Search results for "Cell communication"

showing 10 items of 153 documents

Chemokines enhance immunity by guiding naive CD8+ T cells to sites of CD4+ T cell-dendritic cell interaction.

2005

CD8+ T cells have a crucial role in resistance to pathogens and can kill malignant cells; however, some critical functions of these lymphocytes depend on helper activity provided by a distinct population of CD4+ T cells. Cooperation between these lymphocyte subsets involves recognition of antigens co-presented by the same dendritic cell, but the frequencies of such antigen-bearing cells early in an infection and of the relevant naive T cells are both low. This suggests that an active mechanism facilitates the necessary cell-cell associations. Here we demonstrate that after immunization but before antigen recognition, naive CD8+ T cells in immunogen-draining lymph nodes upregulate the chemok…

CD4-Positive T-LymphocytesReceptors CCR5T cellAntigen presentationCell CommunicationBiologyCD8-Positive T-LymphocytesLymphocyte ActivationInterleukin 21MiceCell MovementmedicineCell AdhesionCytotoxic T cellAnimalsAntigen-presenting cellChemokine CCL4Chemokine CCL3MultidisciplinaryCD28Dendritic cellDendritic CellsMacrophage Inflammatory ProteinsNatural killer T cellmedicine.anatomical_structureChemokines CCImmunologyLymph NodesChemokinesImmunologic MemoryNature
researchProduct

Autocrine transforming growth factor- from chronic lymphocytic leukemia-β cells interferes with proliferative T cell signals

1999

Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of noncycling B cells in lymphatic and extralymphatic tissues. In the present study we investigated the possible contribution of TGF-beta, as secreted by CLL-B cells, on this low proliferative state. CLL-B cells were shown to express TGF-beta RNA and to release bioactive TGF-beta into culture supernatants. Antibody neutralization of endogenously secreted TGF-beta increased the proliferation of CLL-B cells as cultured in the presence of IL-2 or IL-4 or in direct contact with activated CD4+ T cells. In these culture systems, addition of exogenous TGF-beta downregulated basal and cytokineinduced proliferation of CLL-B cell…

CD4-Positive T-LymphocytesT cellPalatine TonsilImmunologyAntineoplastic AgentsCell CommunicationLymphocyte ActivationInterleukin 21Antigens CDTransforming Growth Factor betahemic and lymphatic diseasesmedicineHumansImmunology and AllergyCytotoxic T cellIL-2 receptorAntigen-presenting cellCells CulturedInterleukin 3B-LymphocytesCD40biologyT-Lymphocytes Helper-InducerHematologyLeukemia Lymphocytic Chronic B-CellCoculture TechniquesCell biologyAutocrine Communicationmedicine.anatomical_structurebiology.proteinInterleukin 12Immunobiology
researchProduct

Dendritic Cells Lose Ability to Present Protein Antigen after Stimulating Antigen-Specific T Cell Responses, despite Upregulation of MHC Class II Exp…

2000

Abstract Immature dendritic cells (DC) take up, process and present protein antigens; mature DC are specialized for stimulating primary T cell responses with increased expression of MHC class II and co-stimulatory molecules, but are incapable of processing and presenting soluble protein. The current study examined whether maturation of DC is triggered by T cell recognition of antigens presented by immature DC. Human DC derived from CD34+ progenitor cells by culture with granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-6 (IL-6) in serum-free medium could prime naive CD4+ T cells to keyhole limpet hemocyanin (KLH) and ovalbumin (OVA). The cultured DC retained the abil…

CD4-Positive T-LymphocytesTime FactorsOvalbuminT cellImmunologyCD1Bone Marrow CellsCell CommunicationCulture Media Serum-FreeInterferon-gammaInterleukin 21medicineHumansImmunology and AllergyCytotoxic T cellIL-2 receptorCD40 AntigensAntigen-presenting cellCells CulturedAntigen PresentationMHC class IIbiologyInterleukin-6Tumor Necrosis Factor-alphaHistocompatibility Antigens Class IIGranulocyte-Macrophage Colony-Stimulating FactorCell DifferentiationDendritic CellsHematologyIntercellular Adhesion Molecule-1Natural killer T cellMolecular biologyCoculture Techniquesmedicine.anatomical_structureHemocyaninsB7-1 Antigenbiology.proteinImmunobiology
researchProduct

Membrane vesicles shed by oligodendroglioma cells induce neuronal apoptosis.

