Search results for "regulation"

showing 10 items of 4463 documents

Reconstitution of T Cell Proliferation under Arginine Limitation: Activated Human T Cells Take Up Citrulline via L-Type Amino Acid Transporter 1 and …

2017

In the tumor microenvironment, arginine is metabolized by arginase-expressing myeloid cells. This arginine depletion profoundly inhibits T cell functions and is crucially involved in tumor-induced immunosuppression. Reconstitution of adaptive immune functions in the context of arginase-mediated tumor immune escape is a promising therapeutic strategy to boost the immunological anti-tumor response. Arginine can be recycled in certain mammalian tissues from citrulline via argininosuccinate in a two-step enzymatic process involving the enzymes argininosuccinate synthase (ASS) and argininosuccinate lyase (ASL). Here we demonstrate that anti-CD3/anti-CD28-activated human primary CD4+ and CD8+ T c…

0301 basic medicinelcsh:Immunologic diseases. AllergyArginineT cellArgininosuccinate synthaseImmunologyarginineamino acid transporter03 medical and health scienceschemistry.chemical_compoundDownregulation and upregulationT cell metabolismmedicineCitrullineExtracellularT lymphocyteImmunology and AllergybiologyMolecular biologyArgininosuccinate lyase030104 developmental biologymedicine.anatomical_structurechemistrycitrullinebiology.proteinlcsh:RC581-607CD8Frontiers in Immunology
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Cyclic AMP Represents a Crucial Component of Treg Cell-Mediated Immune Regulation

2016

T regulatory (Treg) cells are one of the key players in the immune tolerance network, and a plethora of manuscripts have described their development and function in the course of the last two decades. Nevertheless, it is still a matter of debate as to which mechanisms and agents are employed by Treg cells, providing the basis of their suppressive potency. One of the important candidates is cyclic AMP (cAMP), which is long known as a potent suppressor at least of T cell activation and function. While this suppressive function by itself is widely accepted, the source and the mechanism of action of cAMP are less clear, and a multitude of seemingly contradictory data allow for, in principle, tw…

0301 basic medicinelcsh:Immunologic diseases. AllergyFOXP3Mini ReviewT cellImmunologyimmune tolerance networkAdenylate kinaseBiologyregulatory T cellsImmune tolerance03 medical and health sciencesmedicineImmunology and Allergycyclic AMPReceptorEffectorimmune regulationFOXP3suppressionAdenosineCell biology030104 developmental biologymedicine.anatomical_structureadenosineImmunologylcsh:RC581-607Intracellularmedicine.drugFrontiers in Immunology
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Editorial: Current concepts of cellular and biological drugs to modulate regulatory T cell activity in the clinic

2016

The Editorial on the Research Topic Current Concepts of Cellular and Biological Drugs to Modulate Regulatory T Cell Activity in the Clinic Regulatory T (Treg) cells are essential for the maintenance of peripheral tolerance and prevent the development of autoimmunity and allergy. While on the one hand being indispensable for the perpetuation of tolerance to harmless antigens or self-antigens, Treg cells contribute to cancer pathogenesis and progression (1). Hence, the potential to treat a multitude of different human diseases by pharmacological modulation of Treg cells is enormous. Consequently, this T cell population is in the focus of biomedical research and development. Currently, isolate…

0301 basic medicinelcsh:Immunologic diseases. AllergyRegulatory T cellT cellImmunologyPopulationAutoimmunitymedicine.disease_causeregulatory T cellsAutoimmunityAutoimmune Diseases03 medical and health sciencesmedicineImmunology and Allergyclinical studieseducationeducation.field_of_studybusiness.industryPeripheral toleranceImmunoregulationT helper cellDendritic CellsTolerance inductionEditorial030104 developmental biologymedicine.anatomical_structureHumanized mouseImmunologybusinesslcsh:RC581-607Frontiers in Immunology
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Novel Insight Into the Molecular and Metabolic Mechanisms Orchestrating IL-17 Production in γδ T Cells

