Search results for "TNF"

showing 10 items of 161 documents

cIAP1 oncogenic properties analysis : contribution of its partners cdc42 and E2F1

2014

The inhibitor of apoptosis protein cIAP1 (cellular inhibitor of apoptosis protein-1) from the IAP family (Inhibitor of Apoptosis Protein) is an oncogene with an E3 ubiquitin ligase activity. cIAP1 is relocalized from the nucleus to the cytoplasm during the differentiation of many kind of cellular models (macrophages, dendritic cells, colon epithelial cells, hematopoietic stem cells, cardiomyocytes) and this relocalization is associated with a proliferation arrest. The well-known functions of cIAP1 are associated with its cytoplasmic localization, where it regulates the TNFa receptors and NF-?B signaling pathways. However, cIAP1 is mainly expressed in the nucleus on many cell types which is …

[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyTNF-aFilipodiaProliferationActin cytoskeleton[SDV.BC]Life Sciences [q-bio]/Cellular BiologyCIAP1E2F1Rho GTPasesHRasCytosquelette d’actineOncogenic transformation[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular Biology[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyCdc42ProliférationFilipodes[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology[SDV.BC] Life Sciences [q-bio]/Cellular BiologyTransformation oncogénique
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Effet anti-tumoral de l'acide docosahexaénoïque : implication des microARNs et du TNFalpha

2015

Docosahexaenoic acid (DHA) is an omega-3 polyunsaturated fatty acid with anti-inflammatory and anti-tumoral properties. The anti-tumor effect of DHA in colorectal cancer might be attributed to direct anti-proliferative action on cancer cells and to its ability to reduce inflammatory status involved in tumor growth. Tumor Necrosis Factor-alpha (TNFa) is an inflammatory cytokine with paradoxical effect in cancer biology. According to the cellular context, TNFa activates RIP1 kinase dependent signaling pathway leading to proliferation or cell death. Our aim was to evaluate the role of TNFa in anti-proliferative effect of DHA in colon cancer cells and to precise the molecular mechanisms regulat…

[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyApoptose[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyAMPKαApoptosisFoxo3a[SDV.BC]Life Sciences [q-bio]/Cellular BiologyAcide docosahexaénoïqueColorectal cancerCancer colorectalDocosahexaenoic acidMiR-21[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathology[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAMPKaTNFα[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRIP1[SDV.BC] Life Sciences [q-bio]/Cellular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Functional relevance of soluble TNF-alpha, transmembrane TNF-alpha and TNF-signal transduction in gastrointestinal diseases with special reference to…

2002

As a result of extensive clinical and basic research, the pivotal role of tumour necrosis factor (TNF) in the pathogenesis of chronic inflammatory diseases such as inflammatory bowel disease (IBD) has now generally been acknowledged. This has led to promising clinically effective anti-TNF-strategies. Of note, there is more and more evidence that TNF seems to play a key role in other gastrointestinal diseases including Helicobacter pylori infection, pancreatitis, viral hepatitis and toxic liver damage, too. The action of TNF at the cellular level is mediated by two cell surface receptors, TNF-R1 (p60) and TNF-R2 (p80). The function of these receptors and the downstream intracellular signal t…

business.industryGastrointestinal DiseasesTumor Necrosis Factor-alphamedicine.medical_treatmentGastroenterologyAntibodies MonoclonalProteinsDiseasemedicine.diseaseInflammatory Bowel DiseasesTNF Receptor-Associated Factor 2Inflammatory bowel diseaseTNF Receptor-Associated Factor 1PathogenesisTransduction (genetics)CytokineImmunologyMedicineHumansTumor necrosis factor alphaSignal transductionbusinessReceptorSignal TransductionZeitschrift fur Gastroenterologie
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Dabīgu imūnmodulatoru kvalitātes kontroles metožu izvērtējums un stimulējošās iedarbības salīdzinājums ar baktēriju endotoksīnu

2016

Darba mērķis bija raksturot dabīga imūnmodulatora AMP dezamināzes aktivitāti saturoša glikoproteīnu kompleksa (AMPD) darbību in vitro un novērtēt, vai šī iedarbība nav saistīta ar iespējamo endotoksīna (LPS) piesārņojumu. Tika izvērtētas AMPD attīrīšanas metodes, salīdzināta AMPD, LPS un lentināna ietekme uz iekaisuma citokīnu sekrēciju mononukleārajās šūnās, kā arī uz dermas fibroblastu proliferāciju. AMPD frakcijas sastāvs un polisaharīda daļas iespējami strukturālā līdzība ar LPS sarežģīja kvalitātes kontroli. Tāpat kā LPS, AMPD stimulēja TNF un IL-6 produkciju un veicināja dermas fibroblastu proliferāciju ar imūnšūnu sekretēto proteīnu starpniecību. LPS neitralizēšanai izmantojamās met…

dabīgi imūnmodulatorimononukleārās šūnasAMP dezamināzeBioloģijabaktēriju endotoksīnsTNF alpha
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The Inflammatory Feed-Forward Loop Triggered by the Complement Component C3 as a Potential Target in Endometriosis

