Search results for "tumor necrosis factor alpha"

showing 10 items of 479 documents

FRI0150 Mtor blockade by rapamycin decreases arthritis and spondylitis development and severity in hla-b27 transgenic rats

2018

Career situation of first and presenting author Student for a master or a PhD. Introduction TNF and IL-17A have been demonstrated as key inflammatory cytokines in Spondyloarthritis (SpA), whereas targeting bone remodeling remains an unmet clinical need in SpA. The mammalian target of rapamycin (mTOR) regulates IL-17 expression and osteogenesis and could therefore be a promising therapeutic target in SpA. Objectives To investigate if blockade of mTOR with rapamycin inhibits the pathological processes in inflammation and bone in SpA. Methods Cytokines were measured by ELISA in the supernatant from SpA patient PBMCs stimulated with anti-CD3/CD28, with various concentrations of rapamycin. SpA F…

musculoskeletal diseases030203 arthritis & rheumatologyHLA-B27business.industryArthritis030209 endocrinology & metabolismInflammationPharmacologymedicine.diseaseBlockadeProinflammatory cytokineBone remodeling03 medical and health sciences0302 clinical medicinemedicineTumor necrosis factor alphamedicine.symptombusinessPI3K/AKT/mTOR pathwayFRIDAY, 15 JUNE 2018
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Association of different tumor necrosis factor α promoter allele frequencies with ankylosing spondylitis in HLA-B27 positive individuals

1998

OBJECTIVE To investigate the potential association of tumor necrosis factor alpha (TNFalpha) promoter alleles with ankylosing spondylitis. METHODS DNA from 141 HLA-B27 positive Caucasian patients with ankylosing spondylitis and 46 B27-positive and 99 B27-negative healthy Caucasian controls was investigated by polymerase chain reaction amplification of the TNFalpha promoter region and subsequent dot-blot analysis with allele-specific oligonucleotides. RESULTS There was a significant decrease in the promoter alleles TNF-238.2 and TNF-308.2 in the ankylosing spondylitis group (266 wild-type alleles, 16 variant alleles) compared with the B27-positive (75 wildtype promoter alleles, 17 variant al…

musculoskeletal diseasesAnkylosing spondylitisImmunologyHaplotypeWild typePromoterBiologymedicine.diseaseGenetic determinismRheumatologyImmunologymedicineImmunology and AllergyPharmacology (medical)Tumor necrosis factor alphaAlleleAllele frequencyArthritis & Rheumatism
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Tumour necrosis factor   in rheumatoid arthritis and osteoarthritis patients in blood serum and synovial fluid

2010

Rheumatoid arthritis (RA) is a chronic autoimmune disease of unknown cause which affects the ability of elderly people to work. There is strong evidence to suggest that inflammatory mediators such as tumour necrosis factor α (TNFα) and interleukin 1 (IL1) have a critical role in the pathogenesis of RA. Biological treatment blocks pathological pathways in the actions of these proinflammatory cytokines. The aim of this study was …

musculoskeletal diseasesAutoimmune diseasebusiness.industryImmunologyInterleukinmedicine.diseaseGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokinePathogenesisBlood serumRheumatologyRheumatoid arthritisImmunologymedicineImmunology and AllergySynovial fluidTumor necrosis factor alphabusinessAnnals of the Rheumatic Diseases
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In-Vitro-Effects of TNF-A and IL-1-Antagonists on the Cytokine Network of Patients with Oligoarticular Idiopathic Arthritis (OJIA)

2011

In-Vitro-Effects of TNF-A and IL-1-Antagonists on the Cytokine Network of Patients with Oligoarticular Idiopathic Arthritis (OJIA)

musculoskeletal diseasesCytokine Networkbusiness.industryPediatrics Perinatology and Child HealthImmunologymedicineArthritisTumor necrosis factor alphaskin and connective tissue diseasesmedicine.diseasebusinessIn vitroPediatric Research
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Deficiency of Nrf2 accelerates the effector phase of arthritis and aggravates joint disease

2011

14 páginas, 8 figuras, 1 tabla.-- et al.

