Search results for "MACROPHAGES"

showing 10 items of 533 documents

Antibodies against tumor necrosis factor (TNF) induce T-cell apoptosis in patients with inflammatory bowel diseases via TNF receptor 2 and intestinal…

2011

Background & Aims The anti–tumor necrosis factor (TNF) antibodies infliximab, adalimumab, and certolizumab pegol have proven clinical efficacy in Crohn's disease. Here, we assessed the effects of anti-TNF antibodies on apoptosis in inflammatory bowel disease (IBD). Methods CD14 + macrophages and CD4 + T cells were isolated from peripheral blood and lamina propria mononuclear cells from patients with IBD and control patients. Cell surface markers and apoptosis were assessed by immunohistology and fluorescence-activated cell sorting techniques. Results Lamina propria CD14 + macrophages showed significantly more frequent and higher membrane-bound TNF (mTNF) expression than CD4 + T cells in IBD…

CD4-Positive T-LymphocytesMaleNecrosisCD14Anti-Inflammatory AgentsLipopolysaccharide ReceptorsApoptosisEnzyme-Linked Immunosorbent AssayBiologyAntibodies Monoclonal HumanizedReal-Time Polymerase Chain ReactionPeripheral blood mononuclear cellPolyethylene GlycolsImmunoglobulin Fab FragmentsYoung AdultmedicineHumansReceptors Tumor Necrosis Factor Type IIAntigen-presenting cellAgedLamina propriaHepatologyCluster of differentiationTumor Necrosis Factor-alphaMacrophagesGastroenterologyAdalimumabAntibodies MonoclonalMiddle AgedFlow CytometryInflammatory Bowel DiseasesInfliximabmedicine.anatomical_structureApoptosisCase-Control StudiesImmunologyCertolizumab PegolTumor necrosis factor alphaFemalemedicine.symptomGastroenterology
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Development of Abdominal Aortic Aneurysm Is Decreased in Mice with Plasma Phospholipid Transfer Protein Deficiency

2013

International audience; Plasma phospholipid transfer protein (PLTP) increases the circulating levels of proatherogenic lipoproteins, accelerates blood coagulation, and modulates inflammation. The role of PLTP in the development of abdominal aortic aneurysm (AAA) was investigated by using either a combination of mechanical and elastase injury at one site of mouse aorta (elastase model) or continuous infusion of angiotensin II in hyperlipidemic ApoE-knockout mice (Ang II model). With the elastase model, complete PLTP deficiency was associated with a significantly lower incidence and a lesser degree of AAA expansion. With the Ang II model, findings were consistent with those in the elastase mo…

CD4-Positive T-LymphocytesMalemedicine.medical_specialty[SDV]Life Sciences [q-bio]Inflammation030204 cardiovascular system & hematologyBiologyPathology and Forensic MedicineMice03 medical and health sciencesAortic aneurysmApolipoproteins E0302 clinical medicinemedicine.arteryPhospholipid transfer proteinInternal medicinemedicineAnimalsPhospholipid Transfer ProteinsPancreatic elastaseAorta030304 developmental biologyInflammationMice Knockout0303 health sciencesAortaPancreatic ElastaseAngiotensin IIMacrophagesElastasemedicine.diseaseAngiotensin IIElastinMice Inbred C57BL[SDV] Life Sciences [q-bio]EndocrinologyLiverImmunologybiology.proteincardiovascular systemCytokinesmedicine.symptomElastinAortic Aneurysm Abdominal
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Methotrexate specifically modulates cytokine production by T cells and macrophages in murine collagen-induced arthritis (CIA): a mechanism for methot…

1999

SUMMARYImmunosuppressive therapy with methotrexate (MTX) has been established as effective treatment for patients with rheumatoid arthritis. To analyse the therapeutic potential and mechanisms of action of MTX, we determined serum cytokine levels and cytokine production by splenic T cells and macrophages in untreated and MTX-treated mice. Furthermore, we assessed the role of MTX in a murine model of experimental arthritis induced by collagen type II (CIA). MTX reduced spontaneous and IL-15-induced tumour necrosis factor (TNF) production by splenic T cells but not by macrophages from healthy mice in vitro in a dose-dependent manner. In contrast, interferon-gamma (IFN-γ) production was less s…