2006

In order to investigate the mechanism by which oligodendrogliomas cause neuronal damage, media conditioned by G26/24 oligodendroglioma cells, were fractionated into shed vesicles and vesicle-free supernatants, and added to primary cultures of rat fetal cortical neurons. After one night treatment with vesicles, a reproducible, dose-dependent, inhibitory effect on neurite outgrowth was already induced and, after 48-72 h of incubation, neuronal apoptosis was evident. Vesicle-free supernatants and vesicles shed by NIH-3T3 cells had no inhibitory effects on neurons. Western blot analyses showed that treated neurons expressed a decreased amount of neurofilament (NF), growth-associated protein (GA…

Cancer ResearchCell signalingProgrammed cell deathPathologymedicine.medical_specialtyNeurofilamentFas Ligand ProteinNeuriteCellOligodendrogliomaApoptosisCell CommunicationBiologyRats Sprague-DawleyMiceWestern blotmedicineAnimalsMyelin SheathCerebral CortexNeuronsmedicine.diagnostic_testVesicleCytoplasmic Vesiclesoligodendroglioma membrane vesicles neuronal apoptosis Fas-L Nogo.Cell biologyRatsmedicine.anatomical_structureOncologyNIH 3T3 CellsNeuronInternational journal of oncology
researchProduct

Cell-cell and cell-collagen interactions influence gelatinase production by human breast-carcinoma cell line 8701-BC

1995

We previously produced evidence that the human mammary-carcinoma cell line 8701-BC expresses several metalloproteinases (MMP-1, -2, -9, and -10) and their tissue inhibitors. In order to obtain a better understanding of the environmental control over gelatinolytic activities, we have tested the enzyme production of 8701-BC cells, at time intervals after plating on different collagen substrates, i.e., types I, III, IV, V and OF/LB, used as films in culture dishes. Proteinase activities, released in the conditioned culture media, were tested by zymography on SDS-PAGE, and by quantificative analyses, using 14C carboxy-methylated transferrin as substrate in a liquid incubation medium. Enzymatic …

Cancer ResearchConfluencyKunitz STI protease inhibitorBreast NeoplasmsCell CommunicationBiologyTrypsinCulture MediaMolecular WeightOncologyBiochemistryCell–cell interactionGelatinasesCell cultureEndopeptidasesTumor Cells CulturedmedicineHumansGelatinaseSerine Proteinase InhibitorsZymographyCollagenCell Divisionmedicine.drugInternational Journal of Cancer
researchProduct

Oligodendroglioma cells shed microvesicles which contain TRAIL as well as molecular chaperones and induce cell death in astrocytes.

2011

Microvesicles (MVs) shed from G26/24 oligodendroglioma cells were previously reported to cause a reproducible, dose-dependent, inhibitory effect on neurite outgrowth, and eventually neuronal apoptosis, when added to primary cultures of rat cortical neurons. These effects were reduced but not abolished by functional monoclonal antibodies against Fas-L. In order to investigate whether MVs contain other factors able to induce cell death, we tested them for TRAIL and found clear evidence of its presence in the vesicles. This finding suggests the possibility that Fas-L and TRAIL cooperate in inducing brain cell death. Aimed at understanding the route through which the vesicles deliver their mess…

Cancer ResearchProgrammed cell deathNeuritemedicine.drug_classOligodendrogliomaCellCell CommunicationBiologyMonoclonal antibodyTNF-Related Apoptosis-Inducing LigandCell-Derived MicroparticlesmedicineAnimalsHSP70 Heat-Shock ProteinsRats WistarCells CulturedCell DeathVesicleHSC70 Heat-Shock ProteinsCell cycleMicrovesiclesRatsCell biologymedicine.anatomical_structureOncologyApoptosisAstrocytesCulture Media Conditionedmicrovesicles oligodendroglioma astrocytes TRAIL Hsp70Molecular Chaperones
researchProduct

The aryl hydrocarbon receptor (AhR) in the regulation of cell–cell contact and tumor growth

2010

The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor, which is activated by a large group of environmental pollutants including polycyclic aromatic hydrocarbons, dioxins and planar polychlorinated biphenyls. Ligand binding leads to dimerization of the AhR with aryl hydrocarbon receptor nuclear translocator and transcriptional activation of several xenobiotic phase I and phase II metabolizing enzymes, such as cytochrome P4501A1 and glutathione- S -transferase, respectively. Since phase I enzymes convert inert carcinogens to active genotoxins, the AhR plays a key role in tumor initiation. Besides this classical route, the AhR mediates tumor promotion and recent evide…

Cancer Researchmedicine.medical_specialtyAryl hydrocarbon receptor nuclear translocatorReviewsTumor initiationCell Communicationmedicine.disease_causeInternal medicineNeoplasmsmedicineCell AdhesionHomeostasisHumansTranscription factorbiologyCell CycleCell MembraneContact inhibitionMembrane ProteinsEpithelial CellsGeneral MedicineAryl hydrocarbon receptorEndocrinologyReceptors Aryl HydrocarbonTumor progressionbiology.proteinCancer researchTumor promotionCarcinogenesisCell DivisionSignal Transduction
researchProduct

