Search results for "Immune system"

showing 10 items of 2885 documents

Activation of MAP kinase p38 is critical for the cell-cycle–controlled suppressor function of regulatory T cells

2007

AbstractRegulatory T cells play an essential role in the control of self-tolerance and processes of adaptive immunity. Tolerogenic IL-10–modulated human dendritic cells (IL-10DCs) induce anergic T cells with strong suppressive properties (iTregs) that inhibit the activation of effector T cells. In this study, we evaluated the interaction between cell-cycle regulation and intracellular signaling in these iTregs. Analysis of signal transduction events revealed a down-regulation of the mitogen-activated protein kinases (MAPKs) Jun N-terminal kinase (JNK) and a nonactivation of extracellular-signal–regulated kinase (ERK) in contrast to a marked activation of p38 MAPK and the p38 effector MAPK-a…

MAPK/ERK pathwayp38 mitogen-activated protein kinasesImmunologyIn Vitro TechniquesProtein Serine-Threonine KinasesBiologyT-Lymphocytes Regulatoryp38 Mitogen-Activated Protein KinasesBiochemistryAldesleukinHumansProtein kinase AMitogen-Activated Protein Kinase KinasesKinaseCell CycleIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesCell BiologyHematologyAcquired immune systemInterleukin-10Cell biologyMitogen-activated protein kinasebiology.proteinSignal transductionCyclin-Dependent Kinase Inhibitor p27Blood
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Extracellular vesicles provide a capsid-free vector for oncolytic adenoviral DNA delivery

2020

Extracellular vesicles (EVs) have been showcased as auspicious candidates for delivering therapeutic cargo, including oncolytic viruses for cancer treatment. Delivery of oncolytic viruses in EVs could provide considerable advantages, hiding the viruses from the immune system and providing alternative entry pathways into cancer cells. Here we describe the formation and viral cargo of EVs secreted by cancer cells infected with an oncolytic adenovirus (IEVs, infected cell-derived EVs) as a function of time after infection. IEVs were secreted already before the lytic release of virions and their structure resembled normally secreted EVs, suggesting that they were not just apoptotic fragments of…

MECHANISM0301 basic medicineOncolytic adenovirusHistologyadenoviruHEPATITIS-B-VIRUSGenetic enhancementvirusesTETRASPANINGene deliveryBiologysolukalvotGENE DELIVERYPATHWAY03 medical and health sciences0302 clinical medicineImmune systemlcsh:QH573-671MICROVESICLESEXOSOMESsyöpähoidotlcsh:CytologyMICROPARTICLESadenoviruksetCell BiologyadenovirusExtracellular vesiclesVirologyMicrovesicles3. Good healthOncolytic virus030104 developmental biologyLytic cycle030220 oncology & carcinogenesisCELLSCancer cellonkolyyttiset virukset1182 Biochemistry cell and molecular biologycancer therapyAUTOPHAGYonkolyyttinen virushoitoextracellular vesiclesResearch ArticleDNA delivery
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CD4+CD25+ regulatory T cells inhibit natural killer cell functions in a transforming growth factor-beta-dependent manner.

2007

Tumor growth promotes the expansion of CD4+CD25+ regulatory T (T reg) cells that counteract T cell–mediated immune responses. An inverse correlation between natural killer (NK) cell activation and T reg cell expansion in tumor-bearing patients, shown here, prompted us to address the role of T reg cells in controlling innate antitumor immunity. Our experiments indicate that human T reg cells expressed membrane-bound transforming growth factor (TGF)–β, which directly inhibited NK cell effector functions and down-regulated NKG2D receptors on the NK cell surface. Adoptive transfer of wild-type T reg cells but not TGF-β−/− T reg cells into nude mice suppressed NK cell–mediated cytotoxicity, redu…

