Search results for " Inbred MRL lpr"

showing 10 items of 12 documents

IL-34–Dependent Intrarenal and Systemic Mechanisms Promote Lupus Nephritis in MRL-Faslpr Mice

2019

Background In people with SLE and in the MRL- Fas lpr lupus mouse model, macrophages and autoantibodies are central to lupus nephritis. IL-34 mediates macrophage survival and proliferation, is expressed by tubular epithelial cells (TECs), and binds to the cFMS receptor on macrophages and to a newly identified second receptor, PTPRZ. Methods To investigate whether IL-34–dependent intrarenal and systemic mechanisms promote lupus nephritis, we compared lupus nephritis and systemic illness in MRL- Fas lpr mice expressing IL-34 and IL-34 knockout (KO) MRL- Fas lpr mice. We also assessed expression of IL-34 and the cFMS and PTPRZ receptors in patients with lupus nephritis. Results Intrarenal IL-3…

0301 basic medicineMice Inbred MRL lprChemokineCell SurvivalLupus nephritisRisk AssessmentMonocytesMice03 medical and health sciences0302 clinical medicineSpecies Specificityimmune system diseasesmedicineAnimalsMacrophageMolecular Targeted Therapyskin and connective tissue diseasesCells CulturedCell ProliferationMice KnockoutSystemic lupus erythematosusCell Deathbiologybusiness.industryInterleukinsMacrophagesGeneral MedicineMonocyte proliferationmedicine.diseaseLupus NephritisMice Inbred C57BLDisease Models AnimalBasic ResearchKidney Tubules030104 developmental biologyGene Expression RegulationNephrology030220 oncology & carcinogenesisImmunologyKnockout mouseDisease Progressionbiology.proteinChemokinesbusinessMacrophage proliferationNephritisJournal of the American Society of Nephrology
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Inducible Co-Stimulator Null MRL-Fas lpr Mice

2005

MRL/MpJ-Tnfrsf6lpr (MRL-Faslpr) mice develop a spontaneous T cell-dependent autoimmune disease that shares features with human lupus, including fatal nephritis, systemic pathology, and autoantibodies (autoAb). The inducible co-stimulator (ICOS) is upregulated on activated T cells and modulates T cell-mediated responses. To investigate whether ICOS has an essential role in regulating autoimmune lupus nephritis and the systemic illness in MRL-Faslpr mice, ICOS null (-/-) MRL Faslpr and ICOS intact (+/+) MRL-Faslpr strains (wild-type [WT]) were generated and compared. It was determined that in ICOS-/- MRL-Faslpr as compared with the WT strain, (1) there is a significant reduction in circulatin…

Antigens Differentiation T-LymphocyteMice Inbred MRL lprT-LymphocytesT cellLupus nephritismedicine.disease_causeBlood Urea NitrogenAutoimmunityInducible T-Cell Co-Stimulator ProteinInterferon-gammaMiceImmune systemimmune system diseasesmedicineAnimalsskin and connective tissue diseasesAutoantibodiesMice Inbred C3HSystemic lupus erythematosusTumor Necrosis Factor-alphabusiness.industryAutoantibodyGeneral Medicinemedicine.diseaseLupus NephritisIsotypeInterleukin-10Mice Inbred C57BLProteinuriamedicine.anatomical_structureNephrologyImmunoglobulin GImmunologyInterleukin-4businessNephritisJournal of the American Society of Nephrology
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The fungal lactone oxacyclododecindione is a potential new therapeutic substance in the treatment of lupus-associated kidney disease.

2013

Recently oxacyclododecindione (Oxa), a macrocyclic lactone isolated from the imperfect fungus Exserohilum rostratum, has been described as a potent transcription inhibitor of inducible proinflammatory and profibrotic genes in cell culture models. As kidney disease in systemic lupus erythematosus is characterized by aberrant expression of inflammatory mediators and infiltration of immune cells, we investigated the effect of Oxa in MRL-Fas(lpr) mice, a model of systemic lupus erythematosus. These mice develop a spontaneous T-cell and macrophage-dependent autoimmune disease including severe glomerulonephritis that shares features with human lupus. Comparable to the results of in vitro models, …

ChemokineMice Inbred MRL lprMacrocyclic CompoundsAnti-Inflammatory AgentsProtein Array AnalysisGene ExpressionInflammationChemokine CXCL9Proinflammatory cytokineInterferon-gammaMiceImmune systemmedicineAnimalsCalgranulin ARNA MessengerChemokine CCL4Chemokine CCL5Chemokine CCL2Autoimmune diseaseSystemic lupus erythematosusbiologyInterleukin-6Tumor Necrosis Factor-alphaGlomerulonephritismedicine.diseaseLupus NephritisChemokine CXCL12Disease Models AnimalNephrologyImmunologybiology.proteinCytokinesFemaleOsteopontinmedicine.symptomKidney diseaseKidney international
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Knockout of the KH-Type Splicing Regulatory Protein Drives Glomerulonephritis in MRL-Faslpr Mice

