Search results for "T cell"

showing 10 items of 2228 documents

Thapsigargin-stimulated MAP kinase phosphorylation via CRAC channels and PLD activation: inhibitory action of docosahexaenoic acid.

2004

AbstractThis study was conducted on human Jurkat T-cells to investigate the role of depletion of intracellular Ca2+ stores in the phosphorylation of two mitogen-activated protein kinases (MAPKs), i.e. extracellular signal-regulated kinase (ERK) 1 and ERK2, and their modulation by a polyunsaturated fatty acid, docosahexaenoic acid (DHA). We observed that thapsigargin (TG) stimulated MAPK activation by store-operated calcium (SOC) influx via opening of calcium release-activated calcium (CRAC) channels as tyrphostin-A9, a CRAC channel blocker, and two SOC influx inhibitors, econazole and SKF-96365, diminished the action of the former. TG-stimulated ERK1/ERK2 phosphorylation was also diminished…

MAPK/ERK pathwayThapsigarginDocosahexaenoic AcidsBiophysicschemistry.chemical_elementCalciumBiochemistryDiglycerideschemistry.chemical_compoundJurkat CellsStructural BiologyGeneticsPhospholipase DHumansPhosphorylationMolecular BiologyProtein kinase CProtein Kinase CDiacylglycerol kinaseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Phospholipase CChemistryKinasePhospholipase DRyanodine Receptor Calcium Release ChannelCell BiologyJurkat T-cellCell biologyEnzyme Activationenzymes and coenzymes (carbohydrates)Docosahexaenoic acidFatty Acids UnsaturatedThapsigarginlipids (amino acids peptides and proteins)CalciumMitogen-Activated Protein KinasesFEBS letters
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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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Differential inhibition of TRAIL-mediated DR5-DISC formation by decoy receptors 1 and 2.

2006

International audience; Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that induces cancer cell death by apoptosis with some selectivity. TRAIL-induced apoptosis is mediated by the transmembrane receptors death receptor 4 (DR4) (also known as TRAIL-R1) and DR5 (TRAIL-R2). TRAIL can also bind decoy receptor 1 (DcR1) (TRAIL-R3) and DcR2 (TRAIL-R4) that fail to induce apoptosis since they lack and have a truncated cytoplasmic death domain, respectively. In addition, DcR1 and DcR2 inhibit DR4- and DR5-mediated, TRAIL-induced apoptosis and we demonstrate here that this occurs through distinct mechanisms. While DcR1 prevents the assembly of the…

MESH : Hela CellsMESH: Membrane GlycoproteinsMESH: Membrane MicrodomainsDecoy Receptor 1ApoptosisMESH : Membrane GlycoproteinsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandJurkat Cells0302 clinical medicineMESH : Tumor Necrosis Factor Decoy ReceptorsMESH: Jurkat CellsDecoy receptorsReceptorCells CulturedMESH : Jurkat CellsMESH : Tumor Necrosis Factor-alpha0303 health sciencesMembrane GlycoproteinsMESH : Protein BindingArticlesMESH : Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsTumor Necrosis Factor Receptor-Associated Peptides and ProteinsCell biology030220 oncology & carcinogenesisCaspasesDeath-inducing signaling complexApoptosis/drug effects; Apoptosis Regulatory Proteins/antagonists & inhibitors; Apoptosis Regulatory Proteins/pharmacology; Caspases/metabolism; Cells Cultured; Death Domain Receptor Signaling Adaptor Proteins; Enzyme Activation/drug effects; GPI-Linked Proteins; HeLa Cells; Humans; Jurkat Cells; Membrane Glycoproteins/antagonists & inhibitors; Membrane Glycoproteins/pharmacology; Membrane Microdomains/drug effects; Protein Binding/drug effects; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor/metabolism; TNF-Related Apoptosis-Inducing Ligand; Tumor Necrosis Factor Decoy Receptors; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins/metabolism; Tumor Necrosis Factor-alpha/antagonists & inhibitors; Tumor Necrosis Factor-alpha/pharmacologyMESH : Apoptosis Regulatory ProteinsMESH: TNF-Related Apoptosis-Inducing LigandProtein BindingMESH: Cells CulturedDeath Domain Receptor Signaling Adaptor ProteinsMESH: Enzyme ActivationBiologyMESH: Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsGPI-Linked Proteins03 medical and health sciencesMembrane MicrodomainsCell surface receptorMESH : Cells Cultured[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyReceptors Tumor Necrosis Factor Member 10cHumansMESH: Protein Binding[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing LigandMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyDeath domainMESH: CaspasesMESH: HumansTumor Necrosis Factor-alphaMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell BiologyMESH: Receptors Tumor Necrosis FactorMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : Receptors Tumor Necrosis FactorEnzyme ActivationMESH: Hela CellsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsApoptosisMESH: Tumor Necrosis Factor-alphaMESH : Membrane MicrodomainsMESH : CaspasesApoptosis Regulatory ProteinsMESH : Enzyme ActivationMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy ReceptorsHeLa CellsMESH: Death Domain Receptor Signaling Adaptor Proteins
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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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Semicarbazide-sensitive amine oxidase/vascular adhesion protein-1 deficiency reduces leukocyte infiltration into adipose tissue and favors fat deposi…