2021

Copyright © 2021 Agostinis, Zorzet, Balduit, Zito, Mangogna, Macor, Romano, Toffoli, Belmonte, Morello, Martorana, Borelli, Ricci, Kishore and Bulla. The complement system is a major component of humoral innate immunity, acting as a first line of defense against microbes via opsonization and lysis of pathogens. However, novel roles of the complement system in inflammatory and immunological processes, including in cancer, are emerging. Endometriosis (EM), a benign disease characterized by ectopic endometrial implants, shows certain unique features of cancer, such as the capacity to invade surrounding tissues, and in severe cases, metastatic properties. A defective immune surveillance against…

endometriosisTHP-1 CellsTNF-amast cellsPeritoneal DiseasesCell DegranulationEndometriumImmunology and AllergyOriginal ResearchMice Knockoutmedicine.diagnostic_testendometriosiComplement C3Hep G2 CellsAntibody opsonizationmedicine.anatomical_structureComplement C3aTumor necrosis factor alphaFemaleInflammation MediatorsSignal TransductionImmunologyBiologySettore MED/08 - Anatomia PatologicaImmunofluorescencePeritoneal cavityPeritoneummedicineAnimalsHumansSettore MED/05 - Patologia ClinicaC3complement system...Innate immune systemTumor Necrosis Factor-alphaPeritoneal fluidC3; endometriosis; mast cells; complement system; TNF-aRC581-607Coculture TechniquesImmunity InnateComplement systemImmunity HumoralMice Inbred C57BLDisease Models AnimalCase-Control StudiesTNF-αCancer researchPeritoneal DiseaseImmunologic diseases. Allergymast cell
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IL-17 and TNF-α Are Key Mediators of Moraxella catarrhalis Triggered Exacerbation of Allergic Airway Inflammation

2017

Alterations of the airway microbiome is often associated with pulmonary diseases. For example, detection of the bacterial pathogen Moraxella catarrhalis in the upper airways is linked with an increased risk to develop or exacerbate asthma. However, the mechanisms by which M. cattarhalis augments allergic airway inflammation (AAI) remains unclear. We here characterized the cellular and soluble mediators of M. catarrhalis triggered excacerbation of AAI in wt and IL-17 deficient as well as in animals treated with TNF-alpha and IL-6 neutralizing antibodies. We compared the type of inflammatory response in M. catarrhalis infected, HDM-allergic and animals infected with M. catarrhalis at differen…

exacerbation of allergic reactionslcsh:Immunologic diseases. Allergy0301 basic medicineExacerbationT cellImmunologyexacerbation of pulmonary inflammationpulmonary inflammationMoraxella catarrhalisAllergic sensitization03 medical and health sciences0302 clinical medicineMoraxellaceae infectionsinfection and allergyImmunology and AllergyMedicineSensitizationOriginal Researchbiologybusiness.industrymicrobial exacerbation of pulmonary inflammationbiology.organism_classificationIL-17030104 developmental biologymedicine.anatomical_structureTNF-αImmunologyTumor necrosis factor alphaInterleukin 17lcsh:RC581-607businessAirway030215 immunologyFrontiers in Immunology
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Role of gene polymorphisms IL 10 (-1082 G/A) and TNFa (-308G/A) in susceptibility to acute myocardial infarction in young man.

2011

gene polymorphisms IL10 (-1082 G/A) and TNF a (-308G/A)acute myocardial infarctionSettore MED/05 - Patologia Clinicayoung man.
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Interleukin 10 restores lipopolysaccharide-induced alterations in synaptic plasticity probed by repetitive magnetic stimulation

