Search results for " Regulator"

showing 10 items of 728 documents

New candidates for CD4 T cell pathogenicity in experimental neuroinflammation and multiple sclerosis

2015

Multiple sclerosis is a chronic autoimmune demyelinating disease of the central nervous system, which is thought to be triggered by environmental factors in genetically susceptible individuals leading to activation of autoreactive T lymphocytes. Large multi-centre genome-wide association studies have identified multiple genetic risk loci in multiple sclerosis. In this study, we investigated T cell transcriptomic changes in experimental autoimmune encephalomyelitis, an animal model for multiple sclerosis. We correlated these findings with the multiple sclerosis risk genes postulated by the most recent Immunochip analysis and found that multiple sclerosis susceptibility genes were significant…

CD4-Positive T-LymphocytesMice KnockoutEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisEffectorMultiple sclerosisT cellExperimental autoimmune encephalomyelitisGenome-wide association studyMERTKBiologymedicine.diseaseMice Inbred C57BLMicemedicine.anatomical_structureImmunologymedicineDemyelinating diseaseAnimalsHumansGene Regulatory NetworksNeurology (clinical)NeuroinflammationBrain
researchProduct

Local blockade of IL-6R signaling induces lung CD4+ T cell apoptosis in a murine model of asthma via regulatory T cells.

2007

We previously reported high levels of the soluble form of the IL-6R (sIL-6R) in the airways of asthmatic subjects. Here, we analyzed the IL-6R effects on Th2 cell survival in the lung by locally antagonizing sIL-6R-mediated trans-signaling with a designer fusion protein (gp130-Fc) as well as IL-6R signaling with an antibody against the gp80 unit of the IL-6R (alphaIL-6R) in a murine model of asthma after ovalbumin peptide (OVA) sensitization and challenge. Blockade of the sIL-6R led to a significant decrease in inflammatory cells by an apoptosis-independent mechanism. In contrast, local treatment with alphaIL-6R antibodies that also block signaling via the membrane-bound IL-6R (mIL-6R) led …

CD4-Positive T-LymphocytesSTAT3 Transcription FactorOvalbuminT cellRecombinant Fusion ProteinsImmunologyGene ExpressionApoptosisBiologyT-Lymphocytes RegulatoryAntibodiesInterleukin 21MicemedicineCytokine Receptor gp130Immunology and AllergyCytotoxic T cellAnimalsIL-2 receptorPhosphorylationLungMice Inbred BALB CInterleukin-6FOXP3Forkhead Transcription FactorsGeneral MedicineT lymphocyterespiratory systemReceptors Interleukin-6AsthmaCoculture TechniquesImmunoglobulin Fc FragmentsDisease Models Animalmedicine.anatomical_structureApoptosisImmunologyCancer researchFemaleImmunizationSignal transductionBronchoalveolar Lavage FluidSignal TransductionInternational immunology
researchProduct

miR-155 inhibition sensitizes CD4+ Th cells for TREG mediated suppression.

2009

BackgroundIn humans and mice naturally occurring CD4(+)CD25(+) regulatory T cells (nTregs) are a thymus-derived subset of T cells, crucial for the maintenance of peripheral tolerance by controlling not only potentially autoreactive T cells but virtually all cells of the adaptive and innate immune system. Recent work using Dicer-deficient mice irrevocably demonstrated the importance of miRNAs for nTreg cell-mediated tolerance.Principal findingsDNA-Microarray analyses of human as well as murine conventional CD4(+) Th cells and nTregs revealed a strong up-regulation of mature miR-155 (microRNA-155) upon activation in both populations. Studying miR-155 expression in FoxP3-deficient scurfy mice …

CD4-Positive T-LymphocytesScienceImmunology/ImmunomodulationBiologyModels BiologicalT-Lymphocytes RegulatoryImmune tolerancemiR-155MiceDownregulation and upregulationImmune ToleranceAnimalsHumansIL-2 receptorOligonucleotide Array Sequence AnalysisMultidisciplinaryInnate immune systemGenetics and Genomics/Functional GenomicsQInterleukin-2 Receptor alpha SubunitRPeripheral toleranceFOXP3Forkhead Transcription FactorsTransfectionImmunity InnateCell biologyUp-RegulationKineticsMicroRNAsImmunologyImmunology/Immune ResponseMedicineGenetics and Genomics/Genetics of the Immune SystemResearch ArticlePLoS ONE
researchProduct

Human CD4+CD25+ regulatory T cells and infectious tolerance.