MESH : CytokinesMESH: Flow CytometryMESH : Immunity NaturalMESH: T-LyLymphocyte ActivationT-Lymphocytes RegulatoryMiceInterleukin 210302 clinical medicineT-Lymphocyte SubsetsTransforming Growth Factor betaNeoplasmsMESH : Receptors ImmunologicMESH : Cell ProliferationImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: AnimalsMESH: NeoplasmsIL-2 receptorReceptors Immunologic0303 health sciencesMESH: Cytokineshemic and immune systemsFlow CytometryNatural killer T cell3. Good healthCell biologyKiller Cells Naturalmedicine.anatomical_structureNK Cell Lectin-Like Receptor Subfamily KInterleukin 12CytokinesReceptors Natural Killer Cell[SDV.IMM]Life Sciences [q-bio]/ImmunologyFranceMESH : Killer Cells NaturalMESH : Cytotoxicity Tests ImmunologicMESH: Killer Cells NaturalMESH: Cell Line TumorMESH : Flow CytometryImmunologychemical and pharmacologic phenomenaMESH: Cytotoxicity Tests ImmunologicMESH : Mice Inbred C57BLBiologyArticleNatural killer cell03 medical and health sciencesMESH: Mice Inbred C57BLCell Line TumorMESH: Cell ProliferationMESH : MicemedicineAnimalsHumansAntigen-presenting cellMESH: Lymphocyte ActivationMESH : FranceMESH: MiceMESH: Receptors ImmunologicMESH : Lymphocyte ActivationCell Proliferation030304 developmental biologyMESH: Immunity NaturalLymphokine-activated killer cellMESH: HumansMESH : Cell Line TumorMESH : HumansCytotoxicity Tests ImmunologicNKG2DMESH : T-LyMESH : NeoplasmsImmunity InnateMice Inbred C57BLMESH: FranceMESH : Animals030215 immunology
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Choice of second-line disease-modifying antirheumatic drugs after failure of methotrexate therapy for rheumatoid arthritis: A decision tree for clini…

2009

Objective To survey rheumatologists' preferences for the choice of a second-line disease-modifying antirheumatic drug (DMARD) after inadequate response with methotrexate (MTX) therapy in rheumatoid arthritis (RA). Methods Thirty-six rheumatologists stated their preferences for RA treatment after inadequate response with MTX therapy (optimal dose at least 6 months). From the initial scenario, we derived 54 vignettes varying by rheumatoid factor or anti–cyclic citrullinated peptide antibody presence, swollen joint count, Disease Activity Score in 28 joints, and structural damage. Respondents stated their preference among 5 therapeutic options: MTX continuation, switch to another conventional …

MESH: Antirheumatic AgentsMESH: Decision TreesMESH: Treatment FailureArthritisMESH: Antibodies Anti-IdiotypicMESH: Logistic ModelsLogistic regressionSeverity of Illness IndexArthritis Rheumatoid0302 clinical medicineimmune system diseasesImmunology and AllergyMESH: Data CollectionPharmacology (medical)Treatment Failure030212 general & internal medicinePractice Patterns Physicians'skin and connective tissue diseasesMESH: Arthritis RheumatoidData CollectionAntibodies Anti-Idiotypic3. Good healthMESH: Interleukin 1 Receptor Antagonist ProteinMESH: Methotrexate[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemAntirheumatic AgentsRheumatoid arthritismedicine.drugmusculoskeletal diseasesmedicine.medical_specialtyMESH: Rheumatoid FactorImmunologyPeptides Cyclic03 medical and health sciencesRheumatologyRheumatoid FactorMESH: Severity of Illness IndexInternal medicineSeverity of illnessmedicineHumansRheumatoid factorMESH: Physician's Practice PatternsMESH: Peptides Cyclic030203 arthritis & rheumatologyAnakinraMESH: HumansTumor Necrosis Factor-alphabusiness.industryDecision Treesmedicine.diseaseRheumatologyInterleukin 1 Receptor Antagonist ProteinLogistic ModelsMethotrexateMESH: Tumor Necrosis Factor-alphaPhysical therapyMethotrexatebusinessArthritis & Rheumatism
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Involvement of complement pathways in patients with bacterial septicemia.

