Search results for "PROLIFERATION"

showing 10 items of 1193 documents

Chronic myeloid leukemia-derived exosomes promote tumor growth through an autocrine mechanism.

2014

Background Chronic myeloid leukemia (CML) is a clonal hematopoietic stem cell disorder in which leukemic cells display a reciprocal t(9:22) chromosomal translocation that results in the formation of the chimeric BCR-ABL oncoprotein, with a constitutive tyrosine kinase activity. Consequently, BCR-ABL causes increased proliferation, inhibition of apoptosis, and altered adhesion of leukemic blasts to the bone marrow (BM) microenvironment. It has been well documented that cancer cells can generate their own signals in order to sustain their growth and survival, and recent studies have revealed the role of cancer-derived exosomes in activating signal transduction pathways involved in cancer cell…

SurvivinMice NudeMice SCIDBiologyAutocrine mechanismsExosomesBiochemistryExosomeInhibitor of Apoptosis ProteinsTransforming Growth Factor beta1Micehemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositiveTGF-β1medicineAnimalsHumansAutocrine signallingMolecular BiologyCell ProliferationTumor microenvironmentCell growthResearchChronic myeloid leukemiaMyeloid leukemiaCell Biologymedicine.diseaseMicrovesiclesCML exosomesCell biologyNeoplasm ProteinsLeukemiaAutocrine CommunicationCancer cellAnti-apoptotic pathwaysApoptosis Regulatory ProteinsSignal TransductionCell communication and signaling : CCS
researchProduct

Sorbitol-penetration enhancer containing vesicles loaded with baicalin for the protection and regeneration of skin injured by oxidative stress and UV…

2018

Abstract Aiming at improving the protective effects of baicalin on the skin, new highly-biocompatible penetration enhancer containing vesicles (PEVs) were developed by modifying the base formulation of transfersomes with sorbitol, thus obtaining sorbitol-PEVs. An extensive evaluation of the physico-chemical features of both transfersomes and sorbitol-PEVs was carried out. Transfersomes were mainly close-packed, multi-compartment vesicles, while sorbitol-PEVs appeared mostly as single, spherical, unilamellar vesicles. All the vesicles were small in size (∼128 nm) and negatively charged (∼−67 mV), without significant differences between the formulations. The in vitro delivery of baicalin to i…

SwineUltraviolet RaysChemistry PharmaceuticalCellPharmaceutical Science02 engineering and technologymedicine.disease_cause030226 pharmacology & pharmacyCell LineExcipients03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineDrug Delivery SystemsCell MovementmedicineAnimalsHumansRegenerationSorbitolParticle SizeCell ProliferationSkinFlavonoidsWound HealingCell growthVesicleRegeneration (biology)fungi3T3 Cells021001 nanoscience & nanotechnologyIn vitroOxidative Stressmedicine.anatomical_structurechemistryBiophysicsSorbitol0210 nano-technologyBaicalinOxidative stressInternational journal of pharmaceutics
researchProduct

Reversible effect of MR and ELF magnetic fields (0.5 T and 0.5 mT) on human lymphocyte activation patterns.

2006

Purpose: The aim of this study was to investigate the effects of magnetic fields (MF) of different intensity generated by a magnetic resonance (MR) unit (0.5 Tesla) and a double cylindrical coil (0.5 mTesla) on human CD4+ T cell lines. Materials and methods: CD4+ T cells were exposed for two hours under isothermal conditions (37 ± 0.5°C) to the above mentioned MF; a control group was provided for each exposed sample. After exposure, the samples were analysed in the laboratory for the following endpoints: Release of cytokines, expression of surface markers, cell proliferation and levels of cytosolic free-calcium. Results: Exposure to MF for 2 h and subsequent in vitro stimulation in the pres…

T cellBiologyLymphocyte ActivationRadiation DosageCell LineNuclear magnetic resonanceElectricitymedicineHumansRadiology Nuclear Medicine and imagingIL-2 receptorLymphocytesMR Biological effectsCell ProliferationRadiological and Ultrasound Technologymedicine.diagnostic_testCell growthMagnetic resonance imagingDose-Response Relationship RadiationMolecular biologyAdaptation PhysiologicalMagnetic Resonance ImagingIn vitroMagnetic fieldCytosolmedicine.anatomical_structureMitogen-activated protein kinasebiology.proteinCytokines
researchProduct

CD4 blockade directly inhibits mouse and human CD4+ T cell functions independent of Foxp3+ Tregs

2013

CD4(+) helper T cells orchestrate protective immunity against pathogens, yet can also induce undesired pathologies including allergies, transplant rejection and autoimmunity. Non-depleting CD4-specific antibodies such as clone YTS177.9 were found to promote long-lasting T cell tolerance in animal models. Thus, CD4 blockade could represent a promising therapeutic approach for human autoimmune diseases. However, the mechanisms underlying anti-CD4-induced tolerance are incompletely resolved. Particularly, multiple immune cells express CD4 including Foxp3(+) regulatory T cells (Tregs) and dendritic cells (DCs), both controlling the activation of CD4(+)Foxp3(-) helper T cells. Utilizing mixed le…