2004

Control of autoaggressive T cells by regulatory T cells (Treg) is essential to ensuring peripheral tolerance. Several subsets of CD(4+) T cells with suppressive properties have been described, including induced T helper (Th) type 3 and T regulatory (Tr) type 1 cells and naturally occurring CD(4+)CD(25+) Treg. CD(4+)CD(25+) Treg suppress the response of conventional T cells in a cell contact-dependent manner, whereas Th3 and Tr1 cells produce immunosuppressive cytokines. Two subsets of human CD(4+)CD(25+) Treg, characterized by expression of the integrins alpha4beta7 or alpha4beta1, are able to convey suppressive capacity to conventional CD(4+) T cells, thereby generating Th suppressor cells…

CD4-Positive T-LymphocytesTransplantationbusiness.industryPeripheral toleranceReceptors Interleukin-2T lymphocyteNatural killer T cellT-Lymphocytes RegulatoryMolecular biologyImmune toleranceInterleukin 21ImmunologyImmune ToleranceHumansCytotoxic T cellMedicineIL-2 receptorbusinessInterleukin 3Transplantation
researchProduct

β-Catenin Signaling Drives Differentiation and Proinflammatory Function of IRF8-Dependent Dendritic Cells

2014

Abstract β-Catenin signaling has recently been tied to the emergence of tolerogenic dendritic cells (DCs). In this article, we demonstrate a novel role for β-catenin in directing DC subset development through IFN regulatory factor 8 (IRF8) activation. We found that splenic DC precursors express β-catenin, and DCs from mice with CD11c-specific constitutive β-catenin activation upregulated IRF8 through targeting of the Irf8 promoter, leading to in vivo expansion of IRF8-dependent CD8α+, plasmacytoid, and CD103+CD11b− DCs. β-Catenin–stabilized CD8α+ DCs secreted elevated IL-12 upon in vitro microbial stimulation, and pharmacological β-catenin inhibition blocked this response in wild-type cells…

CD8 AntigensCellular differentiationImmunologyReceptors Cell SurfaceVaccinia virusPyrimidinonesCD8-Positive T-LymphocytesBiologyParasite LoadArticleProinflammatory cytokineMiceAntigens CDVacciniaAnimalsImmunology and AllergyPromoter Regions Geneticbeta CateninInflammationMice KnockoutCell DifferentiationDendritic CellsT lymphocyteTh1 CellsBridged Bicyclo Compounds HeterocyclicInterleukin-12CD11c AntigenCell biologyEnzyme ActivationMice Inbred C57BLInterferon Regulatory FactorsInterleukin 12FemaleIRF8Signal transductionIntegrin alpha ChainsToxoplasmaSpleenToxoplasmosisCD8Signal TransductionInterferon regulatory factorsThe Journal of Immunology
researchProduct

Advances in haploidentical stem cell transplantation for hematologic malignancies

2016

One of the most important advances in allogeneic hematopoietic stem cell transplantation (allo-HSCT) is the use of alternative donors and cell sources, such as haploidentical transplants (haplo-HSCT) from family donors. Several approaches have been developed to overcome the challenging bidirectional alloreactivity. We discuss these approaches, including ex vivo T-cell-depleted grafts with megadose of CD34(+) cells, not requiring immunosuppression after allogeneic transplantation for graft-versus-host disease (GVHD) prophylaxis, and other strategies using unmanipulated T-cell-replete grafts with intensive immunosuppression or post-transplantation cyclophosphamide to minimize the GVHD. We als…

Cancer ResearchAllogeneic transplantationmedicine.medical_treatmentGraft vs Host DiseaseContext (language use)Hematopoietic stem cell transplantationT-Lymphocytes RegulatoryLymphocyte DepletionDonor Selection03 medical and health sciences0302 clinical medicineReceptors KIRHLA AntigensmedicineHumansCyclophosphamideDonor selectionbusiness.industryHistocompatibility TestingHematopoietic Stem Cell TransplantationImmunosuppressionHematologyAllograftsTransplantationTreatment Outcomesurgical procedures operativeClinical Trials Phase III as TopicOncologyHematologic Neoplasms030220 oncology & carcinogenesisTransplantation HaploidenticalImmunologyStem cellUnrelated DonorsbusinessImmunosuppressive AgentsEx vivo030215 immunologyLeukemia & Lymphoma
researchProduct

Release of IFNγ by Acute Myeloid Leukemia Cells Remodels Bone Marrow Immune Microenvironment by Inducing Regulatory T Cells

2022

Abstract Purpose: The stromal and immune bone marrow (BM) landscape is emerging as a crucial determinant for acute myeloid leukemia (AML). Regulatory T cells (Treg) are enriched in the AML microenvironment, but the underlying mechanisms are poorly elucidated. Here, we addressed the effect of IFNγ released by AML cells in BM Treg induction and its impact on AML prognosis. Experimental Design: BM aspirates from patients with AML were subdivided according to IFNG expression. Gene expression profiles in INFγhigh and IFNγlow samples were compared by microarray and NanoString analysis and used to compute a prognostic index. The IFNγ release effect on the BM microenvironment was investigated in me…

Cancer ResearchBone Marrow CellsMesenchymal Stem CellsSettore MED/08 - Anatomia PatologicaT-Lymphocytes RegulatoryInterferon-gammaLeukemia Myeloid AcuteMiceOncologyBone Marrowhemic and lymphatic diseasesTumor MicroenvironmentAnimalsIFNγ Acute Myeloid Leukemia Bone Marrow Immune Microenvironment
researchProduct

SAHA induces apoptosis in hepatoma cells and synergistically interacts with the proteasome inhibitor Bortezomib.

