Search results for "Immunity"

showing 10 items of 1537 documents

High-Intensity Focused Ultrasound- and Radiation Therapy-Induced Immuno-modulation: Comparison and Potential Opportunities

2017

In recent years, high-intensity focused ultrasound (HIFU) has emerged as a new and promising non-invasive and non-ionizing ablative technique for the treatment of localized solid tumors. Extensive pre-clinical and clinical studies have evidenced that, in addition to direct destruction of the primary tumor, HIFU-thermoablation may elicit long-term systemic host anti-tumor immunity. In particular, an important consequence of HIFU treatment includes the release of tumor-associated antigens (TAAs), the secretion of immuno-suppressing factors by cancer cells and the induction of cytotoxic T lymphocyte (CTL) activity. Radiation therapy (RT) is the main treatment modality used for many types of tu…

0301 basic medicinePathologymedicine.medical_specialtyRadiology Nuclear Medicine and ImagingAcoustics and Ultrasonicsmedicine.medical_treatmentBiophysicsImmunomodulation03 medical and health sciences0302 clinical medicineImmune systemNeoplasmsmedicineBystander effectHumansCancerChemotherapyRadiological and Ultrasound Technologybusiness.industryCancermedicine.diseasePrimary tumorThermal ablationHigh-intensity focused ultrasoundRadiation therapyImmuno-therapyRadiation therapyTumor vaccine030104 developmental biologyBiophysicHigh-intensity focused ultrasound030220 oncology & carcinogenesisCancer cellCancer researchHigh-Intensity Focused Ultrasound AblationAnti-tumor immunitybusinessAnti-tumor immunity; Cancer; High-intensity focused ultrasound; Immuno-therapy; Radiation therapy; Thermal ablation; Tumor vaccine
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Nutritional Wheat Amylase-Trypsin Inhibitors Promote Intestinal Inflammation via Activation of Myeloid Cells.

2016

Background & Aims Wheat amylase-trypsin inhibitors (ATIs) are nutritional activators of innate immunity, via activation of the toll-like receptor 4 (TLR4) on myeloid cells. We aimed to characterize the biologic activity of ATIs in various foods and their effect on intestinal inflammation. Methods We selected 38 different gluten-containing and gluten-free products, either unprocessed (such as wheat, rye, barley, quinoa, amaranth, soya, lentils, and rice) or processed (such as pizza, pasta, bread, and biscuits). ATIs were extracted and their biological activities determined in TLR4-responsive mouse and human cell lines. Effects of oral ATIs on intestinal inflammation were determined in health…

0301 basic medicinePharmacologyAdaptive Immunitychemistry.chemical_compoundMice0302 clinical medicineMesenteric lymph nodesMesenteryMyeloid CellsTriticumPlant ProteinsToll-like receptorDextran SulfateGastroenterologyfood and beveragesColitisIntestinesmedicine.anatomical_structureAmylases030211 gastroenterology & hepatologymedicine.symptomTrypsin InhibitorsInterferon InducersGlutensColonDuodenumInflammationIleumBiologyCell Line03 medical and health sciencesDiet Gluten-FreeIleummedicineAnimalsHumansColitisInflammationInnate immune systemHepatologymedicine.diseaseImmunity InnateMice Inbred C57BLToll-Like Receptor 4Celiac Disease030104 developmental biologyPoly I-CchemistryPolyinosinic:polycytidylic acidImmunologyLymph NodesWheat allergyGastroenterology
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The role of spatial structure in the evolution of viral innate immunity evasion: A diffusion-reaction cellular automaton model

2020

Most viruses have evolved strategies for preventing interferon (IFN) secretion and evading innate immunity. Recent work has shown that viral shutdown of IFN secretion can be viewed as a social trait, since the ability of a given virus to evade IFN-mediated immunity depends on the phenotype of neighbor viruses. Following this idea, we investigate the role of spatial structure in the evolution of innate immunity evasion. For this, we model IFN signaling and viral spread using a spatially explicit approximation that combines a diffusion-reaction model and cellular automaton. Our results indicate that the benefits of preventing IFN secretion for a virus are strongly determined by spatial struct…

0301 basic medicinePhysiologyApoptosisVirus ReplicationBiochemistryVirionsEpitopes0302 clinical medicineInterferonMedicine and Health SciencesBiology (General)Innate Immune Systemeducation.field_of_studyCell DeathEcology3. Good healthCell biologyPhenotypeComputational Theory and MathematicsCell ProcessesModeling and SimulationViral evolutionHost-Pathogen InteractionsVirusesSignal TransductionResearch Articlemedicine.drugEvolutionary ImmunologyQH301-705.5ImmunologyPopulationViral StructureBiologyAntiviral AgentsMicrobiologyViral EvolutionVirusViral Proteins03 medical and health sciencesCellular and Molecular NeuroscienceImmunityVirologyGeneticsmedicineAnimalsHumansComputer SimulationSocial BehavioreducationMolecular BiologySecretionEcology Evolution Behavior and SystematicsImmune EvasionEvolutionary BiologyInnate immune systemVirionBiology and Life SciencesProteinsCell BiologyEvasion (ethics)Immunity InnateOrganismal Evolution030104 developmental biologyViral replicationImmune SystemMicrobial EvolutionInterferonsPhysiological Processes030217 neurology & neurosurgery
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The Immunomodulatory Properties of the Human Amnion-Derived Mesenchymal Stromal/Stem Cells Are Induced by INF-γ Produced by Activated Lymphomonocytes…

