Search results for " CC"

showing 10 items of 188 documents

Analysis of memory and effector CD8+ T cell subsets in chronic graft-versus-host disease.

2009

In humans, the selective depletion of CD8+ cells may prevent GVHD after allogeneic transplantation. These cells can infiltrate and damage target tissues. It is of interest to investigate the phenotypical characteristics and cytotoxic properties of the different CD8+ subsets in cGVHD patients. In a preliminary study we found that patients with cGVHD had a markedly elevated percentage of peripheral blood CCR7−/CD45RA+ cells compared to patients without cGVHD; conversely, the CCR7+/CD45RA+ subsets of CD8+ cells was significantly decreased. In this study, we report in depth on the phenotype of effector T cell subsets in cGVHD patients, as well as their proliferative capability, cytotoxic prope…

MaleReceptors CCR7T cellImmunologyGraft vs Host DiseaseC-C chemokine receptor type 7CD8-Positive T-LymphocytesLymphocyte ActivationGranzymesimmune system diseasesmedicineImmunology and AllergyCytotoxic T cellHumansAgedPharmacologybiologyEffectorChemistryPerforinMiddle Agedmedicine.diseaseGraft-versus-host diseasemedicine.anatomical_structureGranzymePerforinImmunologyChronic Diseasebiology.proteinLeukocyte Common AntigensFemaleImmunologic MemoryCD8International journal of immunopathology and pharmacology
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Docosahexaenoic acid reduces suppressive and migratory functions of CD4CD25 regulatory T-cells

2009

Immunological tolerance is one of the fundamental aspects of the immune system. The CD4(+)CD25(+) regulatory T (Treg) cells have emerged as key players in the development of tolerance to self and foreign antigens. However, little is known about the endogenous factors and mechanisms controlling their suppressive capacity on immune response. In this study, we observed that docosahexaenoic acid (DHA), an n-3 polyunsaturated fatty acid, diminished, in a dose-dependent manner, the capacity of Treg cells to inhibit the CD4(+)CD25(-) effector T-cell proliferation. DHA not only reduced the migration of Treg cells toward chemokines but also downregulated the mRNA expression of CCR-4 and CXCR-4 in Tr…

MaleReceptors CXCR4Chemokineextracellular signal-regulated kinase 1/2Receptors CCR4Docosahexaenoic Acidschemical and pharmacologic phenomenaQD415-436T-Lymphocytes RegulatoryBiochemistryMicehistone desacetylase 7EndocrinologyImmune systemAntigenAntigens CDCell MovementTransforming Growth Factor betaAnimalsCTLA-4 AntigenRNA MessengerIL-2 receptorCells CulturedCell ProliferationDose-Response Relationship DrugbiologySmad7Reverse Transcriptase Polymerase Chain ReactionInterleukin-2 Receptor alpha SubunitFOXP3Forkhead Transcription Factorshemic and immune systemsCell BiologyTransforming growth factor betaInterleukin-10Cell biologyMice Inbred C57BLInterleukin 10Docosahexaenoic acidImmunologybiology.proteinResearch ArticleJournal of Lipid Research
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CD40 ligand and MCP-1 as predictors of cardiovascular events in diabetic patients with stroke.

2009

Aim: Up-regulation of soluble CD40 ligand (sCD40L) and of monocyte chemoattractant protein-1 (MCP-1) has been found in diabetes and in patients with acute cerebral ischemia. We asked whether (i) the two molecules are similarly upregulated among non-lacunar and lacunar diabetic strokes and (ii) sCD40L and/or MCP-1 predict the risk of cardiovascular events in this setting.Methods: Ninety patients with type 2 diabetes mellitus presenting with an acute ischemic stroke (compared with 45 control subjects) were evaluated on admission and up to 36 months (median 24 months) after the event.Results: Diabetic patients with acute stroke had higher plasma CD40L and MCP-1 than controls (p<0.0001), wit…