2007

Histone deacetylase (HDAC) inhibitors represent a promising group of anticancer agents. This paper shows that the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) stimulated at 5-10 microM apoptosis in human hepatoma HepG2 and Huh6 cells, but was ineffective in primary human hepatocytes (PHH). In HepG2 cells SAHA induced the extrinsic apoptotic pathway, increasing the expression of both FasL and FasL receptor and causing the activation of caspase-8. Moreover, SAHA enhanced the level of Bim proteins, stimulated alternative splicing of the Bcl-X transcript with the expression of the proapoptotic Bcl-Xs isoform, induced degradation of Bid into the apoptotic factor t-Bid and dephosphorylat…

Cancer ResearchCarcinoma HepatocellularFas Ligand ProteinClinical BiochemistryPharmaceutical ScienceApoptosisHydroxamic AcidsFas ligandHistone DeacetylasesBortezomibCell Line TumormedicineHumansProtease InhibitorsProtein kinase BVorinostatHDAC inhibitors . HepG2 cells . PHH . Extrinsic and intrinsic apoptotic pathwaysbcl-2-Associated X ProteinPharmacologyMembrane Potential MitochondrialCaspase 8VorinostatbiologyChemistryBortezomibCytochrome cBiochemistry (medical)Cell BiologyBoronic AcidsHistone Deacetylase InhibitorsProteasomeApoptosisPyrazinesProteasome inhibitorbiology.proteinCancer researchApoptosis Regulatory ProteinsProteasome Inhibitorsmedicine.drug
researchProduct

Breast cancer genome-wide association studies: there is strength in numbers.

2012

Breast cancer (BC) is a heterogeneous disease that exhibits familial aggregation. Family linkage studies have identified high-penetrance genes, BRCA1, BRCA2, PTEN and TP53, that are responsible for inherited BC syndromes. Moreover, a combination of family-based and population-based approaches indicated that genes involved in DNA repair, such as CHEK2, ATM, BRIP and PALB2, are associated with moderate risk. Therefore, all of these known genes account for only 25% of the familial aggregation cases. Recently, genome wide association studies (GWAS) in BC revealed single nucleotide polymorphisms (SNPs) in five novel genes associated to susceptibility: TNRC9, FGFR2, MAP3K1, H19 and lymphocyte-spe…

Cancer ResearchMultifactorial InheritanceSettore MED/06 - Oncologia MedicaPALB2PopulationMAP Kinase Kinase Kinase 1Single-nucleotide polymorphismGenome-wide association studyBreast NeoplasmsBiologyPolymorphism Single NucleotideGenetic linkageGeneticsSNPHumansGenetic Predisposition to DiseaseReceptor Fibroblast Growth Factor Type 2educationMolecular BiologyGeneCHEK2Geneticsbreast cancer GWASeducation.field_of_studyMicrofilament ProteinsHigh Mobility Group ProteinsCancer researchTrans-ActivatorsFemaleApoptosis Regulatory ProteinsReceptors ProgesteroneGenome-Wide Association StudyOncogene
researchProduct

Redistribution of CD95, DR4 and DR5 in rafts accounts for the synergistic toxicity of resveratrol and death receptor ligands in colon carcinoma cells.

2004

The natural phytoalexin resveratrol (3, 5, 4'-trihydroxystilbene) exhibits both chemopreventive and antitumor activities through a variety of mechanisms. We have shown previously that resveratrol-induced apoptosis of a human colon cancer cell line involved the redistribution of CD95 (Fas/Apo-1) into lipid rafts. Here, we show that, in colon cancer cells that resist to resveratrol-induced apoptosis, the polyphenol also induces a redistribution of death receptors into lipid rafts. This effect sensitizes these tumor cells to death receptor-mediated apoptosis. In resveratrol-treated cells, tumor necrosis factor (TNF), anti-CD95 antibodies and TNF-related apoptosis-inducing ligand (TRAIL) activa…

Cancer ResearchNystatinTime FactorsApoptosisResveratrolmedicine.disease_causeLigandsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundStilbenesReceptorLipid raftCaspaseMembrane GlycoproteinsbiologyFas receptorFlow CytometryLipidsMitochondriaProto-Oncogene Proteins c-bcl-2CaspasesColonic Neoplasmslipids (amino acids peptides and proteins)Tumor necrosis factor alphaSignal Transductionmedicine.medical_specialtyBlotting WesternTransfectionMembrane MicrodomainsInternal medicineCell Line TumorGeneticsmedicineHumansfas ReceptorMolecular BiologyTumor Necrosis Factor-alphaCarcinomaLipid MetabolismAntineoplastic Agents PhytogenicReceptors TNF-Related Apoptosis-Inducing LigandEndocrinologychemistryApoptosisResveratrolCancer researchbiology.proteinCarcinogenesisApoptosis Regulatory ProteinsOncogene
researchProduct