Mast cells boost myeloid-derived suppressor cell activity and contribute to the development of tumor-favoring microenvironment

2014

Abstract Inflammation plays crucial roles at different stages of tumor development and may lead to the failure of immune surveillance and immunotherapy. Myeloid-derived suppressor cells (MDSC) are one of the major components of the immune-suppressive network that favors tumor growth, and their interaction with mast cells is emerging as critical for the outcome of the tumor-associated immune response. Herein, we showed the occurrence of cell-to-cell interactions between MDSCs and mast cells in the mucosa of patients with colon carcinoma and in the colon and spleen of tumor-bearing mice. Furthermore, we demonstrated that the CT-26 colon cancer cells induced the accumulation of CD11b+Gr1+ imma…

Cancer Researchmedicine.medical_treatmentCD40 LigandImmunologyInflammationCell CommunicationBiologyNitric OxideProinflammatory cytokineInterferon-gammaMiceImmune systemAntigens CD40Animals; Antigens CD40; CD40 Ligand; Cell Line Tumor; Colonic Neoplasms; Humans; Inflammation; Interferon-gamma; Mast Cells; Mice; Mice Inbred BALB C; Mice Knockout; Myeloid Cells; Nitric Oxide; Tumor Microenvironment; Cell Communication; Cancer Research; Immunology; Medicine (all)Cell Line TumormedicineMast cell; Myeloid-Derived Suppressor Cell; tumor microenvironment; colon cancerTumor MicroenvironmentAnimalsHumansMyeloid-Derived Suppressor CellMast CellMyeloid CellsMast CellsCD40 AntigensMyeloid CellInflammationMice KnockoutTumor microenvironmentColonic NeoplasmMice Inbred BALB CCD40AnimalMedicine (all)ImmunotherapyMast cellmedicine.anatomical_structurecolon cancerImmunologyColonic NeoplasmsCancer researchMyeloid-derived Suppressor Cellbiology.proteinmedicine.symptomHuman
researchProduct

Nuclear-mitochondrial interaction.

2007

The biogenesis of mitochondria depends on the coordinated expression of nuclear and mitochondrial genomes. Consequently, the control of mitochondrial biogenesis and function depends on extremely complex processes requiring a variety of well orchestrated regulatory mechanisms. It is clear that the interplay of transcription factors and coactivators contributes to the expression of both nuclear and mitochondrial respiratory genes. In addition, the regulation of mitochondria biogenesis depends on proteins that, interacting with messenger RNAs for mitochondrial proteins, influence their metabolism and expression. Moreover, a tight regulation of the import and final assembly of mitochondrial pro…

Cell NucleusRNA-binding proteinRNA-binding proteinsCell BiologyCell CommunicationBiologyMitochondrionCell biologyEpigenesis GeneticMitochondriamitochondrial fusionMitochondrial biogenesisNeoplasmsMolecular MedicineAnimalsHumansMitochondrial fissionMolecular BiologyTranscription factorPost-transcriptional regulationBiogenesistranscriptional factorpost-transcriptional regulationTranscription FactorsMitochondrion
researchProduct

All-trans retinoic acid restores gap junctional intercellular communication between oral cancer cells with upregulation of Cx32 and Cx43 expressions …

2012

Objective: All-trans retinoic acid (ATRA) has been demonstrated to inhibit tumor growth by restoration of gap junctional intercellular communication (GJIC) via upregulation of connexin (Cx) expression in some solid tumors. However, the relationship between ATRA and GJIC remains unclear in oral squamous cell carcinoma (OSCC). The aim of this study was to investigate the effect of ATRA on the GJIC function of OSCC. Study design: We measured the effects of ATRA on the viability and cell cycle distribution of SCC9 and Tca8113 OSCC cells. The GJIC function was observed using the scrape-loading dye transfer technique, and the mRNA and protein levels of Cx32 and Cx43 were detected by qRT-PCR, West…

Cell cycle checkpointRetinoic acidConnexinAntineoplastic AgentsTretinoinOdontologíaCell CommunicationConnexinschemistry.chemical_compoundDownregulation and upregulationTretinoinmedicineTumor Cells CulturedHumansRNA MessengerGeneral DentistryneoplasmsMouth neoplasmOral Medicine and Pathologyorganic chemicalsGap JunctionsCell cycle:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludbiological factorsUp-RegulationGene Expression Regulation Neoplasticstomatognathic diseasesOtorhinolaryngologychemistryConnexin 43ImmunologyCancer cellUNESCO::CIENCIAS MÉDICASCancer researchCarcinoma Squamous CellSurgeryMouth NeoplasmsResearch-Articlemedicine.drug
researchProduct