2020

Systemic inflammation is associated with alterations in complex brain functions such as learning and memory. However, diagnostic approaches to functionally assess and quantify inflammation-associated alterations in synaptic plasticity are not well-established. In previous work, we demonstrated that bacterial lipopolysaccharide (LPS)-induced systemic inflammation alters the ability of hippocampal neurons to express synaptic plasticity, i.e., the long-term potentiation (LTP) of excitatory neurotransmission. Here, we tested whether synaptic plasticity induced by repetitive magnetic stimulation (rMS), a non-invasive brain stimulation technique used in clinical practice, is affected by LPS-induc…

lcsh:Immunologic diseases. AllergyLipopolysaccharides0301 basic medicinenon-invasive brain stimulationInterleukin-1betaImmunologyTNFα-reporter mouseMice TransgenicStimulationNeurotransmissionHippocampusSynaptic TransmissionneuroinflammationInterferon-gammaMice03 medical and health sciences0302 clinical medicineGenes Reportertranscranial magnetic stimulationAnimalsImmunology and Allergyddc:610NeuroinflammationOriginal ResearchInflammationNeuronsNeuronal Plasticitysynaptic plasticityInterleukin-6Tumor Necrosis Factor-alphaChemistryLong-term potentiationInterleukin-10Mice Inbred C57BLOrganoids030104 developmental biologyBrain stimulationSynaptic plasticityExcitatory postsynaptic potentialTumor necrosis factor alphaMicrogliainterleukin 10lcsh:RC581-607Neuroscience030217 neurology & neurosurgery
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INSAID Variant Classification and Eurofever Criteria Guide Optimal Treatment Strategy in Patients with TRAPS: Data from the Eurofever Registry

2021

Contains fulltext : 231528.pdf (Publisher’s version ) (Closed access) BACKGROUND: TNF receptor-associated periodic syndrome (TRAPS) is a rare autoinflammatory disease caused by dominant mutation of the TNF super family receptor 1A (TNFRSF1A) gene. Data regarding long-term treatment outcomes are lacking. OBJECTIVE: To assess correlations of genotype-phenotypes in patients with TRAPS, as defined by the International Study Group for Systemic Autoinflammatory Diseases (INSAID) classification and Eurofever criteria, with treatment responses. METHODS: Data from 226 patients with variants of the TNFRSF1A gene and enrolled in the Eurofever registry were classified according to the INSAID classifica…

medicine.medical_specialtyAbdominal painAutoinflammatory diseasesGroup AGroup BAA amyloidosis Anakinra Autoinflammatory diseases Colchicine TRAPS Abdominal Pain Colchicine FemaleHumans Mutation Registries Hereditary Autoinflammatory Diseases03 medical and health sciences0302 clinical medicineSettore MED/38 - Pediatria Generale E SpecialisticaAA amyloidosisTNF receptor-associated periodic syndrome (TRAPS) ; TNFRSF1A geneInternal medicinemedicineAA amyloidosisHumansImmunology and AllergyIn patientRegistries030212 general & internal medicineLikely pathogenicAnakinrabusiness.industryHereditary Autoinflammatory DiseasesTRAPSmedicine.diseaseAbdominal PainAnakinra030228 respiratory systemTNF receptor associated periodic syndromeMutationFemalemedicine.symptombusinessColchicineAA amyloidosis; Anakinra; Autoinflammatory diseases; Colchicine; TRAPSInflammatory diseases Radboud Institute for Molecular Life Sciences [Radboudumc 5]medicine.drug
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PReS-FINAL-2088: Risk of severe adverse events in juvenile idiopathic arthritis and pediatric-onset inflammatory bowel disease, treated with anti-tnf…

2013

Introduction: Severe adverse events have been described in children affected by Juvenile Idiopathic Arthritis (JIA) and Inflammatory Bowel Disease (IBD) treated with anti-tnf drugs. Objectives: To define the risk of severe adverse events in patients with JIA and IBD treated with anti-tnf drugs. Methods: This is a retrospective cohort study. All patients with JIA and IBD attending the "IRCCS Burlo Garofolo" of Trieste from 2000 to 2012 were enrolled. They were divided into 2 groups on the basis of the presence or absence of anti-tnf exposure. Severe adverse events were considered the followings: a) infections needing anti-tnf permanent suspension and/or hospitalization; b) autoimmune disease…

medicine.medical_specialtyPathologyPediatric onsetArthritismacromolecular substancesInflammatory bowel diseaseanti-TNF pediatric rheumatology arthritis adverse events inflammatory bowel diseaseRheumatologyinflammatory bowel diseaseInternal medicinemedicineImmunology and AllergyJuvenilePediatrics Perinatology and Child HealthPediatric rheumatologyAdverse effectbusiness.industryanti-TNFmedicine.diseaseadverse eventsdigestive system diseasesRheumatologypediatric rheumatologyarthritisPediatrics Perinatology and Child HealthPoster PresentationTumor necrosis factor alphabusiness
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