T cellImmunologyPriming (immunology)Ki-1 Antigenchemical and pharmacologic phenomenaBiologyCD8-Positive T-LymphocytesLymphocyte ActivationT-Lymphocytes RegulatoryLymphocyte DepletionInterleukin 21MiceImmune systemmedicineImmune ToleranceImmunology and AllergyCytotoxic T cellAnimalsHumansIL-2 receptorCells CulturedAntilymphocyte SerumCell ProliferationMice Inbred BALB CFOXP3Forkhead Transcription Factorshemic and immune systemsDendritic CellsReceptors OX40medicine.diseaseTransplant rejectionMice Inbred C57BLmedicine.anatomical_structureImmunologyCD4 AntigensInterleukin-2
researchProduct

Intrahepatic myeloid-cell aggregates enable local proliferation of CD8+T cells and successful immunotherapy against chronic viral liver infection

2013

Chronic infection is difficult to overcome because of exhaustion or depletion of cytotoxic effector CD8(+) T cells (cytotoxic T lymphoytes (CTLs)). Here we report that signaling via Toll-like receptors (TLRs) induced intrahepatic aggregates of myeloid cells that enabled the population expansion of CTLs (iMATEs: 'intrahepatic myeloid-cell aggregates for T cell population expansion') without causing immunopathology. In the liver, CTL proliferation was restricted to iMATEs that were composed of inflammatory monocyte-derived CD11b(+) cells. Signaling via tumor-necrosis factor (TNF) caused iMATE formation that facilitated costimulation dependent on the receptor OX40 for expansion of the CTL popu…

T cellmedicine.medical_treatmentImmunologyPopulationGreen Fluorescent ProteinsMice TransgenicBiologyCD8-Positive T-LymphocytesLymphocytic ChoriomeningitisMicemedicineImmunology and AllergyCytotoxic T cellAnimalsLymphocytic choriomeningitis virusMyeloid CellseducationCell ProliferationMice Knockouteducation.field_of_studyLiver infectionCD11b AntigenMicroscopy ConfocalLiver DiseasesImmunotherapyReceptors OX40Flow CytometryMice Inbred C57BLCTL*Chronic infectionmedicine.anatomical_structureAnimals NewbornLiverToll-Like Receptor 9ImmunologyChronic DiseaseHost-Pathogen InteractionsImmunotherapyCD8Signal TransductionT-Lymphocytes CytotoxicNature Immunology
researchProduct

Susceptibility to collagen-induced arthritis is modulated by TGFβ responsiveness of T cells

2004

The objective of our study was to determine the regulatory effects that endogenous transforming growth factor beta (TGFbeta) exerts on T cells in the pathogenesis of collagen-induced arthritis (CIA). CIA was induced in transgenic mice expressing a dominant negative TGFbeta type II receptor in T cells under the control of the human CD2 promoter. Clinical and histological arthritis scores were determined and experiments on disease induction and the healing phase of disease were performed. The proliferation and cytokine production of draining lymph node cells in vitro were analyzed. Transgenic mice were more susceptible to induction of CIA. The overall incidence was higher in transgenic mice t…

T-LymphocytesMice Inbred StrainsMice Transgenictransgenic miceTh1 CellsArthritis ExperimentalSeverity of Illness Indexdominant negative TGFβ type II receptorArthritis RheumatoidMiceMice Inbred DBATransforming Growth Factor betaAnimalsCytokinesCattleDisease SusceptibilityLymph NodesCollagen Type IICells CulturedCrosses GeneticResearch ArticleIFNγCell ProliferationArthritis Research & Therapy
researchProduct

Tolerance without clonal expansion: self-antigen-expressing B cells program self-reactive T cells for future deletion.

2008

Abstract B cells have been shown in various animal models to induce immunological tolerance leading to reduced immune responses and protection from autoimmunity. We show that interaction of B cells with naive T cells results in T cell triggering accompanied by the expression of negative costimulatory molecules such as PD-1, CTLA-4, B and T lymphocyte attenuator, and CD5. Following interaction with B cells, T cells were not induced to proliferate, in a process that was dependent on their expression of PD-1 and CTLA-4, but not CD5. In contrast, the T cells became sensitive to Ag-induced cell death. Our results demonstrate that B cells participate in the homeostasis of the immune system by abl…

