2024
Prognostic and therapeutic insights into MIF, DDT, and CD74 in melanoma
Valdez C, Sánchez-Zuno G, Osmani L, Ibrahim W, Galan A, Bacchiocchi A, Halaban R, Kulkarni R, Kang I, Bucala R, Tran T. Prognostic and therapeutic insights into MIF, DDT, and CD74 in melanoma. Oncotarget 2024, 15: 507-520. PMID: 39028303, PMCID: PMC11259151, DOI: 10.18632/oncotarget.28615.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntigens, Differentiation, B-LymphocyteBiomarkers, TumorFemaleHistocompatibility Antigens Class IIHumansImmune Checkpoint InhibitorsIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMaleMelanomaMiddle AgedMutationPrognosisRetrospective StudiesSkin NeoplasmsConceptsMacrophage migration inhibitory factorImmune checkpoint inhibitionD-dopachrome tautomeraseExpression of macrophage migration inhibitory factorDrivers of tumor progressionInflammatory cell markersPatient tumor samplesPatient survival outcomesMigration inhibitory factorStatistically significant differenceCheckpoint inhibitionImmune therapyPrognostic valueSurvival outcomesResistant melanomaGene expressionImproved survivalRetrospective studyInflammatory markersTumor progressionCell markersTumor samplesClinical evidenceMelanomaBulk RNA sequencingDownregulation of adipose LPL by PAR2 contributes to the development of hypertriglyceridemia
Huang Y, Chen L, Li L, Qi Y, Tong H, Wu H, Xu J, Leng L, Cheema S, Sun G, Xia Z, McGuire J, Rodrigues B, Young L, Bucala R, Qi D. Downregulation of adipose LPL by PAR2 contributes to the development of hypertriglyceridemia. JCI Insight 2024, 9: e173240. PMID: 38973609, PMCID: PMC11383372, DOI: 10.1172/jci.insight.173240.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorDevelopment of hypertriglyceridemiaWhite adipose tissueAdipose LPLPAR2 expressionLevels of macrophage migration inhibitory factorElevated plasma TG levelsLPL expressionLipoprotein lipaseIncrease PAR2 expressionPlasma MIF levelsPlasma TG levelsMigration inhibitory factorPalmitic acid dietInhibited Akt phosphorylationMIF levelsLipoprotein lipase geneTG levelsObese humansPlasma TGHypertriglyceridemiaAkt phosphorylationLipid storageInhibitory factorAdipose tissue
2022
“Near Cure” treatment of severe acute EAE in MIF-1-deficient female and male mice with a bifunctional MHCII-derived molecular construct
Vandenbark AA, Meza-Romero R, Wiedrick J, Gerstner G, Seifert H, Kent G, Piechycna M, Benedek G, Bucala R, Offner H. “Near Cure” treatment of severe acute EAE in MIF-1-deficient female and male mice with a bifunctional MHCII-derived molecular construct. Cellular Immunology 2022, 378: 104561. PMID: 35738135, PMCID: PMC9714992, DOI: 10.1016/j.cellimm.2022.104561.Peer-Reviewed Original ResearchConceptsExperimental autoimmune encephalomyelitisAcute experimental autoimmune encephalomyelitisDRα1-MOG-35Multiple sclerosisMIF-1EAE scoresMale miceMIF-2Severe diseaseMacrophage migration inhibitory factorClinical EAE scoresMIF-deficient micePeripheral inflammatory cellsMigration inhibitory factorSpinal cord tissueT cell activationSex-dependent differencesEAE severityAutoimmune encephalomyelitisSerum levelsTreatment of WTInflammatory cellsFemale miceClinical signsCord tissueCD74 ablation rescues type 2 diabetes mellitus-induced cardiac remodeling and contractile dysfunction through pyroptosis-evoked regulation of ferroptosis