2007

The complement system is a major humoral portion of the innate immune system, playing a significant role in host defence against microorganisms. The biological importance of this system is underlined by the fact that at least three different pathways for its activation exist, the classical, the MBL and the alternative pathway. To elucidate the involvement of the classical and/or the MBL pathway during bacterial septicemia, 32 patients with gram-positive and 30 patients with gram-negative bacterial infections were investigated. In patients with gram-positive bacteria, a significant consumption of C1q (p=0.005) but not of mannose-binding lectin (MBL) (p=0.2) was found during the acute phase o…

MESH: Complement Pathway Mannose-Binding LectinLipopolysaccharidesSalmonellaMESH: Complement C1qLipopolysaccharideImmunologychemical and pharmacologic phenomenaBacteremiamedicine.disease_causeGram-Positive BacteriaMannose-Binding LectinMicrobiologyMESH: Gram-Positive Bacteria03 medical and health scienceschemistry.chemical_compoundClassical complement pathway0302 clinical medicinemedicineHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyComplement Pathway ClassicalMESH: BacteremiaMolecular Biology030304 developmental biology0303 health sciencesInnate immune systemMESH: HumansbiologyComplement C1qLectinSalmonella entericaComplement Pathway Mannose-Binding LectinMESH: Complement Pathway Classicalbiology.organism_classificationbacterial infections and mycoses3. Good healthComplement systemMESH: Mannose-Binding LectinchemistryMESH: Salmonella entericaImmunologyAlternative complement pathwaybiology.proteinMESH: LipopolysaccharidesBacteria030215 immunologyMolecular immunology
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The nuclear receptor PPARγ selectively inhibits Th17 differentiation in a T cell–intrinsic fashion and suppresses CNS autoimmunity

2009

T helper cells secreting interleukin (IL)-17 (Th17 cells) play a crucial role in autoimmune diseases like multiple sclerosis (MS). Th17 differentiation, which is induced by a combination of transforming growth factor (TGF)-beta/IL-6 or IL-21, requires expression of the transcription factor retinoic acid receptor-related orphan receptor gamma t (ROR gamma t). We identify the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR gamma) as a key negative regulator of human and mouse Th17 differentiation. PPAR gamma activation in CD4(+) T cells selectively suppressed Th17 differentiation, but not differentiation into Th1, Th2, or regulatory T cells. Control of Th17 differentia…

MESH: Nuclear Receptor Subfamily 1 Group F Member 3Helper-InducerReceptors Retinoic AcidT-LymphocytesMESH: Interleukin-17Cellular differentiationRetinoic AcidPeroxisome proliferator-activated receptorNeurodegenerativeInbred C57BLMedical and Health SciencesMiceInterleukin 210302 clinical medicineGroup FRAR-related orphan receptor gammaMESH: Nuclear Receptor Co-Repressor 2Receptors2.1 Biological and endogenous factorsThyroid HormoneImmunology and AllergyMESH: AnimalsAetiologyEncephalomyelitisPromoter Regions Geneticchemistry.chemical_classificationOrphan receptor0303 health sciencesReceptors Thyroid HormoneInterleukin-17Cell DifferentiationT-Lymphocytes Helper-InducerNuclear Receptor Subfamily 1 Group F Member 33. Good healthCell biologyDNA-Binding Proteinsmedicine.anatomical_structureMESH: Repressor Proteins[SDV.IMM]Life Sciences [q-bio]/ImmunologyInterleukin 17MESH: Cell Differentiationmedicine.medical_specialtyEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisNuclear Receptor Subfamily 1Member 31.1 Normal biological development and functioningT cellImmunologyBiologyAutoimmune DiseasePromoter RegionsExperimental03 medical and health sciencesGeneticUnderpinning researchMESH: Mice Inbred C57BLInternal medicineMESH: Promoter Regions GeneticGeneticsmedicineAnimalsHumansNuclear Receptor Co-Repressor 2MESH: Receptors Thyroid HormoneMESH: T-Lymphocytes Helper-InducerMESH: Encephalomyelitis Autoimmune ExperimentalMESH: Mice030304 developmental biologyMESH: Receptors Retinoic AcidMESH: HumansInflammatory and immune systemNeurosciencesBrief Definitive ReportCorrectionMESH: Multiple SclerosisBrain DisordersMice Inbred C57BLPPAR gammaRepressor ProteinsEndocrinologyMESH: PPAR gammaNuclear receptorchemistryMESH: DNA-Binding Proteins030217 neurology & neurosurgeryAutoimmuneJournal of Experimental Medicine
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Human OX40 tunes the function of regulatory T cells in tumor and nontumor areas of hepatitis C virus-infected liver tissue.