CD4-Positive T-LymphocytesMalemusculoskeletal diseasesT-Lymphocytesmedicine.medical_treatmentImmunologyArthritisMice TransgenicSpleenInterferon-gammaMiceImmune systemAnimalsImmunology and AllergyMedicineheterocyclic compoundsInterferon gammaskin and connective tissue diseasesInterleukin 4Interleukin-15Mice KnockoutMice Inbred BALB CInterleukin-6Tumor Necrosis Factor-alphabusiness.industryMacrophagesOriginal ArticlesImmunotherapymedicine.diseaseArthritis ExperimentalMethotrexatemedicine.anatomical_structureCytokineMice Inbred DBAImmunologyCytokinesTumor necrosis factor alphaCollagenInterleukin-4businessImmunosuppressive AgentsSpleenmedicine.drug
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Impaired immune response to Candida albicans in aged mice

2006

The prevalence of opportunistic fungal infections has increased dramatically among the aged population in recent years. This work investigated the effect of ageing on murine defences against Candida albicans. Aged C57BL/6 mice that were experimentally infected intravenously had a significantly impaired survival and a higher tissue fungal burden compared with young mice. In vitro production of tumour necrosis factor (TNF)-α by macrophages from aged mice in response to yeast cells and hyphae of C. albicans was significantly lower than production by macrophages from young mice. In vitro production of cytokines, such as TNF-α and gamma interferon (IFN-γ), by antigen-stimulated splenocytes from …

CD4-Positive T-LymphocytesMicrobiology (medical)AgingNecrosisBlotting WesternHyphaeMicrobiologyMicrobiologyInterferon-gammaMiceImmune systemAntigenCandida albicansmedicineAnimalsCandida albicansAntibodies FungalCells CulturedbiologyTumor Necrosis Factor-alphaVaccinationCandidiasisGeneral Medicinebiology.organism_classificationAcquired immune systemCorpus albicansMice Inbred C57BLImmunoglobulin GInjections IntravenousImmunologyMacrophages Peritonealbiology.proteinFemaleTumor necrosis factor alphaDisease SusceptibilityFungal Vaccinesmedicine.symptomAntibodySpleenJournal of Medical Microbiology
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Highly focused T cell responses in latent human pulmonary Mycobacterium tuberculosis infection.

2005

Abstract The elucidation of the molecular and immunological mechanisms mediating maintenance of latency in human tuberculosis aids to develop more effective vaccines and to define biologically meaningful markers for immune protection. We analyzed granuloma-associated lymphocytes (GALs) from human lung biopsies of five patients with latent Mycobacterium tuberculosis (MTB) infection. MTB CD4+ and CD8+ T cell response was highly focused in the lung, distinct from PBL, as assessed by TCR-CDR3 spectratyping coupled with a quantitative analysis of TCR VB frequencies. GALs produced IFN-γ in response to autologous macrophages infected with MTB and to defined MTB-derived HLA-A2-presented peptides Ag…

CD4-Positive T-LymphocytesT cellReceptors Antigen T-Cell alpha-betaImmunologyAntigen presentationMolecular Sequence DataEpitopes T-Lymphocytechemical and pharmacologic phenomenaBiologyCD8-Positive T-LymphocytesEpitopeMycobacterium tuberculosisInterferon-gammaAntigenBacterial ProteinsMHC class IHLA-A2 AntigenmedicineImmunology and AllergyHumansAmino Acid SequenceTuberculosis PulmonaryAntigen PresentationAntigens BacterialGranulomaMacrophagesT-cell receptorMycobacterium tuberculosisTh1 Cellsbacterial infections and mycosesbiology.organism_classificationVirologyPeptide FragmentsClone Cellsmedicine.anatomical_structureReceptor-CD3 Complex Antigen T-CellImmunologybiology.proteinCytokinesCD8Protein BindingJournal of immunology (Baltimore, Md. : 1950)
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Mycophenolate mofetil for treatment of active inflammatory bowel disease. Clinical and immunological studies.

