Search results for "immune disease"

showing 10 items of 359 documents

Targeting transcription factor Stat4 uncovers a role for interleukin-18 in the pathogenesis of severe lupus nephritis in mice

2011

Polymorphisms in the transcription factor Stat4 gene have been implicated as risk factors for systemic lupus erythematosus. Although some polymorphisms have a strong association with autoantibodies and nephritis, their impact on pathophysiology is still unknown. To explore this further we used signal transducers and activators of transcription 4 (Stat4) knockout MRL/MpJ-Fas(lpr)/Fas(lpr) (MRL-Fas(lpr)) mice and found that they did not differ in survival or renal function from Stat4-intact MRL-Fas(lpr) mice. Circulating interleukin (IL)-18 levels, however, were elevated in Stat4-deficient compared to Stat4-intact mice, suggesting that this interleukin might contribute to the progression of l…

Malemusculoskeletal diseasesMice Inbred MRL lprchronic inflammationLupus nephritisKidneyInterleukin-23ArticleProinflammatory cytokineOligodeoxyribonucleotides AntisenseGene Knockout TechniquesInterferon-gammaMiceimmune system diseasesmedicineAnimalsskin and connective tissue diseasesSTAT4DNA PrimersAutoimmune diseaseMice Knockoutlupus nephritisMice Inbred BALB CBase Sequencebusiness.industryGene Transfer TechniquesInterleukin-18InterleukinGlomerulonephritishemic and immune systemsSTAT4 Transcription Factormedicine.diseaseInterleukin-12chronic glomerulonephritisNephrologyImmunologyInterleukin 18FemalebusinessNephritisKidney International
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Expression of the multidrug resistance glycoprotein 170 in the peripheral blood lymphocytes of rheumatoid arthritis patients. The percentage of lymph…

1996

International audience; Abstract: The objective was to evaluate the expression of the multidrug resistance P-glycoprotein (P-gp) in peripheral blood lymphocytes (PBL) of patients with rheumatoid arthritis (RA). PBL from 68 RA patients and 44 controls were evaluated. RA patients had a mean disease duration of 10.7 yr, with a mean number of past resistances to DMARDs of 0.82, and were treated with NSAIDs (n = 34), DMARDs (n = 25) and prednisolone (n = 40). Fluorescence flow cytometry was used to assess P-gp membrane expression on PBL. In the RA group, the percentage of PBL expressing P-gp was higher in patients treated with prednisolone than in other patients [mean +/- S.D.: 10.7 +/- 15.8% vs…

Malerheumatoid arthritismedicine.drug_classmedicine.medical_treatmentLymphocytePrednisolone[INFO.INFO-IM] Computer Science [cs]/Medical ImagingDrug resistanceArthritis Rheumatoidresistance03 medical and health sciences0302 clinical medicineRheumatologyImmunopathologyMDRmedicine[INFO.INFO-IM]Computer Science [cs]/Medical ImagingHumansPharmacology (medical)ATP Binding Cassette Transporter Subfamily B Member 1Lymphocytes030304 developmental biologyAgedAutoimmune disease0303 health sciencesChemotherapytreatmentglucocorticoids[ INFO.INFO-IM ] Computer Science [cs]/Medical Imagingbusiness.industryAnti-Inflammatory Agents Non-SteroidaldrugMiddle Agedmedicine.diseaseDrug Resistance Multiple3. Good healthmedicine.anatomical_structure030220 oncology & carcinogenesisRheumatoid arthritisAntirheumatic AgentsImmunologyMultivariate AnalysisPrednisoloneCorticosteroidRegression AnalysisFemalebusinessmedicine.drug
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Ruolo delle heat shock proteins nella patogenesi della miastenia gravis

2010

Myasthenia Gravis (MG) is an autoimmune disorder of the neuromuscolar junction mediated by specific antibodies to the nicotinic acetylcholine receptors. Several clinical and experimental studies have confirmed that the HSPs are involved in the process of regulation of some autoimmune disorders such as arthritis, diabetes, atherosclerosis and multiple sclerosis. The involvement of HSPs within different autoimmune disorders allows to hypothesize their presence in the pathogenesis of the MG, i.e. as suggested by the existence of a cross-reactivity among the antigenic epitopes of Hsp60 and AChR. Moreover, since a cross-reactivity between human and bacterial epitopes of Hsp60 has also been descr…

Medicine (all)Autoimmune diseaseHsp60Chaperonin
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The Role of Exosomes Derived From Mesenchymal Stromal Cells in Dermatology

2021

This study has been funded by the Carlos III Health Institute of Spain through the PI13/02576 and PI17/02083 projects [cofunded by European Regional Development Fund "A way to make Europe" and Andalusian Regional Government Finance (SAS PI-0458-2016)]. The work of MQ-V was supported by a predoctoral fellowship (BOE 22/10/2019) from the Spanish Ministry of Science, Innovation and Universities. This study is part of her doctoral research in the Biomedicine program at the University of Granada.