Chen L, Yin Z, Qin X, Zhu X, Chen X, Ding G, Sun D, Wu NN, Fei J, Bi Y, Zhang J, Bucala R, Ren J, Zheng Q. CD74 ablation rescues type 2 diabetes mellitus-induced cardiac remodeling and contractile dysfunction through pyroptosis-evoked regulation of ferroptosis. Pharmacological Research 2022, 176: 106086. PMID: 35033649, DOI: 10.1016/j.phrs.2022.106086.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnimalsAntigens, Differentiation, B-LymphocyteCell LineDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2FemaleFerroptosisGene ExpressionHistocompatibility Antigens Class IIHumansMacrophage Migration-Inhibitory FactorsMaleMice, KnockoutMiddle AgedMyocardial ContractionMyocardiumNLR Family, Pyrin Domain-Containing 3 ProteinOxidative StressOxygen ConsumptionPyroptosisRatsVentricular RemodelingConceptsHigh glucose/high fatMacrophage migration inhibitory factorCardiac remodelingContractile dysfunctionCell death domainGene Ontology termsInhibitors of MIFRecombinant macrophage migration inhibitory factorCytokine macrophage migration inhibitory factorType 2 diabetes mellitusOntology termsDeath domainLipid peroxidationGlobal metabolic defectsKEGG analysisPlasma MIF levelsInjection of streptozotocinMitochondrial defectsHigh-fat dietMigration inhibitory factorInhibitor of NLRP3Cell deathPrecise interplayMitochondrial dysfunctionCognate receptors
2021
MIF but not MIF-2 recruits inflammatory macrophages in an experimental polymicrobial sepsis model
Tilstam PV, Schulte W, Holowka T, Kim BS, Nouws J, Sauler M, Piecychna M, Pantouris G, Lolis E, Leng L, Bernhagen J, Fingerle-Rowson G, Bucala R. MIF but not MIF-2 recruits inflammatory macrophages in an experimental polymicrobial sepsis model. Journal Of Clinical Investigation 2021, 131: e127171. PMID: 34850744, PMCID: PMC8631602, DOI: 10.1172/jci127171.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCytokinesDisease Models, AnimalFemaleFlow CytometryGene Expression ProfilingInflammationIntramolecular OxidoreductasesLeukocyte CountMacrophage Migration-Inhibitory FactorsMacrophagesMacrophages, PeritonealMaleMiceMice, Inbred C57BLMice, TransgenicPeritoneal LavagePhenotypeProtein BindingRNA-SeqSepsisSignal TransductionConceptsMacrophage migration inhibitory factorSmall peritoneal macrophagesLarge peritoneal macrophagesPolymicrobial sepsisPeritoneal macrophagesMIF receptor CD74MIF promoter polymorphismsMIF-2Migration inhibitory factorPolymicrobial sepsis modelMIF deficiencyAdoptive transferSeptic shockSurvival benefitInfectious insultsMIF antibodyExcessive inflammationInflammatory cytokinesReceptor CD74Sepsis modelProtective effectPeritoneal cavityDifferent infectionsPromoter polymorphismInflammatory macrophagesIntravesical CD74 and CXCR4, macrophage migration inhibitory factor (MIF) receptors, mediate bladder pain
Ye S, Ma F, Mahmood DFD, Meyer-Siegler KL, Menard RE, Hunt DE, Leng L, Bucala R, Vera PL. Intravesical CD74 and CXCR4, macrophage migration inhibitory factor (MIF) receptors, mediate bladder pain. PLOS ONE 2021, 16: e0255975. PMID: 34424927, PMCID: PMC8382170, DOI: 10.1371/journal.pone.0255975.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorHigh mobility group box 1Bladder painMIF receptorHMGB1 releaseBladder hyperalgesiaMobility group box 1MIF receptor CD74Migration inhibitory factorGroup box 1Primary urothelial cellsInhibitory factor receptorWarrants further investigationCD74 receptorReceptor CD74Micturition parametersReceptor antagonistReceptor 4Box 1PainInhibitory factorHyperalgesiaCD74Urothelial cellsNovel target17‐a‐estradiol late in life extends lifespan in aging UM‐HET3 male mice; nicotinamide riboside and three other drugs do not affect lifespan in either sex