2009

1525-2191 (Electronic) Journal Article; Obesity is associated with low-grade inflammation and leukocyte infiltration in white adipose tissue (WAT) and is linked to diabetic complications. Semicarbazide-sensitive amine oxidase, also known as vascular adhesion protein-1 (SSAO/VAP-1), is a membrane protein that is highly expressed in adipocytes and is also present on the endothelial cell surface where it is involved in leukocyte extravasation. We studied fat deposition and leukocyte infiltration in WAT of mice with a null mutation in the amine oxidase copper-containing-3 (AOC3) gene encoding SSAO/VAP-1. Both epididymal and inguinal WATs were larger in 6-month-old AOC3-KO males than in age-matc…

MESH: SemicarbazidesAOC3Obesity/geneticsAdipose tissueMESH: Flow CytometryWhite adipose tissueInbred C57BLMESH: Mice KnockoutTransgenicMiceLeukocytesMESH: ObesityMESH: AnimalsMice KnockoutAmine oxidase (copper-containing)food and beveragesNatural killer T cellFlow CytometryLeukocyte extravasationSemicarbazidesCell Adhesion Molecules/*deficiency/*geneticsAdipose TissueMESH: Cell Adhesion MoleculesLeukocytes/*physiologyAmine Oxidase (Copper-Containing)medicine.symptomInfiltration (medical)MESH: Adipose Tissuemedicine.medical_specialtyMESH: Mice TransgenicKnockoutMice TransgenicInflammation[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyMESH: Monoamine OxidasePathology and Forensic MedicineMESH: LeukocytesMonoamine Oxidase/*deficiencyMESH: Mice Inbred C57BLInternal medicinemedicineAnimalsHumansObesityMonoamine OxidaseMESH: Mice[SDV.BC] Life Sciences [q-bio]/Cellular BiologyMESH: HumansAmine Oxidase (Copper-Containing)/*deficiency/*geneticsmedicine.diseaseAdipose Tissue/pathology/*physiologyMice Inbred C57BLEndocrinologyImmunologyMESH: Amine Oxidase (Copper-Containing)Semicarbazides/*pharmacologyCell Adhesion MoleculesRegular Articles
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Major histocompatibility complex class I-restricted activation of cloned T cells by a soluble protein in the absence of accessory cells.

1989

A T-cell clone, 10BK.1, was established from the draining lymph nodes of (B10 x B10.BR)F1 mice immunized with ovalbumin (OVA) according to standard protocols. Upon coculture with the antigen, 10BK.1 cells reacted by production of lymphokines and by proliferation despite the absence of additional antigen-presenting cells. These T cells do not express major histocompatibility complex (MHC) class II molecules on the cell surface as assessed on the basis of several criteria: by cytofluorometric analysis I-A and I-E determinants were not detectable; 10BK.1 cells could not act as antigen-presenting cells for long-term-cultured MHC class II-restricted T-cell clones; and monoclonal antibodies direc…

MHC class IIMultidisciplinarybiologyOvalbuminT-LymphocytesHistocompatibility Antigens Class IAntigen presentationCD1chemical and pharmacologic phenomenaMHC restrictionLymphocyte ActivationVirologyMolecular biologyAntibodiesCell LineClone CellsMiceAntigenMHC class Ibiology.proteinAnimalsCytotoxic T cellAntigen-presenting cellResearch ArticleProceedings of the National Academy of Sciences
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Evidence for T cell receptor-HLA class II molecule interaction in the response to superantigenic bacterial toxins

1991

The staphylococcal enterotoxins and related microbial T cell mitogens stimulate T cells by cross-linking variable parts of the T cell receptor (TcR) with MHC class II molecules on accessory or target cells. In this report we describe that a given combination of T cell, accessory cell (AC) and toxin can be non-stimulatory. However, the same T cell can respond to the same toxin on another AC and the same AC can present the same toxin to another T cell. This indicates that in the complex formed between TcR, toxin and class II molecule an interaction between TcR and class II molecule takes place.