Mesenchymal stem cell-derived exosomesregenerative medicinemesenchymal stem cell-derived exosomesReviewimmunomodulationRegenerative medicineskin autoimmune diseasesImmunomodulationCell and Developmental Biologyexosomes-based therapyMedicineSkin wound healinglcsh:QH301-705.5Skin repairintegumentary systembusiness.industryRegeneration (biology)Mesenchymal stem cellCell BiologyExosomes-based therapyMicrovesicleslcsh:Biology (General)skin wound healingRegenerative medicineCancer researchSkin autoimmune diseasesWound healingbusinessDevelopmental BiologyFrontiers in Cell and Developmental Biology
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T-bet as a possible therapeutic target in autoimmune disease

2002

The prominent role of pro-inflammatory cytokines produced by T helper-1 (T(H1)) cells in regulating autoimmune responses in vitro and in vivo has been demonstrated. Recent observations of T cell polarisation by regulatory transcription factors--especially T-bet (T-box expressed in T cells)--raise the question of their influence in controlling autoimmune diseases. Here, the authors summarise recent observations of the role of T-bet in controlling chronic inflammatory and autoimmune diseases and discuss the implications of these findings for future therapeutic approaches.

Mice Inbred MRL lprTranscription GeneticTransgeneT cellCellular differentiationClinical BiochemistryMice TransgenicLymphocyte ActivationAutoimmune DiseasesInterferon-gammaMiceTh2 CellsCrohn DiseaseDrug DiscoverymedicineAnimalsLupus Erythematosus SystemicIL-2 receptorIntestinal MucosaMice KnockoutPharmacologyAutoimmune diseaseLupus erythematosusbusiness.industryZAP70Cell DifferentiationTh1 CellsColitisInflammatory Bowel Diseasesmedicine.diseaseCeliac DiseaseDisease Models Animalmedicine.anatomical_structureCTLA-4ImmunologyCytokinesMolecular MedicineT-Box Domain ProteinsbusinessTranscription FactorsExpert Opinion on Therapeutic Targets
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Correlation of renal tubular epithelial cell-derived interleukin-18 up-regulation with disease activity in MRL-Faslpr mice with autoimmune lupus neph…

2002

Objective MRL-Faslpr mice spontaneously develop an autoimmune disease that mimics systemic lupus erythematosus in humans. Infiltrating T cells expressing interferon-γ (IFNγ) are responsible for the autoimmune kidney destruction in MRL-Faslpr mice, and interleukin-18 (IL-18) released by mononuclear phagocytes stimulates T cells to produce the IFNγ. Since MRL-Faslpr T cells are characterized by an overexpression of the IL-18 receptor accessory chain, we sought to determine the impact of IL-18 on the progression of lupus nephritis in MRL-Faslpr mice. Methods IL-18 expression in sera and kidney tissues from MRL-Faslpr mice was determined by enzyme-linked immunosorbent assay (ELISA), reverse tra…

Mice Inbred MRL lprmedicine.medical_treatmentImmunologyBlotting WesternLupus nephritisEnzyme-Linked Immunosorbent AssayBiologymedicine.disease_causeAutoimmunityAutoimmune DiseasesMiceRheumatologyimmune system diseasesInterferonmedicineImmunology and AllergyMacrophageAnimalsPharmacology (medical)Interferon gammaskin and connective tissue diseasesLupus erythematosusCell adhesion moleculeReverse Transcriptase Polymerase Chain ReactionCaspase 1Interleukin-18Epithelial Cellsmedicine.diseaseMolecular biologyImmunohistochemistryLupus NephritisUp-RegulationCytokineKidney TubulesImmunologymedicine.drugArthritis and rheumatism
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Early Development of the Gut Microbiota and Immune Health

2014

In recent years, the increase in human microbiome research brought about by the rapidly evolving “omic” technologies has established that the balance among the microbial groups present in the human gut, and their multipronged interactions with the host, are crucial for health. On the other hand, epidemiological and experimental support has also grown for the ‘early programming hypothesis’, according to which factors that act in utero and early in life program the risks for adverse health outcomes later on. The microbiota of the gut develops during infancy, in close interaction with immune development, and with extensive variability across individuals. It follows that the specific process of…

Microbiology (medical)atopylcsh:MedicineReviewDiseaseinfant gutBiologyGut floraHealth outcomesantibioticsImmune systemHuman gutImmunology and Allergyearly programmingmicrobe-host interactionsMolecular BiologyGut colonizationIntrauterine transmissionnecrotizing enterocolitisgut microbiotaGeneral Immunology and Microbiologylcsh:RHuman microbiomehuman microbiomebiology.organism_classificationintrauterine transmissionInfectious DiseasesImmunologyimmune diseasePathogens
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A bioinformatical approach suggests the function of the autoimmune hepatitis target antigen soluble liver antigen/liver pancreas