Harrison DE, Strong R, Reifsnyder P, Kumar N, Fernandez E, Flurkey K, Javors MA, Lopez‐Cruzan M, Macchiarini F, Nelson JF, Markewych A, Bitto A, Sindler AL, Cortopassi G, Kavanagh K, Leng L, Bucala R, Rosenthal N, Salmon A, Stearns TM, Bogue M, Miller RA. 17‐a‐estradiol late in life extends lifespan in aging UM‐HET3 male mice; nicotinamide riboside and three other drugs do not affect lifespan in either sex. Aging Cell 2021, 20: e13328. PMID: 33788371, PMCID: PMC8135004, DOI: 10.1111/acel.13328.Peer-Reviewed Original ResearchCD74 is a regulator of hematopoietic stem cell maintenance
Becker-Herman S, Rozenberg M, Hillel-Karniel C, Gil-Yarom N, Kramer M, Barak A, Sever L, David K, Radomir L, Lewinsky H, Levi M, Friedlander G, Bucala R, Peled A, Shachar I. CD74 is a regulator of hematopoietic stem cell maintenance. PLOS Biology 2021, 19: e3001121. PMID: 33661886, PMCID: PMC7963458, DOI: 10.1371/journal.pbio.3001121.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnimalsAntigens, Differentiation, B-LymphocyteBone Marrow CellsBone Marrow TransplantationCell LineageFemaleHealthy VolunteersHematopoietic Stem CellsHistocompatibility Antigens Class IIHumansIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMaleMiceMice, Inbred C57BLSignal TransductionConceptsMacrophage migration inhibitory factorHematopoietic stem cellsBone marrowCytokine macrophage migration inhibitory factorMigration inhibitory factorNumber of HSPCsTransplant protocolsCD18 expressionClinical transplantationInduced SurvivalCD74Inhibitory factorBM nicheCell surface receptorsSelf-renewal propertiesClinical insightsProgenitor cellsBlood cell lineagesSurface receptorsStem cellsHematopoietic stemCell lineagesCellsUndifferentiated cellsHematopoietic stem cell maintenanceHsp90-stabilized MIF supports tumor progression via macrophage recruitment and angiogenesis in colorectal cancer
Klemke L, De Oliveira T, Witt D, Winkler N, Bohnenberger H, Bucala R, Conradi LC, Schulz-Heddergott R. Hsp90-stabilized MIF supports tumor progression via macrophage recruitment and angiogenesis in colorectal cancer. Cell Death & Disease 2021, 12: 155. PMID: 33542244, PMCID: PMC7862487, DOI: 10.1038/s41419-021-03426-z.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenic ProteinsAnimalsAntigens, Differentiation, B-LymphocyteAntineoplastic AgentsColitis-Associated NeoplasmsDisease Models, AnimalFemaleHCT116 CellsHEK293 CellsHistocompatibility Antigens Class IIHSP90 Heat-Shock ProteinsHumansInflammation MediatorsIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMaleMice, Inbred C57BLMice, KnockoutNeovascularization, PathologicOrganoidsProtein StabilitySignal TransductionTumor BurdenTumor-Associated MacrophagesConceptsMacrophage migration inhibitory factorMIF levelsMacrophage recruitmentAction of MIFColitis-associated colorectal cancer (CAC) mouse modelTumor growthTumor progressionFunction of MIFColorectal cancer mouse modelHigher MIF levelsHost inflammatory pathwaysTumor-specific functionsEpithelial cellsShorter overall survivalCRC tumor progressionClinical correlation studiesMigration inhibitory factorCRC tumor growthCancer mouse modelWild-type organoidsTumor epithelial cellsHSP90 inhibitor treatmentCD74 expressionOverall survivalCRC patientsUnexpected Pro-Fibrotic Effect of MIF in Non-Alcoholic Steatohepatitis Is Linked to a Shift in NKT Cell Populations