musculoskeletal diseasesGenetically modified mouseMedicinaNF-E2-Related Factor 2PhysiologyChemokine CXCL1Clinical BiochemistryNitric Oxide Synthase Type IIArthritisMice Transgenicmedicine.disease_causeenvironment and public healthBiochemistryNrf2MicemedicineAnimalsMolecular BiologyGeneral Environmental SciencebiologyInterleukin-6Effectorbusiness.industryArthritisInflammation and degenerationCell Biologyrespiratory systemmedicine.diseaseArthritis ExperimentalInfection and autoimmunity Auto-immunity transplantation and immunotherapy [NCMLS 1]Disease Models AnimalOxidative StressEicosanoidCyclooxygenase 2Rheumatoid arthritisTumor Necrosis FactorsImmunologyOsteocalcinbiology.proteinGeneral Earth and Planetary SciencesJointsTumor necrosis factor alphaImmune Regulation Auto-immunity transplantation and immunotherapy [NCMLS 2]businessOxidation-ReductionHeme Oxygenase-1Oxidative stress
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Targeting of the transcription factor STAT4 by antisense phosphorothioate oligonucleotides suppresses collagen-induced arthritis

2007

Abstract The transcription factor STAT4 mediates signals of various proinflammatory cytokines, such as IL-12, IL-15, and IL-23, that initiate and stabilize Th1 cytokine production. Although Th1 cytokine production has been suggested to play a major pathogenic role in rheumatoid arthritis, the role of STAT4 in this disease is poorly understood. In this study, we demonstrate a key functional role of STAT4 in murine collagen-induced arthritis (CIA). In initial studies we found that STAT4 expression is strongly induced in CD4+ T cells and to a lesser extent in CD11b+ APCs during CIA. To analyze the role of STAT4 for arthritis manifestation, we next investigated the outcome of interfering with S…

musculoskeletal diseasesImmunologyAntigen-Presenting CellsCodon InitiatorArthritisBiologyProinflammatory cytokineArthritis RheumatoidPathogenesisMiceimmune system diseasesmedicineAnimalsImmunology and Allergyskin and connective tissue diseasesSTAT4Cells CulturedMice KnockoutMice Inbred BALB CCD11b Antigenhemic and immune systemsOligonucleotides AntisenseSTAT4 Transcription FactorTh1 CellsThionucleotidesmedicine.diseaseArthritis ExperimentalIntegrin alpha MRheumatoid arthritisImmunologybiology.proteinExperimental pathologyTumor necrosis factor alpha
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Update on intravitreal anti-tumor necrosis factor alpha therapies for ocular disorders

2014

Abstract Tumor necrosis factor alpha (TNF-?) is an important pro-inflammatory cytokine associated with a variety of ocular diseases. The currently available TNF-? inhibitors are etanercept, infliximab, adalimumab, golimumab, and certolizumab. Experimental and clinical studies on the intravitreal use of these agents have been reported with etanercept, infliximab, and adalimumab: etanercept has shown limited efficacy in scarce reports; infliximab has been associated with local safety concerns but appears to benefit certain cases; adalimumab has shown no efficacy in cases of age-related macular degeneration (AMD) or diabetic macular edema (DME), but the combination with bevacizumab may be effe…

musculoskeletal diseasesOncologymedicine.medical_specialtyPathologygenetic structuresBevacizumabReviewCertolizumabEtanerceptEtanerceptIntravitreal injectionInternal medicineOcular disordersmedicineAdalimumabskin and connective tissue diseasesTumor necrosis factor alphabusiness.industryAdalimumabMacular degenerationmedicine.diseaseInfliximabeye diseasesGolimumabInfliximabOphthalmologyInfectious DiseasesTumor necrosis factor alphasense organsbusinessmedicine.drugJournal of Ophthalmic Inflammation and Infection
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Levetiracetam‐induced pediatric toxic epidermal necrolysis successfully treated with etanercept

2020

Successful management of toxic epidermal necrolysis (TEN) with tumor necrosis factor-α inhibitors has been described in adults, but few cases have been reported in children. To date, only four pediatric cases of TEN treated with infliximab and one with etanercept have been published. We present the case of an 8-year-old boy diagnosed with TEN induced by levetiracetam, successfully treated with etanercept, systemic corticosteroids, and intravenous immunoglobulin.

musculoskeletal diseasesmedicine.medical_specialtybiologybusiness.industryDermatologymedicine.diseaseDermatologyToxic epidermal necrolysisInfliximabEtanercept030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicine030220 oncology & carcinogenesisPediatrics Perinatology and Child Healthbiology.proteinmedicineTumor necrosis factor alphaLevetiracetamAntibodyskin and connective tissue diseasesbusinessmedicine.drugPediatric Dermatology
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Treatment with a CO-releasing molecule (CORM-3) reduces joint inflammation and erosion in murine collagen-induced arthritis.

