Search results for "Systemic Lupus erythematosus"

showing 10 items of 62 documents

Ovarian stimulation for ovulation induction and in vitro fertilization in patients with systemic lupus erythematosus and antiphospholipid syndrome.

2008

Objective To review the current evidence regarding the relationship between systemic lupus erythematosus (SLE) and antiphospholipid syndrome and female infertility, as well as the risks associated with ovarian stimulation for ovulation induction and IVF. To establish, based on this information, guidelines for safe and successful assisted reproductive technology (ART). Design A MEDLINE computer search was performed to identify relevant articles. Result(s) Systemic lupus erythematosus and antiphospholipid syndrome are not related to infertility, except for cases of amenorrhea accompanying severe flares, renal insufficiency-related hypofertility, and ovarian failure secondary to cyclophosphami…

Infertilitymedicine.medical_specialtymedicine.medical_treatmentOvarian hyperstimulation syndromeFertilization in VitroOvulation Inductionimmune system diseasesAntiphospholipid syndromePregnancyRisk FactorsmedicineHumansLupus Erythematosus Systemicskin and connective tissue diseasesIn vitro fertilisationLupus erythematosusSystemic lupus erythematosusbusiness.industryObstetricsFemale infertilityObstetrics and Gynecologymedicine.diseaseAntiphospholipid SyndromeReproductive MedicineImmunologyOvulation inductionFemalebusinessInfertility FemaleFertility and sterility
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Functional analysis of the classical, alternative, and MBL pathways of the complement system: standardization and validation of a simple ELISA.

2004

Primary defence against invading microorganisms depends on a functional innate immune system and the complement system plays a major role in such immunity. Deficiencies in one of the components of the complement system can cause severe and recurrent infections, systemic diseases, such as systemic lupus erythematosus (SLE) and renal disease. Screening for complement deficiencies in the classical or alternative complement pathways has mainly been performed by haemolytic assays. Here, we describe a simple ELISA-based format for the evaluation of three pathways of complement activation. The assays are based on specific coatings for each pathway in combination with specific buffer systems. We ha…

Innate immune systemSystemic lupus erythematosusImmunologyComplement Pathway AlternativeComplement Pathway Mannose-Binding LectinEnzyme-Linked Immunosorbent AssayComplement System ProteinsBiologyComplement fixation testmedicine.diseaseMannose-Binding LectinComplement systemComplement (complexity)Immune systemImmunologymedicineImmunology and AllergyHumansLupus Erythematosus SystemicComplement Pathway ClassicalReagent Kits DiagnosticFicolinComplement ActivationMannan-binding lectinJournal of immunological methods
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TD-09 IL-34 promotes macrophage-mediated lupus nephritis in MRL-Faslpr mice

2018

Background Nephritis is the major cause of mortality and morbidity in patients with lupus. Macrophages (Mo) are central to kidney destruction in lupus-prone mice and patients. CSF-1, and the newly identified IL-34, mediate Mo survival and proliferation. However, IL-34 and CSF-1 differ during development and disease. While CSF-1 and IL-34 share the CSF-1 receptor (cFMS), expressed by Mo, IL-34 binds to a second receptor, Protein-Tyrosine Phosphatase ζ (PTPRZ) in inflamed kidneys. Intra-renal IL-34, cFMS, and PTPRZ are increased during the progression of lupus nephritis in MRL-Faslpr mice. Therefore, we hypothesized that IL-34 is a potential therapeutic target for lupus nephritis. Methods and…

KidneySystemic lupus erythematosusbusiness.industryLupus nephritisMonocyte proliferationmedicine.diseasePathogenesismedicine.anatomical_structureImmunologymedicineBone marrowbusinessReceptorNephritisTissue Damage
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SPARC regulation of PMN clearance protects from pristane induced lupus and rheumatoid arthritis

2020

AbstractOne step along the pathogenesis of Systemic lupus erythematosus (SLE) is associated with polymorphonuclear leukocyte (PMN) death and their ineffective removal by M2-macrophages. The secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein with unexpected immunosuppressive function in M2-macrophages and myeloid cells. To investigate the role of SPARC in autoimmunity, we adopted a pristane–induced model of lupus in mice, which recapitulates clinical manifestations of human SLE. Sparc-/- mice developed earlier and more severe renal disease, lung and liver parenchymal damage than the WT counterpart. Most prominently, Sparc-/- mice had anticipated and severe occurr…

LungSystemic lupus erythematosusbusiness.industryMatricellular proteinArthritisDendritic cellmedicine.diseasemedicine.disease_causeAutoimmunityPathogenesismedicine.anatomical_structureRheumatoid arthritisImmunologymedicineCancer researchMacrophagebusiness
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Absence of Anti-Glomerular Basement Membrane Antibodies in 200 Patients With Systemic Lupus Erythematosus With or Without Lupus Nephritis: Results of…

2020

IntroductionAnti-glomerular basement membrane (GBM) antibodies are pathogenic antibodies first detected in renal-limited anti-GBM disease and in Goodpasture disease, the latter characterized by rapidly progressive crescentic glomerulonephritis combined with intra-alveolar hemorrhage. Studies have suggested that anti-GBM antibody positivity may be of interest in lupus nephritis (LN). Moreover, severe anti-GBM vasculitis cases in patients with systemic lupus erythematosus (SLE) have been described in the literature, but few studies have assessed the incidence of anti-GBM antibodies in SLE patients.ObjectiveThe main study objective was to determine if positive anti-GBM antibodies were present …