Heinrichs D, Brandt EF, Fischer P, Köhncke J, Wirtz TH, Guldiken N, Djudjaj S, Boor P, Kroy D, Weiskirchen R, Bucala R, Wasmuth HE, Strnad P, Trautwein C, Bernhagen J, Berres ML. Unexpected Pro-Fibrotic Effect of MIF in Non-Alcoholic Steatohepatitis Is Linked to a Shift in NKT Cell Populations. Cells 2021, 10: 252. PMID: 33525493, PMCID: PMC7918903, DOI: 10.3390/cells10020252.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkersCell PolarityDietDisease ProgressionFibrosisGene Expression RegulationHepatic Stellate CellsHepatocytesHumansLiverMacrophage Migration-Inhibitory FactorsMaleMice, Inbred C57BLModels, BiologicalNatural Killer T-CellsNon-alcoholic Fatty Liver DiseaseReceptors, ImmunologicConceptsMacrophage migration inhibitory factorNon-alcoholic fatty liver diseaseNAFLD progressionLiver fibrogenesisNKT cell populationNKT cell subpopulationsChronic liver injuryFatty liver diseaseNon-alcoholic steatohepatitisAnti-fibrotic propertiesPro-fibrotic effectsMigration inhibitory factorPleiotropic inflammatory cytokineLiver injury modelPro-fibrotic phenotypeMIF expressionMurine resultsNASH patientsNKT cellsLiver injuryLiver diseaseFibrosis markersInflammatory cytokinesDiet feedingInjury model
2020
Designed CXCR4 mimic acts as a soluble chemokine receptor that blocks atherogenic inflammation by agonist-specific targeting
Kontos C, El Bounkari O, Krammer C, Sinitski D, Hille K, Zan C, Yan G, Wang S, Gao Y, Brandhofer M, Megens RTA, Hoffmann A, Pauli J, Asare Y, Gerra S, Bourilhon P, Leng L, Eckstein HH, Kempf WE, Pelisek J, Gokce O, Maegdefessel L, Bucala R, Dichgans M, Weber C, Kapurniotu A, Bernhagen J. Designed CXCR4 mimic acts as a soluble chemokine receptor that blocks atherogenic inflammation by agonist-specific targeting. Nature Communications 2020, 11: 5981. PMID: 33239628, PMCID: PMC7689490, DOI: 10.1038/s41467-020-19764-z.Peer-Reviewed Original ResearchMeSH KeywordsAgedAnimalsAntigens, CDAtherosclerosisBinding SitesCarotid Artery, CommonChemokine CXCL12Crystallography, X-RayDisease Models, AnimalDrug DesignDrug Evaluation, PreclinicalEndarterectomy, CarotidFemaleHumansIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMaleMiceMice, Knockout, ApoEMiddle AgedPeptide FragmentsReceptors, CXCR4SialyltransferasesSignal TransductionConceptsMacrophage migration inhibitory factorCXC motif chemokine receptor 4Chemokine receptorsChemokine/receptor axisCXCR4/CXCL12 interactionHuman carotid endarterectomy specimensMigration inhibitory factorChemokine receptor 4MIF/CD74Carotid endarterectomy specimensAtherogenic inflammationCXCL12 interactionReceptor axisReceptor 4MIF inhibitorsReceptor-based strategiesAtherosclerotic plaquesAtherosclerosisAtypical chemokineLeukocyte adhesionCell activityProtective pathwaysInflammationChemokinesPlaques
2001
Up-regulation of macrophage migration inhibitory factor in acute renal allograft rejection in the rat
Brown F, Nikolic-Paterson D, Metz C, Bucala R, Atkins R, Lan H. Up-regulation of macrophage migration inhibitory factor in acute renal allograft rejection in the rat. Clinical & Experimental Immunology 2001, 118: 329-336. PMID: 10540199, PMCID: PMC1905421, DOI: 10.1046/j.1365-2249.1999.01048.x.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorMIF mRNA expressionAcute renal allograft rejectionAcute allograft rejectionRenal allograft rejectionAllograft rejectionMigration inhibitory factorDay 5MIF expressionRenal allograftsMRNA expressionDay 1Inhibitory factorLocal MIF productionMIF protein expressionNormal renal functionT-cell infiltratesCell-mediated diseaseSevere tubular damageCellular immune responsesImmune cell-mediated diseasesSevere tubulitisSevere rejectionCreatinine clearanceMIF productionLysozyme Enhances Renal Excretion of Advanced Glycation Endproducts In Vivo and Suppresses Adverse AGE-mediated Cellular Effects In Vitro: A Potential AGE Sequestration Therapy for Diabetic Nephropathy?