1998

CD4-Positive T-Lymphocytesmedicine.medical_specialtybusiness.industryTumor Necrosis Factor-alphaGeneral NeuroscienceMacrophagesT-LymphocytesMycophenolic AcidMycophenolatemedicine.diseaseInflammatory Bowel DiseasesInflammatory bowel diseaseGastroenterologyGeneral Biochemistry Genetics and Molecular BiologyHistory and Philosophy of ScienceInternal medicinemedicineHumansbusinessCells CulturedImmunosuppressive AgentsAnnals of the New York Academy of Sciences
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Differential expression of alternative H2-M isoforms in B cells, dendritic cells and macrophages by proinflammatory cytokines.

1999

Major histocompatibility (MHC) class II heterodimers bind peptides generated by degradation of endocytosed antigens and display them on the surface of antigen presenting cells (APCs) for recognition by CD4+ T cells. Efficient loading of MHC class II molecules with peptides is catalyzed by the MHC class II-like molecule H2-M. The coordinate regulation of MHC class II and H2-M expression is a prerequisite for efficient MHC class II/peptide assembly in APCs determining both the generation of the T cell repertoire in the thymus and cellular immune responses in the periphery. Here we show that expression of H2-M and MHC class II genes is coordinately and cell type-specific regulated in splenic B…

CD74ImmunologyAntigen presentationGenes MHC Class IICD1Antigen-Presenting CellsGene ExpressionIn Vitro TechniquesMHC Class II GeneMiceMHC class IAnimalsProtein IsoformsMolecular BiologyDNA PrimersMHC class IIB-LymphocytesHLA-D AntigensMice Inbred BALB CbiologyBase SequenceAntigen processingHistocompatibility Antigens Class IIDendritic CellsMHC restrictionMolecular biologybiology.proteinMacrophages PeritonealCytokinesInflammation MediatorsMolecular immunology
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Glioblastoma cells induce differential glutamatergic gene expressions in human tumor-associated microglia/macrophages and monocyte-derived macrophages

2015

Glioblastoma cells produce and release high amounts of glutamate into the extracellular milieu and subsequently can trigger seizure in patients. Tumor-associated microglia/macrophages (TAMs), consisting of both parenchymal microglia and monocytes-derived macrophages (MDMs) recruited from the blood, are known to populate up to 1/3 of the glioblastoma tumor environment and exhibit an alternative, tumor-promoting and supporting phenotype. However, it is unknown how TAMs respond to the excess extracellular glutamate in the glioblastoma microenvironment. We investigated the expressions of genes related to glutamate transport and metabolism in human TAMs freshly isolated from glioblastoma resecti…

Cancer ResearchAntigens Differentiation MyelomonocyticGlutamic AcidglutamateAMPA receptorSLC7A11Antigens CDTumor Cells CulturedExtracellularmedicineHumansReceptors AMPAGRIA2PharmacologyCD11b AntigenbiologyMicrogliaBrain NeoplasmsMacrophagesmonocyte-derived macrophagesCalcium-Binding ProteinsMicrofilament Proteinsglioblastomatumor-associated microglia/macrophagesGlutamate receptorSLC1A2Coculture TechniquesDNA-Binding ProteinsGlutaminemedicine.anatomical_structureGene Expression RegulationOncologyAstrocytesImmunologybiology.proteinCancer researchLeukocyte Common AntigensMolecular MedicineMicrogliaResearch PaperCancer Biology & Therapy
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Dual regulation of SPI1/PU.1 transcription factor by heat shock factor 1 (HSF1) during macrophage differentiation of monocytes

