease modifying therapies or treatments have so far been detected. The crucial step in AD pathogenesis is the production of amyloid-42 peptide, which causes chronic inflammation. Activated cells in the central nervous system (CNS) produce pro- inflammatory mediators that lead to the recruitment of myeloid or lymphocytic cells. As a consequence, the communication between the CNS and peripheral blood of AD subjects could influence the lymphocyte distribution and/or the expression of phenotypic markers. In the present paper, we show a significant decrease in total CD19 + B l…

MaleReceptors CCR6Receptors CCR7MyeloidLymphocyteB-Lymphocyte SubsetsC-C chemokine receptor type 7InflammationC-C chemokine receptor type 6Immunoglobulin DCD19Cohort StudiesAlzheimer DiseasemedicineHumansB cellAgedAged 80 and overSettore MED/04 - Patologia GeneralebiologyGeneral NeuroscienceGeneral MedicineImmunoglobulin DFlow CytometryTumor Necrosis Factor Receptor Superfamily Member 7Psychiatry and Mental healthClinical Psychologymedicine.anatomical_structurePhenotypeAlzheimer's Disease Inflammation B CellsImmunoglobulin GImmunologybiology.proteinFemaleSettore MED/26 - NeurologiaGeriatrics and Gerontologymedicine.symptomMental Status Schedule
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Monocytes/macrophages but not T lymphocytes are the major targets of the CCL3/CCL4 chemokines produced by CD38(+)CD49d(+) chronic lymphocytic leukaem…

2010

ChemokineChronic lymphocytic leukemiaT-LymphocytesCCL3CD38Settore MED/08 - Anatomia PatologicaCD49dMonocytesMacrophages; Tumor Cells Cultured; Leukemia Lymphocytic Chronic B-Cell; Humans; Monocytes; Chemokine CCL4; Chemokine CCL3; T-LymphocytesTumor Cells CulturedMedicineMacrophageHumansChronicChemokine CCL4Chemokine CCL3CulturedLeukemiabiologybusiness.industryMonocyteMacrophagesB-CellHematologyT lymphocytemedicine.diseaseLeukemia Lymphocytic Chronic B-CellLymphocyticTumor Cellsmedicine.anatomical_structureImmunologybiology.proteinbusinessSettore MED/15 - Malattie del SangueCCL3/CCL4 CD38CD49d chronic lymphocitic leukemia
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Content of blood cell components, inflammatory cytokines and growth factors in autologous platelet-rich plasma obtained by various methods.

2022

BACKGROUND The evaluation of the efficacy of platelet-rich plasma (PRP) in clinical practice yields conflicting results and raises numerous controversies. This may be due to different concentrations of biologically active components in PRP obtained with the use of different methods of gravity separation. AIM To compare the content, repeatability and correlations between biologically active components in PRP obtained with four different commercial systems. METHODS From a whole blood sample of each of 12 healthy male volunteers, 4 PRP samples were prepared using 4 different commercial kits [Arthrex Autologous Conditioned Plasma (ACP), Mini GPS III, Xerthra, Dr. PRP] in accordance with the ins…

Orthopedics and Sports MedicinePlatelet-rich plasma; Cytokines; Chemokines; Growth factorsWorld journal of orthopedics
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IL-33/ST2 pathway regulates neutrophil migration and predicts outcome in patients with severe alcoholic hepatitis.

2020

Background & Aims Severe alcoholic hepatitis (SAH) is associated with a high risk of infection. The IL-33/ST2 pathway is involved in sepsis control but data regarding its role in alcohol-related liver disease (ALD) are lacking. We aimed to characterize the role of IL-33/ST2 in the polymorphonuclear neutrophils (PMNs) of patients with ALD and SAH. Methods Serum and circulating neutrophils were collected from patients with SAH, alcoholic cirrhosis and healthy controls. We quantified IL-33/ST2 pathway activity and CXCR2 at baseline and after exposure to IL-33. We also determined the migration capacity of PMNs. Results The decoy receptor of IL-33 (soluble ST2 [sST2]) was increased in SAH vs. ci…