MaleRiskCD40 ligand stroke diabetesmedicine.medical_specialtystrokeCD40L MCP-1Settore MED/09 - Medicina Internacerebral ischemia; chemokines; cytokines; diabetes mellitusCD40 LigandIschemiachemokinesDiseasecerebral ischemiaCohort StudiesDiabetes ComplicationsInternal medicineDiabetes mellitusInternal MedicineDiabetes MellitusMedicineCD40LHumanscardiovascular diseasesStrokeChemokine CCL2Ageddiabetesbusiness.industryProportional hazards modelBiochemistry (medical)Type 2 Diabetes MellitusMiddle Agedmedicine.diseasecytokinesSurgeryStrokeTreatment OutcomeQuartileGene Expression RegulationCardiologyRegression AnalysisFemaleCardiology and Cardiovascular MedicinebusinessCohort studyMCP-1
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Thyroid hormone induction of the adrenoleukodystrophy-related gene (ABCD2).

2003

X-linked adrenoleukodystrophy (X-ALD) is a demyelinating disorder associated with impaired very-long-chain fatty-acid (VLCFA) beta-oxidation caused by mutations in the ABCD1 (ALD) gene that encodes a peroxisomal membrane ABC transporter. ABCD2 (ALDR) displays partial functional redundancy because when overexpressed, it is able to correct the X-ALD biochemical phenotype. The ABCD2 promoter contains a putative thyroid hormone-response element conserved in rodents and humans. In this report, we demonstrate that the element is capable of binding retinoid X receptor and 3,5,3'-tri-iodothyronine (T3) receptor (TRbeta) as a heterodimer and mediating T3 responsiveness of ABCD2 in its promoter conte…

MaleThyroid HormonesReceptors Retinoic AcidGene ExpressionATP-binding cassette transporterRetinoid X receptorRats Sprague-DawleyMiceABCD3Gene expressionABCD2medicineAnimalsHumansReceptorAdrenoleukodystrophyPromoter Regions GeneticGeneCells CulturedRepetitive Sequences Nucleic AcidPharmacologyChemokine CCL22Mice KnockoutReceptors Thyroid Hormonebiologymedicine.diseaseCell biologyRatsUp-RegulationOligodendrogliaRetinoid X ReceptorsLiverAstrocytesChemokines CCbiology.proteinCancer researchMolecular MedicineTriiodothyronineAdrenoleukodystrophyChemokine CCL17Transcription FactorsMolecular pharmacology
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Incidence of Abcd1 level on the induction of cell death and organelle dysfunctions triggered by very long chain fatty acids and TNF-alpha on oligoden…

2012

X-linked adrenoleukodystrophy (X-ALD) is characterized by ABCD1 deficiency. This disease is associated with elevated concentrations of very long chain fatty acids (C24:0 and C26:0) in the plasma and tissues of patients. Under its severe form, brain demyelination and inflammation are observed. Therefore, we determined the effects of C24:0 and C26:0 on glial cells:oligodendrocytes, which synthesize myelin, and astrocytes, which participate in immune response. So, 158N murine oligodendrocytes, rat C6 glioma cells, rat primary cultures of neuronal-glial cells, and of oligodendrocytes were treated for various periods of time in the absence or presence of C24:0 and C26:0 used at plasmatic concent…

MaleTime FactorsVacuoleMitochondrionToxicologyATP Binding Cassette Transporter Subfamily D Member 1chemistry.chemical_compoundMice0302 clinical medicineRNA Small InterferingAdrenoleukodystrophyCells CulturedComputingMilieux_MISCELLANEOUSMembrane Potential MitochondrialNeurons0303 health sciencesGeneral NeuroscienceFatty AcidsBrainPeroxisomeCatalaseFlow Cytometry3. Good healthCell biologyMitochondriaOligodendrogliamedicine.anatomical_structureFemaleProgrammed cell deathChromatography GasBiologyGas Chromatography-Mass SpectrometryStatistics Nonparametric03 medical and health sciencesMicroscopy Electron TransmissionLysosomeOrganellemedicineAnimalsHumansPropidium iodideRNA MessengerRats Wistar030304 developmental biologyCell SizeChemokine CCL22OrganellesDose-Response Relationship DrugCell growthTumor Necrosis Factor-alphaRatschemistryAnimals NewbornAstrocytesATP-Binding Cassette Transporters[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgery
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CXCR2 blockade impairs angiotensin II-induced CC chemokine synthesis and mononuclear leukocyte infiltration.