2019

Increasing evidence has demonstrated that IL-17-producing γδ T cells (γδ T17) play a tumor-promoting role in a series of cancers via various mechanisms in mice and human cancers, though the relationship between γδ T17 and human tumors has yet to be extensively characterized and established. Molecular signals such as intrinsic cascade, environmental cues and cellular metabolic pathways including nutrient uptake and utilization in γδ T17 cells are significantly important for their activation, differentiation, and function. Understanding the molecular mechanisms and metabolic pathways of γδ T17 cells in both the physiological setting and tumor environment would contribute to the development of…

0301 basic medicinelcsh:Immunologic diseases. Allergymedicine.medical_treatmentMini ReviewMetabolic reprogrammingImmunologyBiology03 medical and health sciences0302 clinical medicineCancer immunotherapyNeoplasmsmedicineTranscriptional regulationTumor MicroenvironmentImmunology and AllergyAnimalsHumansmetabolic reprogrammingtranscriptional regulationinnate immune cellsIntraepithelial Lymphocytescancer immunotherapyMicrobiotaInterleukin-17Immunotherapy3. Good healthCell biologyMetabolic pathway030104 developmental biologyInterleukin 17γδ T17 cellslcsh:RC581-607Function (biology)030215 immunologyFrontiers in Immunology
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Elevated sodium leads to the increased expression of HSP60 and induces apoptosis in HUVECs

2017

Atherosclerosis is the leading cause of death in the world. We have previously shown that expression of heat shock protein 60 (HSP60) on the surface of endothelial cells is the main cause of initiating the disease as it acts as a T cell auto-antigen and can be triggered by classical atherosclerosis risk factors, such as infection (e.g. Chlamydia pneumoniae), chemical stress (smoking, oxygen radicals, drugs), physical insult (heat, shear blood flow) and inflammation (inflammatory cytokines, lipopolysaccharide, oxidized low density lipoprotein, advanced glycation end products). In the present study, we show that increasing levels of sodium chloride can also induce an increase in intracellular…

0301 basic medicinelcsh:MedicineApoptosisBlood PressureSodium Chloride030204 cardiovascular system & hematologyVascular MedicineHeat Shock ResponseEpitheliumUmbilical veinWhite Blood CellsSpectrum Analysis Techniques0302 clinical medicineAnimal CellsGlycationMedicine and Health Scienceslcsh:ScienceCellular Stress ResponsesMultidisciplinaryCell DeathT CellsFlow CytometryProtein TransportChemistryCell ProcessesSpectrophotometryPhysical SciencesHypertensionCytophotometryCellular TypesAnatomymedicine.symptomIntracellularResearch Articlemedicine.medical_specialtyImmune CellsSodiumImmunologychemistry.chemical_elementInflammationBiologyResearch and Analysis MethodsImmunophenotypingProinflammatory cytokine03 medical and health sciencesInternal medicineHeat shock proteinHuman Umbilical Vein Endothelial CellsmedicineHumansHeat shockBlood CellsSodiumlcsh:RChemical CompoundsBiology and Life SciencesEndothelial CellsEpithelial CellsChaperonin 60Cell BiologyAtherosclerosisBiological Tissue030104 developmental biologyEndocrinologyGene Expression RegulationchemistryImmunologySaltslcsh:QBiomarkersPLOS ONE
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The Unfolded Protein Response Plays a Predominant Homeostatic Role in Response to Mitochondrial Stress in Pancreatic Stellate Cells.