Male0301 basic medicineAlcoholic liver diseaseCirrhosisPolymorphonuclear neutrophilsNeutrophils[SDV.MHEP.PHY] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]ApoptosisGastroenterologyReceptors Interleukin-8BLiver disease0302 clinical medicineCell MovementLiver Cirrhosis AlcoholicProspective StudiesCXC chemokine receptorsReceptorCells CulturedMigrationMiddle AgedPrognosisRecombinant Proteins3. Good healthCirrhosisAlcoholic hepatitis;Cirrhosis;Infection;Interleukin-33;Migration;Polymorphonuclear neutrophilsFemale030211 gastroenterology & hepatologyAlcoholic hepatitisInfectionSignal TransductionAdultmedicine.medical_specialtyAlcoholic hepatitisSepsis03 medical and health sciencesInternal medicinemedicine[SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]Humanscardiovascular diseasesAgedHepatologyHepatitis Alcoholicbusiness.industrymedicine.diseaseInterleukin-33Interleukin-1 Receptor-Like 1 Proteinnervous system diseasesInterleukin 33030104 developmental biologyCase-Control StudiesbusinessFollow-Up Studies
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Systemic Immune Responses in Alzheimer's Disease: In Vitro Mononuclear Cell Activation and Cytokine Production

2010

To investigate the systemic signs of immune-inflammatory responses in Alzheimer's disease (AD), in the present study we have analyzed blood lymphocyte subsets and the expression of activation markers on peripheral blood mononuclear cells (PBMCs) from AD patients and age-matched healthy controls (HC) activated in vitro by recombinant amyloid-beta peptide (rAbeta42). Our study of AD lymphocyte subpopulations confirms the already described decrease of the absolute number and percentage of B cells when compared to HC lymphocytes, whereas the other subsets are not significantly different in patients and controls. We report the increased expression of the activation marker CD69 and of the chemoki…

MaleEotaxinCCR2ChemokineTime Factorsmedicine.medical_treatmentPeripheral blood mononuclear cellChemokine receptorImmune systemAlzheimer’s disease chemokine cytokine PBMC rAβ42Alzheimer DiseasemedicineHumansLymphocytesIL-2 receptorCells CulturedAgedSettore MED/04 - Patologia GeneraleAged 80 and overAnalysis of VarianceAmyloid beta-Peptidesbiologybusiness.industryGeneral NeuroscienceGeneral MedicineMiddle AgedFlow CytometryPeptide FragmentsPsychiatry and Mental healthClinical PsychologyCytokineGene Expression RegulationCase-Control StudiesImmunologyLeukocytes Mononuclearbiology.proteinCytokinesFemaleGeriatrics and GerontologybusinessJournal of Alzheimer's Disease
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Insulin resistance aggravates atherosclerosis by reducing vascular smooth muscle cell survival and increasing CX3CL1/CX3CR1 axis.

2014

Aims Insulin resistance (IR) is a major risk factor for cardiovascular disease and atherosclerosis. Life-threatening acute events are mainly due to rupture of unstable plaques, and the role of vascular smooth muscle cells (VSMCs) in this process in IR, Type 2 diabetes mellitus, and metabolic syndrome (T2DM/MetS) has not been fully addressed. Therefore, the role of VSMC survival in the generation of unstable plaques in T2DM/MetS and the involvement of inflammatory mediators was investigated. Methods and results Defective insulin receptor substrate 2 (IRS2)-mediated signalling produced insulin-resistant VSMCs with reduced survival, migration, and higher apoptosis than control cells. Silencing…

medicine.medical_specialtyVascular smooth musclePhysiologyCell Survivalmedicine.medical_treatmentMyocytes Smooth MuscleCX3C Chemokine Receptor 1InflammationMice TransgenicBiologyMuscle Smooth VascularInsulin resistanceApolipoproteins EPhysiology (medical)Internal medicinemedicineAnimalsHumansProtein kinase BPI3K/AKT/mTOR pathwayCells CulturedMice KnockoutChemokine CX3CL1Insulinmedicine.diseaseAtherosclerosisIRS2Mice Inbred C57BLAtheromaEndocrinologyDiabetes Mellitus Type 2cardiovascular systemReceptors Chemokinemedicine.symptomInsulin ResistanceCardiology and Cardiovascular MedicineSignal TransductionCardiovascular research
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Mboat7 down-regulation by hyper-insulinemia induces fat accumulation in hepatocytes.