2008

Contains fulltext : 70589.pdf (Publisher’s version ) (Closed access) OBJECTIVE: CO-releasing molecules (CO-RMs) are a novel class of anti-inflammatory agents. We have examined the possible therapeutic effects of CORM-3 in collagen-induced arthritis (CIA). METHODS: Arthritis was induced in DBA-1/J mice by type II collagen. Animals were treated with CORM-3 (5 and 10 mg/kg/day, intraperitoneally) or the inactive compound iCORM-3 (10 mg/kg/day, intraperitoneally) unable to release CO, from days 22 to 31. Production of anti-type II collagen antibodies, cytokines and cartilage olimeric matrix protein (COMP) was evaluated by enzyme-linked immunosorbent assay, and prostaglandin E(2) (PGE(2)) by rad…

musculoskeletal diseasesmedicine.medical_treatmentImmunologyAnti-Inflammatory AgentsDrug Evaluation PreclinicalType II collagenArthritisInflammationPharmacologyAuto-immunity transplantation and immunotherapy [N4i 4]DinoprostoneGeneral Biochemistry Genetics and Molecular BiologyMiceRheumatologyOrganometallic CompoundsPerception and Action [DCN 1]medicineAnimalsImmunology and AllergyChronic inflammation and autoimmunity [UMCN 4.2]Dose-Response Relationship Drugbiologybusiness.industryRANK LigandInterleukinIntercellular Adhesion Molecule-1medicine.diseaseArthritis ExperimentalPathogenesis and modulation of inflammation [N4i 1]Cellular infiltrationCyclooxygenase 2Mice Inbred DBARANKLImmunologybiology.proteinCytokinesTumor necrosis factor alphaMicrobial pathogenesis and host defense [UMCN 4.1]Inflammation Mediatorsmedicine.symptombusinessInfection and autoimmunity [NCMLS 1]Heme Oxygenase-1Immunity infection and tissue repair [NCMLS 1]Prostaglandin E
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A novel intrinsically disordered outer membrane lipoprotein ofAggregatibacter actinomycetemcomitansbinds various cytokines and plays a role in biofil…

2017

Intrinsically disordered proteins (IDPs) do not have a well-defined and stable 3-dimensional fold. Some IDPs can function as either transient or permanent binders of other proteins and may interact with an array of ligands by adopting different conformations. A novel outer membrane lipoprotein, bacterial interleukin receptor I (BilRI) of the opportunistic oral pathogen Aggregatibacter actinomycetemcomitans binds a key gatekeeper proinflammatory cytokine interleukin (IL)-1b. Because the amino acid sequence of the novel lipoprotein resembles that of fibrinogen binder A of Haemophilus ducreyi, BilRI could have the potential to bind other proteins, such as host matrix proteins. However, from th…

outer membrane lipoproteinsbacterial cytokine receptorbiofilm matrix composition0301 basic medicineMicrobiology (medical)Virulence FactorsLipoproteinsInterleukin-1beta030106 microbiologyImmunologyGingivaBiologyIntrinsically disordered proteinsAggregatibacter actinomycetemcomitansMicrobiologybacterial cytokine receptors03 medical and health sciencesHumansInterleukin 8Periodontal Diseasesouter membrane lipoproteinTumor Necrosis Factor-alphaInterleukin-8ta1182Biochemistry and Molecular BiologyBiofilmAggregatibacter actinomycetemcomitansReceptors Interleukin-1food and beveragesintrinsically disordered proteinbiology.organism_classificationInterleukin-10Cell biologyIntrinsically Disordered ProteinsInterleukin 10EditorialInfectious DiseasesBiochemistryBiofilmsParasitologyTumor necrosis factor alphabiofilm matrix compositionsintrinsically disordered proteinsBacterial outer membraneBiokemi och molekylärbiologiResearch PaperBacterial Outer Membrane ProteinsLipoproteinVirulence
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