2016

Activated pancreatic stellate cells (PaSC) are key participants in the stroma of pancreatic cancer, secreting extracellular matrix proteins and inflammatory mediators. Tumors are poorly vascularized, creating metabolic stress conditions in cancer and stromal cells that necessitate adaptive homeostatic cellular programs. Activation of autophagy and the endoplasmic reticulum unfolded protein response (UPR) have been described in hepatic stellate cells, but the role of these processes in PaSC responses to metabolic stress is unknown. We reported that the PI3K/mTOR pathway, which AMPK can regulate through multiple inputs, modulates PaSC activation and fibrogenic potential. Here, using primary a…

0301 basic medicinelcsh:MedicineApoptosisMitochondrionAMP-Activated Protein KinasesEndoplasmic ReticulumBiochemistrychemistry.chemical_compoundMiceeIF-2 KinasePhosphatidylinositol 3-Kinases0302 clinical medicineFluorescence MicroscopyCell SignalingTumor Microenvironment2.1 Biological and endogenous factorsSmall interfering RNAsAetiologylcsh:ScienceEnergy-Producing OrganellesCancerMice KnockoutMicroscopyMultidisciplinarySecretory PathwayCell DeathTOR Serine-Threonine KinasesLight MicroscopySignaling CascadesCell biologyMitochondriaNeoplasm ProteinsUp-RegulationNucleic acidsCell Processes030220 oncology & carcinogenesisCellular Structures and OrganellesResearch ArticleSignal TransductionProgrammed cell deathCell PhysiologyGeneral Science & TechnologyAutophagic Cell DeathKnockoutBiologyBioenergeticsResearch and Analysis MethodsStress Signaling Cascade03 medical and health sciencesGeneticsAutophagyAnimalsNon-coding RNAPancreasPI3K/AKT/mTOR pathwaylcsh:RAutophagyAMPKBiology and Life SciencesCell BiologyCell MetabolismGene regulationPancreatic NeoplasmsEnzyme Activation030104 developmental biologychemistryHepatic stellate cellUnfolded protein responseUnfolded Protein ResponseRNAlcsh:QGene expressionInterleukin-4Digestive DiseasesRottlerinTranscription Factor CHOP
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Dynamics of a Protein Interaction Network Associated to the Aggregation of polyQ-Expanded Ataxin-1

2020

Background: Several experimental models of polyglutamine (polyQ) diseases have been previously developed that are useful for studying disease progression in the primarily affected central nervous system. However, there is a missing link between cellular and animal models that would indicate the molecular defects occurring in neurons and are responsible for the disease phenotype in vivo. Methods: Here, we used a computational approach to identify dysregulated pathways shared by an in vitro and an in vivo model of ATXN1(Q82) protein aggregation, the mutant protein that causes the neurodegenerative polyQ disease spinocerebellar ataxia type-1 (SCA1). Results: A set of common dysregulated pathwa…

0301 basic medicinelcsh:QH426-470Ataxin 1Mice TransgenicNerve Tissue ProteinsProtein aggregationBlood–brain barrierblood-brain-barrierArticledrugspolyQ03 medical and health sciences0302 clinical medicineataxin-1Interaction networkIn vivoMutant proteinCerebellumGeneticsmedicineAnimalsGene Regulatory NetworksProtein Interaction MapsGenetics (clinical)NeuronsbiologypathwayGene Expression Profilingmedicine.diseaselcsh:Genetics030104 developmental biologymedicine.anatomical_structureGene Expression Regulationnetworkbiology.proteinSpinocerebellar ataxiaPeptidesNeuroscience030217 neurology & neurosurgeryFunction (biology)Genes
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Functional insights into the infective larval stage of Anisakis simplex s.s., Anisakis pegreffii and their hybrids based on gene expression patterns

2018

[Background]: Anisakis simplex sensu stricto and Anisakis pegreffii are sibling species of nematodes parasitic on marine mammals. Zoonotic human infection with third stage infective larvae causes anisakiasis, a debilitating and potentially fatal disease. These 2 species show evidence of hybridisation in geographical areas where they are sympatric. How the species and their hybrids differ is still poorly understood. [Results]: Third stage larvae of Anisakis simplex s.s., Anisakis pegreffii and hybrids were sampled from Merluccius merluccius (Teleosti) hosts captured in waters of the FAO 27 geographical area. Specimens of each species and hybrids were distinguished with a diagnostic genetic m…