2001

Antibodies to a soluble liver antigen/liver pancreas (SLA/LP) appear to be highly specific for the diagnosis of autoimmune hepatitis. The SLA/LP target antigen was recently identified as a hitherto unknown gene encoding 474 amino acid residues. The function of this antigen remains unclear, because it does not share sequence homology with proteins of known function stored in any of the publicly accessible databases. Therefore we used a new theoretical method called fold recognition and could show that the SLA/LP sequence is compatible with the architecture of the superfamily of pyridoxal phosphate (PLP; vitamin B6)-dependent transferases. Its function is likely to be that of a serine hydroxy…

Models MolecularAutoimmune diseaseHepatitisHepatologySelenocysteineMolecular Sequence DataComputational BiologyAutoimmune hepatitisBiologymedicine.diseaseAutoantigensHepatitis Autoimmunechemistry.chemical_compoundchemistryBiochemistryAntigenSerine hydroxymethyltransferasebiology.proteinmedicineHumansAmino Acid SequenceAntibodyPyridoxal phosphateHepatology
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Gain-of-function mutations in IFIH1 cause a spectrum of human disease phenotypes associated with upregulated type I interferon signaling.

2014

The type I interferon system is integral to human antiviral immunity. However, inappropriate stimulation or defective negative regulation of this system can lead to inflammatory disease. We sought to determine the molecular basis of genetically uncharacterized cases of the type I interferonopathy Aicardi-Goutières syndrome, and of other patients with undefined neurological and immunological phenotypes also demonstrating an upregulated type I interferon response. We found that heterozygous mutations in the cytosolic double-stranded RNA receptor gene IFIH1 (MDA5) cause a spectrum of neuro-immunological features consistently associated with an enhanced interferon state. Cellular and biochemica…

Models MolecularInterferon-Induced Helicase IFIH1Molecular Sequence DataHDE NEU PEDElectrophoretic Mobility Shift AssayBiologymedicine.disease_causeNervous System MalformationsReal-Time Polymerase Chain ReactionArticleDEAD-box RNA HelicasesImmune systemAutoimmune Diseases of the Nervous SystemDownregulation and upregulationAnalysis of Variance; Autoimmune Diseases of the Nervous System; Base Sequence; DEAD-box RNA Helicases; Electrophoretic Mobility Shift Assay; Exome; HEK293 Cells; Humans; Interferon Type I; Microsatellite Repeats; Molecular Sequence Data; Mutation; Nervous System Malformations; Real-Time Polymerase Chain Reaction; Sequence Analysis DNA; Signal Transduction; Spectrum Analysis; Models Molecular; Phenotype; GeneticsModelsInterferonGeneticsmedicineHumansExomeMutationAnalysis of VarianceBase SequenceSpectrum AnalysisMolecularRNAMDA5DNASequence Analysis DNAMolecular biology3. Good healthInterferon Tipo IHEK293 CellsPhenotypeInterferon Type IMutationCancer researchSignal transductionSequence AnalysisInterferon type Imedicine.drugMicrosatellite RepeatsSignal TransductionNature genetics
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Acquired C1 inhibitor (C1-INH) deficiency type II. Replacement therapy with C1-INH and analysis of patients' C1-INH and anti-C1-INH autoantibodies

1989

Abstract The response of two patients with autoantibody-mediated C1-inhibitor (C1-INH) deficiency to replacement therapy with C1-INH was studied over a period of 3 d. In patient 1 an acute attack of angioedema was successfully managed by infusion of 1,000 U of C1-INH concentrate. C1-INH function returned to normal levels within 30 min, while CH50 and C4 peaked after 6-7 h and C1 hemolytic activity reached 50-60% of normal after 3 d. Immediately after the injection an increase in C1-INH-anti-C1-INH complexes was observed. Based on NH2-terminal sequence analysis of the patients' Mr 96,000 C1-INH, it is concluded that this fragment is generated after cleavage of C1-INH in its active site by on…

Molecular Sequence DataPharmacologyComplement C1 Inactivator ProteinsEpitopeC1-inhibitorAutoimmune DiseasesAntibody SpecificityImmunopathologyBlood plasmamedicineHumansheterocyclic compoundsAmino Acid SequenceAngioedemaInfusions IntravenousAutoantibodiesAngioedemabiologybusiness.industryAutoantibodyAntibody titerGeneral Medicinebiochemical phenomena metabolism and nutritionrespiratory systembacterial infections and mycosesrespiratory tract diseasesImmunologybiology.proteinmedicine.symptomAntibodybusinessResearch Article
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