Zheng F, Cai W, Mitsuhashi T, Vlassara H, Bucala R. Lysozyme Enhances Renal Excretion of Advanced Glycation Endproducts In Vivo and Suppresses Adverse AGE-mediated Cellular Effects In Vitro: A Potential AGE Sequestration Therapy for Diabetic Nephropathy? Molecular Medicine 2001, 7: 737-747. PMID: 11788787, PMCID: PMC1950004, DOI: 10.1007/bf03401963.Peer-Reviewed Original ResearchConceptsAdvanced glycation endproductsSerum advanced glycation endproductsDb/db miceNon-obese diabeticSerum AGEsMesangial cellsDb miceAGE-BSAGlycation endproductsIGF-I productionDiabetic renal damageSprague-Dawley ratsAGE clearanceSuppress macrophagesNOD miceDiabetic nephropathyRenal damageRenal excretionNormal ratsMMP-9Type IV collagenHost defense proteinsExcretionMRNA levelsMiceMacrophage migration inhibitory factor is an important mediator in the pathogenesis of gastric inflammation in rats
Huang X, Hui C, Chen Y, Chun B, Wong Y, Fung P, Metz C, Cho C, Hui W, Bucala R, Lam S, Lan H. Macrophage migration inhibitory factor is an important mediator in the pathogenesis of gastric inflammation in rats. Gastroenterology 2001, 121: 619-630. PMID: 11522746, DOI: 10.1053/gast.2001.27205.Peer-Reviewed Original ResearchMeSH KeywordsAcetic AcidAcute DiseaseAnimalsAntibodies, MonoclonalDisease Models, AnimalGastritisGene ExpressionIn Situ HybridizationIn Vitro TechniquesIntercellular Adhesion Molecule-1Macrophage Migration-Inhibitory FactorsMacrophagesMaleNeutrophilsNitric Oxide SynthaseNitric Oxide Synthase Type IIRatsRats, Sprague-DawleyRNA, MessengerStomach UlcerTumor Necrosis Factor-alphaWound HealingConceptsAcute gastric ulcerMigration inhibitory factorInducible nitric oxide synthaseGastric ulcerNitric oxide synthaseGastric inflammationMIF antibodyOxide synthaseRole of MIFRat gastric ulcer modelsInhibitory factorMacrophage migration inhibitory factorIntercellular adhesion molecule-1Tumor necrosis factor alphaGastric ulcer modelImmune-mediated diseasesKey inflammatory mediatorsMajor inflammatory cellsAccumulation of macrophagesNecrosis factor alphaAdhesion molecule-1Sites of inflammationNeutrophil accumulationMIF productionUlcer sizeNeuroendocrine properties of macrophage migration inhibitory factor (MIF)
Fingerle‐Rowson G, Bucala R. Neuroendocrine properties of macrophage migration inhibitory factor (MIF). Immunology And Cell Biology 2001, 79: 368-375. PMID: 11488984, DOI: 10.1046/j.1440-1711.2001.01024.x.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorMigration inhibitory factorInhibitory factorCytokine macrophage migration inhibitory factorPro-inflammatory actionsMIF expressionSeptic shockNeuroendocrine mediatorsInflammatory diseasesPathogenic roleEndocrine circuitsNeuroendocrine propertiesImmune systemEndocrine tissuesImmune tissuesNeuroendocrine mechanismsDiseaseTissueArthritisNeuroendocrineFactorsURINE MACROPHAGE MIGRATION INHIBITORY FACTOR CONCENTRATIONS AS A DIAGNOSTIC TOOL IN HUMAN RENAL ALLOGRAFT REJECTION1