2020

Background: Naturally occurring variation in Membrane-bound O-acyltransferase domain-containing 7 (MBOAT7), encoding for an enzyme involved in phosphatidylinositol acyl-chain remodelling, has been associated with fatty liver and hepatic disorders. Here, we examined the relationship between hepatic Mboat7 down-regulation and fat accumulation. Methods: Hepatic MBOAT7 expression was surveyed in 119 obese individuals and in experimental models. MBOAT7 was acutely silenced by antisense oligonucleotides in C57Bl/6 mice, and by CRISPR/Cas9 in HepG2 hepatocytes. Findings: In obese individuals, hepatic MBOAT7 mRNA decreased from normal liver to steatohepatitis, independently of diabetes, inflammatio…

Research paperTGFβ Transforming Growth Factor BetaIntracellular SpaceCRISPR Clustered Regularly Interspaced Short Palindromic RepeatshHEPS Human HepatocytesMice0302 clinical medicineLPIAT1DAG Diacylglyceroli.p. Intraperitonealmedia_commonFatty AcidsGeneral Medicine3. Good health030220 oncology & carcinogenesisHOMA-IR homeostasis Model Assessment of Insulin ResistanceMPO morpholinolcsh:Medicine (General)medicine.medical_specialtyPE Phosphatidyl-EthanolamineNashGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesTNFα tumor Necrosis Factor AlphaLDL Low Density LipoproteinsHyperinsulinismNAFLDSD Standard Dietmedia_common.cataloged_instanceHumansCPT1 Carnitine Palmitoyltransferase IPhosphatidylinositolGene SilencingEuropean unionVLDL Very Low Density Lipoproteinlcsh:RhHSC Human Hepatic Stellate Cellsmedicine.diseaseLipid MetabolismOA Oleic AcidCI Confidence IntervalMboat7 Membrane bound O-acyltransferase domain containing 7MCD methionine choline deficient diet030104 developmental biologyEndocrinologychemistryCDP Cytidine-DiphosphateFOXO1 Forkhead Box protein O1NAFLD nonalcoholic fatty liver diseaseSteatohepatitisBMI Body Mass IndexCL CardiolipinAcyltransferases0301 basic medicineAlcoholic liver diseaseCXCL10 C-X-C Motif Chemokine 10lcsh:Medicinechemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseIFG Impaired Fasting GlucoseAPOB Apolipoprotein BNonalcoholic fatty liver diseasePIP Phosphatidyl-Inositol-PhosphateSteatohepatitisqRT-PCR quantitative Real Time Polymerase Chain ReactionMice Knockoutlcsh:R5-920ORO Oil Red O StainingPI PhosphatidylinositolFatty liverTM6SF2 Transmembrane 6 Superfamily Member 2PhospholipidTAG TriglyceridesNASH Nonalcoholic SteatohepatitisLipogenesisLPA Lyso-Phosphatidic AcidPhosphatidylinositolSignal TransductionPS Phosphatidyl-SerinePA Palmitic AcidALD alcoholic liver diseasePC Phosphatidylcholinei.v. IntravenousFATP1 Fatty Acid Transport Protein 1Models BiologicalInternal medicinemedicineAnimalsNonalcoholic fatty liver diseasePPARα Peroxisome Proliferator-Activated Receptor alphaObesityG3P Glyceraldehyde-3-PhosphateSREBP1c Sterol Regulatory Element-Binding Protein 1HDL High Density Lipoproteinsbusiness.industryPI3K Phosphatidylinositol 3 KinaseMembrane ProteinsNHEJ Non-Homologues End JoiningPNPLA3 Patatin-like Phospholipase Domain-containing-3MTTP Microsomal Triglyceride Transfer ProteinLPIAT1 Lysophosphatidylinositol Acyltransferase 1TMC4 Transmembrane Channel-Like 4Disease Models AnimalGene Expression RegulationHepatocytesFOXA2 Forkhead Box A2mTOR mammalian target of RapamycinSteatosisInsulin ResistancebusinessPG Phosphatidyl-GlycerolFABP1 Fatty Acid-Binding Protein 1 FAS Fatty Acid SynthaseT2DM Type 2 Diabetes MellitusEBioMedicine
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