T-LymphocytesProgrammed Cell Death 1 ReceptorAutoimmunityAntigens CD/biosynthesisAntigens CD5/geneticsAutoantigensInterleukin 21MiceImmunology and AllergyCytotoxic T cellHomeostasisCTLA-4 AntigenIL-2 receptorAntigens Differentiation/biosynthesisB-LymphocytesAntigens CD/geneticsB-Lymphocytes/immunologyT-Lymphocytes/metabolismNatural killer T cellCell biologymedicine.anatomical_structureHomeostasis/immunology2723 Immunology and AllergyAntigens CD5/biosynthesisAntigens Differentiation/geneticsAntigens CD5/immunologyT cellImmunologyAntigens CD/immunologyClonal Deletion610 Medicine & healthchemical and pharmacologic phenomenaMice TransgenicBiologyAutoantigens/biosynthesisCD5 AntigensAutoimmunity/physiologyAutoantigens/immunologyAntigens CDmedicineAnimalsB-Lymphocytes/metabolismAntigen-presenting cellCell Proliferation2403 ImmunologyAntigens Differentiation/immunologyGene Expression Regulation/immunologyCD40Clonal Deletion/physiologyT-Lymphocytes/immunologyAntigens Differentiation10040 Clinic for NeurologyB-1 cellGene Expression Regulationbiology.protein
researchProduct

T Cells Integrate Local and Global Cues to Discriminate between Structurally Similar Antigens

2015

International audience; T lymphocytes' ability to discriminate between structurally related antigens has been attributed to the unique signaling properties of the T cell receptor. However, recent studies have suggested that the output of this discrimination process is conditioned by environmental cues. Here, we demonstrate how the IL-2 cytokine, collectively generated by strongly activated T cell clones, can induce weaker T cell clones to proliferate. We identify the PI3K pathway as being critical for integrating the antigen and cytokine responses and for controlling cell-cycle entry. We build a hybrid stochastic/deterministic computational model that accounts for such signal synergism and …

T-Lymphocytesmedicine.medical_treatmentT cellEFFECTORMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyLYMPHOCYTESArticleGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineACTIVATIONMicePhosphatidylinositol 3-KinasesAntigenmedicineAnimalsAntigenslcsh:QH301-705.5Sensory cuePI3K/AKT/mTOR pathwayAFFINITYIL-2T-cell receptorMEMORYPROLIFERATIONRECOGNITIONCell biologyMice Inbred C57BLCytokinemedicine.anatomical_structureDIFFERENTIATIONlcsh:Biology (General)ImmunologyCytokinesInterleukin-2Signal transductionTCRSignal Transduction
researchProduct

A Regulatory Mechanism Involving TBP-1/Tat-Binding Protein 1 and Akt/PKB in the Control of Cell Proliferation

2011

Abstract TBP-1 /Tat-Binding Protein 1 (also named Rpt-5, S6a or PSMC3) is a multifunctional protein, originally identified as a regulator of HIV-1-Tat mediated transcription. It is an AAA-ATPase component of the 19S regulative subunit of the proteasome and, as other members of this protein family, fulfils different cellular functions including proteolysis and transcriptional regulation. We and others reported that over expression of TBP-1 diminishes cell proliferation in different cellular contexts with mechanisms yet to be defined. Accordingly, we demonstrated that TBP-1 binds to and stabilizes the p14ARF oncosuppressor increasing its anti-oncogenic functions. However, TBP-1 restrains cell…

TBP-1/Tat-Binding Protein 1lcsh:Medicinemacromolecular substancesBiologymTORC2Cell GrowthTBP-1/Tat-Binding Protein 1; cell proliferationp14arfMolecular Cell BiologyGeneticsCancer GeneticsTranscriptional regulationGene Networkslcsh:ScienceBiologyProtein kinase BPI3K/AKT/mTOR pathwayMultidisciplinaryCell growthAKTBinding proteinlcsh:RMolecular biologySignaling CascadesCell biologyTBP-1enzymes and coenzymes (carbohydrates)cell proliferationbiology.proteinMdm2lcsh:QCell DivisionResearch ArticleSignal TransductionPLoS ONE
researchProduct

The high-performance technology CRISPR/Cas9 improves knowledge and management of acute myeloid leukemia

2021

Knowledge on acute myeloid leukemia pathogenesis and treatment has progressed recently, but not enough to provide ideal management. Improving the prognosis of acute myeloid leukemia patients depends on advances in molecular biology for the detection of new therapeutic targets and the production of effective drugs. The CRISPR/Cas9 technology allows gene insertions and deletions and it is the first step in investigating the function of their encoded proteins. Thus, new experimental models have been developed and progress has been made in understanding protein metabolism, antitumor activity, leukemic cell maintenance, differentiation, growth, apoptosis, and self-renewal, the combined pathogene…

TechnologyCD38acute myeloid leukemiamedicine.disease_causeGeneral Biochemistry Genetics and Molecular Biologycd38bcl2chemistry.chemical_compoundcrispr/cas9flt3 inhibitorshemic and lymphatic diseasesmedicineCRISPRHumansMidostaurinProtein Kinase InhibitorsCell ProliferationMutationCas9business.industryCell growthRMyeloid leukemiamedicine.diseaseidh2LeukemiaLeukemia Myeloid Acutechemistryfms-Like Tyrosine Kinase 3MutationCancer researchMedicineCRISPR-Cas SystemsbusinessBiomedical Papers
researchProduct