2020

Human mesenchymal stromal/stem cells (MSCs), being immunoprivileged and having immunomodulatory ability, represent a promising tool to be applied in the field of regenerative medicine. Based on numerous in vitro evidences, the immunological effects of MSCs on immune cells could depend on different mechanisms as cell-to-cell contact and paracrine signals. Furthermore, recent studies have shown that the immunomodulatory activity of MSCs is initiated by activated immune cells; thus, their interaction represents a potential homeostatic mechanism by which MSCs regulate the immune response. MSCs also release exosomes able to give different effects, in a paracrine manner, by influencing inflammato…

0301 basic medicineProgrammed Cell Death 1 ReceptorCell CommunicationLymphocyte ActivationimmunomodulationB7-H1 AntigenMonocytes0302 clinical medicineImmunology and AllergyOriginal ResearchChemistryCell DifferentiationHealthy VolunteersI-kappa B KinaseCell biologymedicine.anatomical_structureprimed-hAMSCsMonocyte differentiationCytokinesStem celllcsh:Immunologic diseases. AllergyStromal cellT cellPrimary Cell CultureImmunologyregenerative medicineexosomesInterferon-gamma03 medical and health sciencesParacrine signallingImmune systeminterferon-γmedicineHumansImmunologic FactorsAmnionhuman amnion-derived mesenchymal stem cellsCell ProliferationImmunosuppression TherapyPDL-1Mesenchymal stem cellImmunityM2-like monocytesMesenchymal Stem CellsCoculture TechniquesMicrovesiclesMicroRNAs030104 developmental biologyLeukocytes Mononuclearlcsh:RC581-607Interferon Regulatory Factor-1030215 immunologyFrontiers in Immunology
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Viral Bcl2s' transmembrane domain interact with host Bcl2 proteins to control cellular apoptosis

2020

© The Author(s) 2020.

0301 basic medicineProgrammed cell deathScienceProtein domainGeneral Physics and AstronomyApoptosisBiologyVirus-host interactionsArticleGeneral Biochemistry Genetics and Molecular BiologyFluorescenceCell Line03 medical and health sciences0302 clinical medicineProtein Domainsimmune system diseaseshemic and lymphatic diseasesmedicineHumansAmino Acid SequenceAuthor CorrectionPeptide sequenceneoplasmsMultidisciplinaryVirus–host interactionsQCell MembraneGeneral ChemistryViral proteinsmedicine.diseaseControl cellLymphomaCell biologyVirusTransmembrane domain030104 developmental biologyProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisDoxorubicin030220 oncology & carcinogenesisbiological phenomena cell phenomena and immunityProtein MultimerizationHydrophobic and Hydrophilic InteractionsProteïnesProtein Binding
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E2F1 interacts with BCL-xL and regulates its subcellular localization dynamics to trigger cell death

2018

International audience; E2F1 is the main pro-apoptotic effector of the pRB-regulated tumor suppressor pathway by promoting the transcription of various pro-apoptotic proteins. We report here that E2F1 partly localizes to mitochondria, where it favors mitochondrial outer membrane permeabilization. E2F1 interacts with BCL-xL independently from its BH3 binding interface and induces a stabilization of BCL-xL at mitochondrial membranes. This prevents efficient control of BCL-xL over its binding partners, in particular over BAK resulting in the induction of cell death. We thus identify a new, non-BH3-binding regulator of BCL-xL localization dynamics that influences its anti-apoptotic activity.

0301 basic medicineProgrammed cell deathTranscription Geneticbcl-X ProteinRegulatorBcl-xL[SDV.CAN]Life Sciences [q-bio]/CancerBCL-xL mobilityMitochondrionBiochemistrylaw.invention[ SDV.CAN ] Life Sciences [q-bio]/CancerE2F1 Subject Category Autophagy & Cell Death03 medical and health sciences[SDV.CAN] Life Sciences [q-bio]/CancerlawBCL-2 familyCell Line TumorGeneticsJournal ArticleHumansE2F1Molecular BiologyCell DeathbiologyManchester Cancer Research CentreEffectorChemistryResearchInstitutes_Networks_Beacons/mcrcScientific ReportsapoptosisSubcellular localizationMitochondriaCell biologyProtein Transportbcl-2 Homologous Antagonist-Killer Protein030104 developmental biologyGene Expression RegulationProto-Oncogene Proteins c-bcl-2biology.proteinSuppressorbiological phenomena cell phenomena and immunityExtracellular SpaceE2F1 Transcription FactorProtein Binding
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Parasites Dampen Dendritic Cell Activation to Ensure Their Survival

2017

Dendritic cells (DCs) are critical for induction of protective immunity against Leishmania major. However, DC activation occurs only several weeks after parasite transmission. Parasites synthesize a macrophage-inducible C-type lectin (Mincle) ligand. Engagement of Mincle by the parasite ligand dampens DC activation, thus delaying induction of interferon-γ-producing T cells responsible for parasite eradication.