MHC class IIT-LymphocytesT cellBacterial ToxinsImmunologyT-cell receptorAntigen presentationHistocompatibility Antigens Class IIReceptors Antigen T-CellAntigen-Presenting Cellsfood and beveragesT lymphocyteBiologyLymphocyte ActivationMicrobiologyCell biologymedicine.anatomical_structuremedicinebiology.proteinHumansImmunology and AllergyCytotoxic T cellAntigen-presenting cellCD8European Journal of Immunology
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Toxoplasma gondii down-regulates MHC class II gene expression and antigen presentation by murine macrophages via interference with nuclear translocat…

2001

The obligate intracellular protozoan parasite Toxoplasma gondii is able to establish persistent infections within human and animal hosts. We have shown recently that T. gondii down-regulates IFN-γ-induced MHC class II expression in murine bone marrow-derived macrophages (BMMΦ). As shown in this study, the capacity of IFN-γ-activated murine BMMΦ to present ovalbumin to CD4+ T cell hybridomas was dose-dependently inhibited by T. gondii. IFN-γ-induced up-regulation of H2-Aa, H2-Ab, H2-Eb, H2-Ma, H2-Mb, H2-Oa and invariant chain transcripts was prominently down-regulated by T. gondii. Furthermore, mRNA levels of class II transactivator and interferon-regulatory factor-1 were significantly dimin…

MHC class IIbiologyT cellImmunologyAntigen presentationToxoplasma gondiibiology.organism_classificationMolecular biologyMHC Class II Genemedicine.anatomical_structureparasitic diseasesbiology.proteinSTAT proteinmedicineImmunology and AllergySTAT1Signal transductionEuropean Journal of Immunology
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γδ T cells and their clinical application in colon cancer

2023

In recent years, research has focused on colorectal cancer to implement modern treatment approaches to improve patient survival. In this new era, γδ T cells constitute a new and promising candidate to treat many types of cancer because of their potent killing activity and their ability to recognize tumor antigens independently of HLA molecules. Here, we focus on the roles that γδ T cells play in antitumor immunity, especially in colorectal cancer. Furthermore, we provide an overview of small-scale clinical trials in patients with colorectal cancer employing either in vivo activation or adoptive transfer of ex vivo expanded γδ T cells and suggest possible combinatorial approaches to treat co…

MHC- unrestricted activationtumorcolon rectal cancerImmunologyImmunology and Allergygamma delta T cellsimmunotherapy
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Aminopropyltransferases involved in polyamine biosynthesis localize preferentially in the nucleus of plant cells

2012

Plant aminopropyltransferases consist of a group of enzymes that transfer aminopropyl groups derived from decarboxylated S-adenosyl-methionine (dcAdoMet or dcSAM) to propylamine acceptors to produce polyamines, ubiquitous metabolites with positive charge at physiological pH. Spermidine synthase (SPDS) uses putrescine as amino acceptor to form spermidine, whereas spermine synthase (SPMS) and thermospermine synthase (TSPMS) use spermidine as acceptor to synthesize the isomers spermine and thermospermine respectively. In previous work it was shown that both SPDS1 and SPDS2 can physically interact with SPMS although no data concerning the subcellular localization was reported. Here we study the…

Macromolecular AssembliesProteomicsS-AdenosylmethioninePlant anatomyImmunohistoquímicaArabidopsislcsh:MedicineSecondary MetabolismSpermineExpressionPlant ScienceSpermidine synthaseBiochemistrychemistry.chemical_compoundBimolecular fluorescence complementationCytosolMolecular Cell BiologyPolyaminesPlant Genomicslcsh:SciencePlant Growth and DevelopmentMultidisciplinarybiologyPlant BiochemistryArabidopsis-ThalianaGenomicsImmunohistochemistryMetabolismeFunctional GenomicsBiochemistrySpermine synthasePlant proteinPlant PhysiologyMechanismResearch ArticleHistologyAcyltransferasePlant Cell BiologyActive Transport Cell NucleusSpermidine SynthaseBimolecular fluorescence complementationProtein InteractionsBiologyCell NucleusCrystal-Structurelcsh:RHistologiaBotanyProtein interactionsSubcellular localizationAnatomia vegetalExpressió gènicaMolecular WeightSpermidineMetabolismchemistryDecarboxylasebiology.proteinPutrescineBotànicalcsh:QGene expressionSpermidine synthase
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