2007

Objective—Angiotensin II (Ang-II) and mononuclear leukocytes are involved in atherosclerosis. This study reports the inhibition of Ang-II–induced mononuclear cell recruitment by CXCR2 antagonism and the mechanisms involved.Methods and Results—Ang-II (1 nmol/L, i.p. in rats) induced CXC and CC chemokines, followed by neutrophil and mononuclear cell recruitment. Administration of the CXCR2 antagonist, SB-517785-M, inhibited the infiltration of both neutrophils (98%) and mononuclear cells (60%). SB-517785-M had no effect on the increase in CXC chemokine levels but reduced MCP-1, RANTES, and MIP-1α release by 66%, 63%, and 80%, respectively. Intravital microscopy showed that pretreatment with S…

Malemedicine.medical_specialtyChemokineCXCR3Peripheral blood mononuclear cellLosartanReceptors Interleukin-8BRats Sprague-DawleyChemokine receptorInternal medicinemedicineCell AdhesionCCL17AnimalsHumansCXC chemokine receptorsSplanchnic CirculationChemokine CCL7Chemokine CCL4Chemokine CCL5Cells CulturedChemokine CCL2Chemokine CCL3InflammationbiologyAngiotensin IIMicrocirculationEndothelial CellsMacrophage Inflammatory ProteinsAtherosclerosisAngiotensin IIMonocyte Chemoattractant ProteinsRatsMononuclear cell infiltrationChemotaxis LeukocyteEndocrinologyNeutrophil Infiltrationbiology.proteinLeukocytes MononuclearCardiology and Cardiovascular MedicineAngiotensin II Type 1 Receptor BlockersArteriosclerosis, thrombosis, and vascular biology
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Atorvastatin in stable angina patients lowers CCL2 and ICAM1 expression: Pleiotropic evidence from plasma mRNA analyses

2013

Objective: Statin pleiotropy is still an evolving concept, and the lack of clarity on this subject is due at least in part to the lack of a definitive biomarker for statin pleiotropy. Using plasma mRNA analysis as a novel research tool for the non-invasive in vivo assessment of gene expression in vascular beds, we hypothesised that atorvastatin lowers the plasmamRNA level from statin pleiotropy-target genes, and the reduction is independent of the reduction of low-density lipoprotein cholesterol (LDL-C). Design and methods: Forty-four patients with stable angina received atorvastatin therapy (20 mg/day, 10 weeks). Plasma chemokine (C-C motif) ligand 2 (CCL2) and intercellular adhesion molec…

Malemedicine.medical_specialtyChemokineStatinmedicine.drug_classAtorvastatinClinical BiochemistryGene ExpressionDrug Administration ScheduleIn vivoInternal medicineGene expressionAtorvastatinmedicineHumansPyrrolesAngina StableRNA MessengerSerum amyloid AChemokine CCL2AgedbiologyAnticholesteremic AgentsAtorvastatin CCL2 ICAM1 Interventional trial mRNA in plasma Pleiotropic effectsC-reactive proteinCholesterol LDLGeneral MedicineMiddle AgedIntercellular Adhesion Molecule-1EndocrinologyHeptanoic AcidsHMG-CoA reductasebiology.proteinFemalelipids (amino acids peptides and proteins)medicine.drugClinical Biochemistry
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Influence of HMB Supplementation and Resistance Training on Cytokine Response to Resistance Exercise

2014

The purpose of this study was to determine the effects of a multinutritional supplement including amino acids, β-hydroxy-β-methylbutyrate (HMB), and carbohydrates on cytokine responses to resistance exercise and training.Seventeen healthy, college-aged men were randomly assigned to a Muscle Armor™ (MA; Abbott Nutrition, Columbus, OH) or placebo supplement group and 12 weeks of resistance training. An acute resistance exercise protocol was administered at 0, 6, and 12 weeks of training. Venous blood samples at pre-, immediately post-, and 30-minutes postexercise were analyzed via bead multiplex immunoassay for 17 cytokines.After 12 weeks of training, the MA group exhibited decreased interfer…