2014

International audience; : In addition to their cytoprotective role in stressful conditions, heat shock proteins (HSPs) are involved in specific differentiation pathways, e.g. we have identified a role for HSP90 in macrophage differentiation of human peripheral blood monocytes exposed to Macrophage Colony-Stimulating Factor (M-CSF). Here, we show that deletion of the main transcription factor involved in heat shock gene regulation, heat shock factor 1 (HSF1), affects M-CSF-driven differentiation of mouse bone marrow cells. HSF1 transiently accumulates in the nucleus of human monocytes undergoing macrophage differentiation, including M-CSF-treated peripheral blood monocytes and phorbol ester-…

Cancer ResearchCellular differentiation[SDV]Life Sciences [q-bio][SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Mice0302 clinical medicineHeat Shock Transcription FactorsHSF1[SDV.BDD]Life Sciences [q-bio]/Development BiologyCells CulturedComputingMilieux_MISCELLANEOUSRegulation of gene expression0303 health sciencesMice Inbred BALB C[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyHematology[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]3. Good healthDNA-Binding ProteinsOncology030220 oncology & carcinogenesismonocytesProteasome Endopeptidase ComplexAntigens Differentiation MyelomonocyticReceptors Cell Surface[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiology03 medical and health sciencesAntigens CDHeat shock proteinProto-Oncogene Proteinstranscription factorsAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyTranscription factor030304 developmental biologySPI1Macrophagesheat-shock proteinsfungi[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMolecular biologyHsp70Heat shock factorMice Inbred C57BLcell differentiationGene Expression RegulationTrans-Activators[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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CD38/CD31, the CCL3 and CCL4 chemokines, and CD49d/vascular cell adhesion molecule-1 are interchained by sequential events sustaining chronic lymphoc…

2009

AbstractCD38 and CD49d are associated negative prognosticators in chronic lymphocytic leukemia (CLL). Despite evidence that both molecules are involved in interactions occurring between CLL and normal cells in the context of CLL-involved tissues, a functional link is still missing. Using gene expression profiles comparing CD38+CD49d+ versus CD38−CD49d− CLL cells, we showed overexpression of the CCL3 and CCL4 chemokines in cells from the former group. These chemokines were also up-regulated by CD38 signals in CLL; moreover, CCL3 was expressed by CLL cells from bone marrow biopsies (BMB) of CD38+CD49d+ but not CD38−CD49d− cases. High levels of CCR1 and, to a lesser extent, CCR5, the receptors…

Cancer ResearchChemokineChronic lymphocytic leukemiaIntegrin alpha4ApoptosisCD38immune system diseaseshemic and lymphatic diseasesReceptorsChronicMacrophages; Apoptosis; Membrane Glycoproteins; Humans; Integrin alpha4; Antigens CD38; Vascular Cell Adhesion Molecule-1; Endothelial Cells; Receptors Chemokine; Antigens CD31; Cell Survival; Bone Marrow Cells; Leukemia Lymphocytic Chronic B-Cell; Antigens CD; Up-Regulation; Chemokine CCL4; Chemokine CCL3; Cell LineChemokine CCL4Chemokine CCL3Membrane GlycoproteinsLeukemiaCell adhesion moleculehemic and immune systemsLymphocyticCDUp-RegulationPlatelet Endothelial Cell Adhesion Molecule-1Leukemiamedicine.anatomical_structureOncologyChemokineReceptors ChemokineTumor necrosis factor alphaStromal cellCell SurvivalVascular Cell Adhesion Molecule-1Bone Marrow CellsBiologyCell LineAntigens CDmedicineHumansAntigensMonocyteMacrophagesB-CellEndothelial Cellsmedicine.diseaseADP-ribosyl Cyclase 1Leukemia Lymphocytic Chronic B-CellCLL integrins chemokines CD49d CD38 prognosis.Cancer researchbiology.proteinCD31Settore MED/15 - Malattie del SangueCD38
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