0301 basic medicineProtective immunityLigandLectinmacromolecular substancesDendritic cellBiologybiology.organism_classificationCell biology03 medical and health sciences030104 developmental biologyInfectious Diseasesbiology.proteinParasite hostingParasitologyParasite transmissionLeishmania majorTrends in Parasitology
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Lack of NFATc1 SUMOylation prevents autoimmunity and alloreactivity

2020

A novel transgenic mouse, in which the transcription factor NFATc1 bears lysine-to-arginine mutations that prevent modification by SUMO, develops normally and is healthy. However, SUMO-insensitive NFATc1 transmits strong tolerogenic signals, thus preventing autoimmune and alloimmune T cell responses.

0301 basic medicineProtein sumoylationEncephalomyelitis Autoimmune ExperimentalT cellStem Cells & RegenerationImmunologySUMO proteinAutoimmunityBiologyenvironment and public healthT-Lymphocytes RegulatoryArticleMinor Histocompatibility AntigensMice03 medical and health sciences0302 clinical medicineImmune systemNeuroinflammationAldesleukinSTAT5 Transcription FactormedicineAnimalsImmunology and AllergyTranscription factorMice Knockoutintegumentary systemNFATC Transcription FactorsExperimental autoimmune encephalomyelitisSumoylationNFATmedicine.diseaseCell biologyenzymes and coenzymes (carbohydrates)030104 developmental biologymedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisCytokinesPositive Regulatory Domain I-Binding Factor 1Journal of Experimental Medicine
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Bacterial-viral load and the immune response in stable and exacerbated COPD: significance and therapeutic prospects.

2016

Silvestro Ennio D’Anna,1 Bruno Balbi,2 Francesco Cappello,3,4 Mauro Carone,2 Antonino Di Stefano21Department of Rehabilitation, Cardiorespiratory Unit, Fondazione Istituto G. Giglio di Cefalù, 2Pneumology Unit and Laboratory of Cytoimmunopathology of Heart and Lung, Fondazione Salvatore Maugeri, IRCCS, Veruno (NO) and Cassano delle Murge (BA), 3Human Anatomy Section, Department of Experimental Biomedicine and Clinical Neuroscience, University of Palermo, Palermo, Italy; 4Euro-Mediterranean Institute of Science and Technology, Palermo, ItalyAbstract: Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation and an abnormal inflammatory respon…

0301 basic medicinePulmonary and Respiratory MedicinePulmonary diseasemicrobiomeReview03 medical and health sciencesPulmonary Disease Chronic Obstructive0302 clinical medicineImmune systemexacerbationsmedicineHumansMicrobiomeRespiratory systemlcsh:RC705-779COPDImmunity CellularLungseverity of COPDbusiness.industryBiomarkers; COPD phenotype; Exacerbations; Microbiome; Severity of COPD; Pulmonary and Respiratory Medicine; Public Health Environmental and Occupational Health; Health PolicyHealth PolicyPublic Health Environmental and Occupational HealthbiomarkersExacerbationlcsh:Diseases of the respiratory systemBiomarkerGeneral MedicineViral Loadmedicine.diseaseBacterial Loadrespiratory tract diseases030104 developmental biologymedicine.anatomical_structure030228 respiratory systemImmunologyDisease ProgressionCOPD phenotypebusinessViral loadRespiratory tractInternational journal of chronic obstructive pulmonary disease
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A T cell-specific deletion of HDAC1 protects against experimental autoimmune encephalomyelitis.

2017

Multiple sclerosis (MS) is a human neurodegenerative disease characterized by the invasion of autoreactive T cells from the periphery into the CNS. Application of pan-histone deacetylase inhibitors (HDACi) ameliorates experimental autoimmune encephalomyelitis (EAE), an animal model for MS, suggesting that HDACi might be a potential therapeutic strategy for MS. However, the function of individual HDAC members in the pathogenesis of EAE is not known. In this study we report that mice with a T cell-specific deletion of HDAC1 (using the Cd4-Cre deleter strain; HDAC1-cKO) were completely resistant to EAE despite the ability of HDAC1cKO CD4+ T cells to differentiate into Th17 cells. RNA sequencin…

0301 basic medicineReceptors CCR6Encephalomyelitis Autoimmune ExperimentalMultiple SclerosisReceptors CCR4T cellImmunologyCCR4Histone Deacetylase 1C-C chemokine receptor type 6Biologymedicine.disease_causeAutoimmunity03 medical and health sciencesChemokine receptorMice0302 clinical medicineCell MovementmedicineImmunology and AllergyAnimalsHumansCells CulturedMice KnockoutChimeraMultiple sclerosisExperimental autoimmune encephalomyelitisGene targetingmedicine.diseaseMolecular biologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureSTAT1 Transcription FactorCancer researchTh17 Cells030215 immunologyJournal of autoimmunity
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