2014

International audience; Regulatory T cells (Tregs) can be considered as a mixed population of distinct subsets, endowed with a diverse extent and quality of adaptation to microenvironmental signals. Here, we uncovered an opposite distribution of Treg expansion, phenotype, and plasticity in different microenvironments in the same organ (liver) derived from patients with chronic hepatitis C: On the one side, cirrhotic and tumor fragments were moderately and highly infiltrated by Tregs, respectively, expressing OX40 and a T-bet high IFN-c – " T-helper (Th)1-suppressing " phenotype; on the other side, noncirrhotic liver specimens contained low frequencies of Tregs that expressed low levels of O…

MESH: Receptors OX40/metabolism*MESH: Interleukin-12/metabolismLiver CirrhosisMaleMacrophagemedicine.disease_causeMESH: Carcinoma Hepatocellular/immunology*T-Lymphocytes RegulatoryMESH: OX40 Ligand/metabolism0302 clinical medicineMESH: Aged 80 and overMESH: T-Lymphocytes Regulatory/physiology*MESH: Up-RegulationOX40MESH: AgedAged 80 and over0303 health scienceseducation.field_of_studyT REGMESH: Middle AgedMedicine (all)MESH: Liver Cirrhosis/immunology*Liver Neoplasmshemic and immune systemsMiddle AgedMESH: Liver Neoplasms/immunology*PhenotypeHepatitis CInterleukin-123. Good healthUp-RegulationPhenotypeLiver Neoplasm[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/VirologyInterleukin 12[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemalemedicine.symptomMESH: Hepatitis C/immunology*OX40; T REG; HEPATITIS C VIRUSHumanmedicine.medical_specialtyCarcinoma HepatocellularHepatitis C virusLiver CirrhosiPopulationInflammationchemical and pharmacologic phenomena[SDV.CAN]Life Sciences [q-bio]/CancerOX40 LigandBiologyMESH: PhenotypeMESH: Liver Neoplasms/virology03 medical and health sciencesIkaros Transcription FactorDownregulation and upregulationInternal medicinemedicineHumansMESH: Macrophages/metabolismeducation030304 developmental biologyAgedMESH: HumansHepatologyMacrophagesHEPATITIS C VIRUSMESH: Carcinoma Hepatocellular/virologyHepatologyReceptors OX40MESH: Ikaros Transcription Factor/metabolismMESH: Hepatitis C/complicationsMESH: MaleOX40 ligandImmunologyMESH: Liver Cirrhosis/virologyMESH: Female030215 immunology
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Modulation of MHC Class II Determinants on Rat Langerhans Cells During Short Term Culture

1993

Epidermal Langerhans cells (LC) are regarded as the most peripheral outpost of the immune system. They play a pivotal role during the onset of an immune response in the skin. One of the principal functions of LC is reflected in their extraordinary potency to present antigen to high activation requiring naive T cells.

MHC class IIImmune systemintegumentary systemAntigenImmunologybiology.proteinPotencyHigh activationBiologyInvariant chain
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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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CSF-1 signals directly to renal tubular epithelial cells to mediate repair in mice

2009

金沢大学医薬保健研究域医学系

Macrophage colony-stimulating factorPathologymedicine.medical_specialtymedicine.medical_treatmenteducation030232 urology & nephrologyApoptosisReceptor Macrophage Colony-Stimulating FactorBiology03 medical and health sciencesParacrine signallingMice0302 clinical medicineFibrosismedicineAnimalsHumansRegenerationAutocrine signalling030304 developmental biologyCell Proliferation0303 health sciencesMice Inbred C3HGrowth factorMacrophage Colony-Stimulating FactorMacrophageshemic and immune systemsEpithelial CellsGeneral Medicinemedicine.diseaseFibrosis3. Good healthKidney TubulesIntegrin alpha MApoptosisReperfusion Injurybiology.proteinCancer researchReperfusion injurytissuesResearch Article
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