Malemedicine.medical_specialtyStrength trainingmedicine.medical_treatmentInterleukin-1betaMedicine (miscellaneous)Immune functionGranulocytePlaceboBody Mass IndexInterferon-gammaYoung AdultDouble-Blind MethodMuscle damageInternal medicineMyokineMyokinemedicineDietary CarbohydratesValeratesHumansMicronutrientsAmino Acidsta315Chemokine CCL4Immune function; Muscle damage; Myokine; Nutrition; Strength trainingChemokine CCL2NutritionNutrition and DieteticsInterleukin-13business.industryInterleukin-6MonocyteBody WeightInterleukin-8InterleukinResistance TrainingVenous bloodHealthy VolunteersInterleukin-10Cytokinemedicine.anatomical_structureEndocrinologyNutrition AssessmentImmunologyDietary SupplementsCytokinesStrength trainingbusiness
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Enzymatically Degraded, Nonoxidized LDL Induces Human Vascular Smooth Muscle Cell Activation, Foam Cell Transformation, and Proliferation

2000

Background —Enzymatic, nonoxidative modification transforms LDL to an atherogenic molecule (E-LDL) that activates complement and macrophages and is present in early atherosclerotic lesions. Methods and Results —We report on the atherogenic effects of E-LDL on human vascular smooth muscle cells (SMC). E-LDL accumulated in these cells, and this was accompanied by selective induction of monocyte chemotactic protein-1 in the absence of effects on the expression of interleukin (IL)-8, RANTES, or monocyte inflammatory proteins-1α and -β). Furthermore, E-LDL stimulated the expression of gp130, the signal-transducing chain of the IL-6 receptor (IL-6R) family, and the secretion of IL-6. E-LDL invok…

Malemedicine.medical_specialtyVascular smooth muscleArteriosclerosismedicine.medical_treatmentBiologyFibroblast growth factorMuscle Smooth VascularStatistics NonparametricPhysiology (medical)Internal medicinemedicineHomeostasisHumansRNA MessengerAutocrine signallingAortaCells CulturedChemokine CCL2AgedFoam cellInterleukin-6Cell growthGrowth factorMonocyteCholesterol LDLReceptors Interleukin-6EnzymesCell biologymedicine.anatomical_structureEndocrinologyFemaleCardiology and Cardiovascular MedicineCell activationOxidation-ReductionCell DivisionFoam CellsCirculation
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A human CCT5 gene mutation causing distal neuropathy impairs hexadecamer assembly in an archaeal model

2014

Chaperonins mediate protein folding in a cavity formed by multisubunit rings. The human CCT has eight non-identical subunits and the His147Arg mutation in one subunit, CCT5, causes neuropathy. Knowledge is scarce on the impact of this and other mutations upon the chaperone's structure and functions. To make progress, experimental models must be developed. We used an archaeal mutant homolog and demonstrated that the His147Arg mutant has impaired oligomeric assembly, ATPase activity, and defective protein homeostasis functions. These results establish for the first time that a human chaperonin gene defect can be reproduced and studied at the molecular level with an archaeal homolog. The major…

Models MolecularProtein FoldingProtein ConformationProtein subunitMutantMolecular Sequence Datahuman CCT5 gene mutation molecular dynamics neuropathy archaeal modelSequence alignmentGene mutationBiologyArticleChaperonin03 medical and health sciences0302 clinical medicineProtein structureHumansProtein Interaction Domains and MotifsAmino Acid Sequence030304 developmental biologyGenetics0303 health sciencesMultidisciplinarySettore BIO/16 - Anatomia UmanaArchaeaSettore CHIM/08 - Chimica FarmaceuticaChaperone (protein)Mutationbiology.proteinThermodynamicsProtein foldingProtein MultimerizationSequence Alignment030217 neurology & neurosurgeryChaperonin Containing TCP-1
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