0301 basic medicinelcsh:QH426-470Virulence Factorslcsh:BiotechnologyAnisakis simplexBreedingBiologyAnisakisTranscriptomeFish Diseases03 medical and health scienceslcsh:TP248.13-248.65parasitic diseasesGeneticsAnimalsAlleleGeneGeneticsSequence Analysis RNAGene Expression ProfilingAnisakis simplexMolecular Sequence AnnotationHelminth Proteins030108 mycology & parasitologyAllergensbiology.organism_classificationA. PegreffiiAnisakisGene expression profilingGadiformeslcsh:Genetics030104 developmental biologyGene Expression RegulationSympatric speciationGenetic markerLarvaGene expressionEnergy MetabolismTranscriptomeResearch ArticleBiotechnologyBMC Genomics
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PFN1 and integrin‐β1/mTOR axis involvement in cornea differentiation of fibroblast limbal stem cells

2019

Abstract Ex vivo limbal stem cell transplantation is the main therapeutic approach to address a complete and functional re‐epithelialization in corneal blindness, the second most common eye disorder. Although important key points were defined, the molecular mechanisms involved in the epithelial phenotype determination are unclear. Our previous studies have demonstrated the pluripotency and immune‐modulatory of fibroblast limbal stem cells (f‐LSCs), isolated from the corneal limbus. We defined a proteomic profile especially enriched in wound healing and cytoskeleton‐remodelling proteins, including Profilin‐1 (PFN1). In this study we postulate that pfn‐1 knock down promotes epithelial lineage…

0301 basic medicinelimbal stem cellApoptosisintegrin-β1Settore MED/13 - EndocrinologiaProfilins0302 clinical medicinesignallingCells CulturedCorneal epitheliumIntegrin beta1TOR Serine-Threonine KinasesEpithelium CornealCell DifferentiationCell biologymedicine.anatomical_structuremTOR pathway030220 oncology & carcinogenesisMolecular MedicineOriginal ArticleStem cellHomeobox protein NANOGintegrin‐β1regenerative medicineBiologyLimbus CorneaeCorneal limbus03 medical and health sciencesstem cellsmedicineHumansprofilinFibroblastlimbal stem cellsPI3K/AKT/mTOR pathwayCell ProliferationWound HealingSettore MED/30 - Malattie Apparato VisivoCell BiologyOriginal ArticlesFibroblastseye diseasesepithelial differentiation030104 developmental biologyGene Expression RegulationEye disordersense organscorneal regenerationWound healingBiomarkersJournal of Cellular and Molecular Medicine
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Long Non-coding Antisense RNA TNRC6C-AS1 Is Activated in Papillary Thyroid Cancer and Promotes Cancer Progression by Suppressing TNRC6C Expression

2018

Context: Evidences have shown the important role of long non-coding antisense RNAs in regulating its cognate sense gene in cancer biology. Objective: Investigate the regulatory role of a long non-coding antisense RNA TNRC6C-AS1 on its sense partner TNRC6C, and their effects on the aggressiveness and iodine-uptake ability of papillary thyroid cancer (PTC). Design: TNRC6C-AS1 was identified as the target long non-coding RNA in PTC by using microarray analysis and computational analysis. In vitro gain/loss-of-function experiments were performed to investigate the effects of TNRC6C-AS1 and TNRC6C on proliferation, apoptosis, migration, invasion and iodine-uptake ability of TPC1 cells. Expressio…

0301 basic medicinelong non-coding antisense RNAendocrine system diseasesEndocrinology Diabetes and MetabolismTNRC6C-AS1lcsh:Diseases of the endocrine glands. Clinical endocrinologyPapillary thyroid cancer03 medical and health sciencesEndocrinology0302 clinical medicineDownregulation and upregulationSense (molecular biology)medicinepapillary thyroid cancerTNRC6COriginal Researchiodine accumulationGene knockdownMessenger RNAlcsh:RC648-665ChemistryMicroarray analysis techniquesRNAmedicine.diseaseAntisense RNA030104 developmental biology030220 oncology & carcinogenesisCancer researchFrontiers in Endocrinology
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