2021

KH-type splicing regulatory protein (KSRP) is an RNA-binding protein that promotes mRNA decay and thereby negatively regulates cytokine expression at the post-transcriptional level. Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by dysregulated cytokine expression causing multiple organ manifestations

MaleChemokineMice Inbred MRL lprQH301-705.5medicine.medical_treatmentLupus nephritisBiologyKidneyArticleImmune systemsystemic lupus erythematosusimmune system diseasesmedicinecytokineAnimalsCD11a AntigenRNA MessengerKSRPBiology (General)skin and connective tissue diseasesRegulation of gene expressionMice KnockoutSystemic lupus erythematosusFOXP3RNA-Binding ProteinsGlomerulonephritisGeneral Medicinemedicine.diseaseMice Inbred C57BLCytokineCancer researchbiology.proteinTrans-ActivatorsFemaleLymph NodesChemokinesBiomarkersglomerulonephritispost-transcriptional regulationCells
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Circulating CSF-1 Promotes Monocyte and Macrophage Phenotypes that Enhance Lupus Nephritis

2009

Macrophages mediate kidney disease and are prominent in a mouse model (MRL- Fas lpr ) of lupus nephritis. Colony stimulating factor-1 (CSF-1) is the primary growth factor for macrophages, and CSF-1 deficiency protects MRL- Fas lpr mice from kidney disease and systemic illness. Whether this renoprotection derives from a reduction of macrophages and whether systemic CSF-1, as opposed to intrarenal CSF-1, promotes macrophage-dependent lupus nephritis remain unclear. Here, we found that increasing systemic CSF-1 hastened the onset of lupus nephritis in MRL- Fas lpr mice. Using mutant MRL- Fas lpr strains that express high, moderate, or no systemic CSF-1, we detected a much higher tempo of kidne…

MaleMacrophage colony-stimulating factorMice Inbred MRL lprLupus nephritisMice TransgenicInflammationKidneyMonocytesMiceimmune system diseasesmedicineAnimalsHumansskin and connective tissue diseasesCell ProliferationInflammationMice Inbred BALB CMice Inbred C3HSystemic lupus erythematosusbiologyCD68business.industryMacrophage Colony-Stimulating FactorMacrophagesMonocyteGeneral MedicineMonocyte proliferationmedicine.diseaseLupus NephritisMice Inbred C57BLDisease Models AnimalBasic ResearchPhenotypemedicine.anatomical_structureIntegrin alpha MNephrologyImmunologybiology.proteinFemalemedicine.symptombusinessJournal of the American Society of Nephrology
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Dynamic in vivo Imaging of Microvasculature and Perfusion by Miniaturized Confocal Laser Microscopy

2008

<i>Introduction:</i> Microvasculature and associated pathologies mandate dynamic imaging. We evaluated a novel miniaturized confocal laser scanning probe for in vivo visualization of blood vessels, blood flow, cell tracking and perfusion in both healthy rodents and disease models.<i> Methods:</i> The hand-held confocal microscopy system allowed a 500- to 2,400-fold magnification at a dynamically variable imaging depth. Different intravital stains were used alone or in combination for tissue, nuclear, plasma and vascular endothelial cell staining and for blood flow visualization, and targeted staining for individual cell populations. <i>Results:</i> Precis…

MaleMice Inbred MRL lprPathologymedicine.medical_specialtyMaterials scienceLaser scanningDynamic imagingConfocalCell Communicationlaw.inventionMiceImaging Three-DimensionalIn vivoConfocal microscopylawMicroscopyLeukocytesmedicineAnimalsFluorescent DyesInflammationMicroscopy ConfocalMiniaturizationMicrocirculationBrainEndothelial CellsThrombosisLupus NephritisMice Inbred C57BLDisease Models AnimalMicrovesselsFemaleSurgeryIntracranial ThrombosisGerbillinaePerfusionBlood Flow VelocityPreclinical imagingBiomedical engineeringEuropean Surgical Research
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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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Activation of the lectin pathway in murine lupus nephritis.

2004

In systemic lupus erythematosus (SLE), hypocomplementaemia and complement deposition have been described both in man and in experimental models. A major involvement of the classical pathway of complement activation has been demonstrated in this disease, however relatively little is known about the involvement of the lectin pathway. Therefore in the present study we have analyzed the activity of all three pathways of complement activation in murine models of SLE. In the mouse, MBL is expressed in two forms, namely MBL-A and MBL-C. In the present study young and old MRL-lpr and control MRL+/+ mice were compared for the levels of complement activity with specific attention for the lectin pathw…

Mice Inbred MRL lprImmunologychemical and pharmacologic phenomenaurologic and male genital diseasesmedicine.disease_causeAutoimmunityClassical complement pathwayMiceImmune systemimmune system diseasesMurine lupusLectinsmedicineAnimalsskin and connective tissue diseasesMolecular BiologyAutoantibodiesChemistrybacterial infections and mycosesmedicine.diseaseLupus NephritisComplement systemLectin pathwayImmunologyAlternative complement pathwayNephritisMolecular immunology
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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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