MaleAnti-Glomerular Basement Membrane Disease[SDV]Life Sciences [q-bio]Lupus nephritisAucunurologic and male genital diseasesSeverity of Illness IndexGastroenterologyanti-glomerular basement membrane antibodies0302 clinical medicinesystemic lupus erythematosusLupus Erythematosus SystemicImmunology and Allergy030212 general & internal medicineOriginal Researchmedicine.diagnostic_testbiologyanti-GBM glomerulonephritisGlomerular basement membraneIIfMiddle Aged3. Good healthTitermedicine.anatomical_structure[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleAntibodyVasculitisAdultlcsh:Immunologic diseases. Allergymedicine.medical_specialtyImmunology03 medical and health sciencesAntigenInternal medicineanti-GBM antibodiesmedicineHumansAutoantibodiesRetrospective Studies030203 arthritis & rheumatologylupus nephritisbusiness.industryGoodpasture diseasemedicine.diseaseCase-Control StudiesImmunoassaybiology.proteinbusinesslcsh:RC581-607BiomarkersFrontiers in Immunology
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Per-protocol repeat kidney biopsy portends relapse and long-term outcome in incident cases of proliferative lupus nephritis

2019

Abstract Objectives In patients with LN, clinical and histological responses to treatment have been shown to be discordant. We investigated whether per-protocol repeat kidney biopsies are predictive of LN relapses and long-term renal function impairment. Methods Forty-two patients with incident biopsy-proven active proliferative (class III/IV±V) LN from the database of the UCLouvain were included in this retrospective study. Per-protocol repeat biopsies were performed after a median [interquartile range (IQR)] time of 24.3 (21.3–26.2) months. The National Institutes of Health activity index (AI) and chronicity index (CI) scores were assessed in all biopsies. Results Despite a moderate corre…

MaleBiopsy030232 urology & nephrologyKidneyGastroenterologychemistry.chemical_compound0302 clinical medicinesystemic lupus erythematosusRecurrenceInterquartile rangePharmacology (medical)Proteinuriamedicine.diagnostic_testHazard ratioPrognosisLupus NephritisProteinuriaKidney TubulesCreatinineDisease ProgressionhistopathologyFemaleRenal biopsymedicine.symptomRituximabImmunosuppressive AgentsAdultlong-term outcomemedicine.medical_specialtyRenal functionMethylprednisoloneYoung Adult03 medical and health sciencesrenal biopsyRheumatologyInternal medicineBiopsymedicineHumansImmunologic FactorsCyclophosphamideGlucocorticoidsProportional Hazards ModelsRetrospective Studieslupus nephritisrepeat biopsy030203 arthritis & rheumatologyCreatininebusiness.industryrenal functionMycophenolic AcidchemistryPulse Therapy DrugHistopathologybusinessRheumatology
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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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Lupus Erythematosus Quality of Life Questionnaire (LEQoL): Development and Psychometric Properties

2020

Lupus erythematosus (LE) affects patients&rsquo

MalePsychometricsHealth Toxicology and MutagenesisPsychological interventionlcsh:MedicineArticle03 medical and health sciences0302 clinical medicineCronbach's alphaQuality of lifeimmune system diseasesSurveys and QuestionnairesmedicineHumansLupus Erythematosus Systemicinstrument030212 general & internal medicineskin and connective tissue diseasesReliability (statistics)030203 arthritis & rheumatologyFinal versionSystemic lupus erythematosusLupus erythematosusbusiness.industrycutaneouslcsh:RPublic Health Environmental and Occupational HealthReproducibility of Resultssystemicmedicine.diseaseTest (assessment)Cross-Sectional Studiesquality of lifeFemalebusinesslupus erythematosusClinical psychologyInternational Journal of Environmental Research and Public Health
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Molecular Basis of Hereditary C1q Deficiency

1998

Abstract Complete selective deficiencies of the complement component C1q are rare genetic disorders which are associated with recurrent infections and a high prevalence of lupus erythematosus-like symptoms. The improvements in molecular biology techniques have facilitated the analysis of such genetic defects to a great extend. To date the basis of C1q deficiencies from 13 families have been studied at the genetic level. In each case single base mutations leading to either termination codons, frame shift or amino acid exchanges were thought to be responsible for these defects as no other aberrations were found. In addition to DNA analysis, conventional immunochemical and biochemical methods …

MaleRecurrent infectionsGenotypeTurkeyImmunologySaudi ArabiaBiologyAutoimmune DiseasesFrameshift mutationchemistry.chemical_compoundC1q DeficiencyGermanyComplement component C1qmedicineHumansLupus Erythematosus SystemicPoint MutationImmunology and AllergyGenetic Predisposition to DiseaseSequence DeletionGeneticsSystemic lupus erythematosusComplement C1qImmunologic Deficiency SyndromesHematologymedicine.diseaseStructure and functionAmino Acid SubstitutionchemistryChromosomes Human Pair 1Codon NonsenseFemaleDNAImmunobiology
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