Brown F, Nikolic-Paterson D, Chadban S, Dowling J, Jose M, Metz C, Bucala R, Atkins R. URINE MACROPHAGE MIGRATION INHIBITORY FACTOR CONCENTRATIONS AS A DIAGNOSTIC TOOL IN HUMAN RENAL ALLOGRAFT REJECTION1. Transplantation 2001, 71: 1777-1783. PMID: 11455258, DOI: 10.1097/00007890-200106270-00013.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorAcute rejectionMIF concentrationsRenal transplant patientsCyA toxicityTransplant patientsProspective studyRetrospective studyNormal controlsSerum macrophage migration inhibitory factorUrine macrophage migration inhibitory factorAcute renal allograft rejectionStable renal transplant patientsDay 1 posttransplantationEpisodes of biopsyLocal MIF productionRenal allograft patientsRENAL ALLOGRAFT REJECTION1Renal transplant dysfunctionSerum MIF concentrationsSerum MIF levelsTransplant patient groupsRenal allograft rejectionPro-inflammatory cytokinesNormal healthy controlsPurification and Characterization of Macrophage Migration Inhibitory Factor as a Secretory Protein from Rat Epididymis: Evidences for Alternative Release and Transfer to Spermatozoa
Eickhoff R, Wilhelm B, Renneberg H, Wennemuth G, Bacher M, Linder D, Bucala R, Seitz J, Meinhardt A. Purification and Characterization of Macrophage Migration Inhibitory Factor as a Secretory Protein from Rat Epididymis: Evidences for Alternative Release and Transfer to Spermatozoa. Molecular Medicine 2001, 7: 27-35. PMID: 11474125, PMCID: PMC1949991, DOI: 10.1007/bf03401836.Peer-Reviewed Original ResearchConceptsOuter dense fibersSequence analysisDense fibersSecretion modeCDNA fragmentsN-terminal signal sequenceEndoplasmic reticulumMacrophage migration inhibitory factorEpithelial cellsCytokine macrophage migration inhibitory factorN-terminal amino acid sequence analysisAmino acid sequence analysisApical cell surfaceAcid sequence analysisEpididymal epithelial cellsRat epididymisSignal sequenceCDNA sequenceWestern blot experimentsPlasma membraneMigration inhibitory factorSecretory proteinsCytoskeletal elementsExpression patternsN-terminus
2000
Peripheral blood fibrocytes: Mesenchymal precursor cells and the pathogenesis of fibrosis
Chesney J, Bucala R. Peripheral blood fibrocytes: Mesenchymal precursor cells and the pathogenesis of fibrosis. Current Rheumatology Reports 2000, 2: 501-505. PMID: 11123104, DOI: 10.1007/s11926-000-0027-5.Peer-Reviewed Original ResearchConceptsPeripheral blood fibrocytesBlood fibrocytesTissue injuryDistinct cell surface phenotypePersistent T-cell activationNaïve T cellsPathogenesis of fibrosisCell surface phenotypeT cell activationCognate immunityAutoimmune disordersConnective tissue cellsImmunohistochemical studyForeign antigensT cellsSurface phenotypeMesenchymal precursor cellsScar formationFibrotic tissueFibrocytesGrowth factorPrecursor cellsNovel populationMatrix depositionInjuryInvolvement of Macrophage Migration Inhibitory Factor (MIF) in Experimental Uric Acid Nephropathy
Kim Y, Huang X, Suga S, Mazzali M, Tang D, Metz C, Bucala R, Kivlighn S, Johnson R, Lan H. Involvement of Macrophage Migration Inhibitory Factor (MIF) in Experimental Uric Acid Nephropathy. Molecular Medicine 2000, 6: 837-848. PMID: 11126199, PMCID: PMC1949919, DOI: 10.1007/bf03401822.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorUric acid crystal depositionMigration inhibitory factorUric acid nephropathyGranuloma formationMIF mRNAMIF proteinOxonic acidInhibitory factorCrystal depositionAcute uric acid nephropathyAreas of granulomasMIF mRNA expressionProgressive tubulointerstitial injuryRoutine light microscopyUrate nephropathyWestern blot analysisMIF expressionLocal cellular responseMIF secretionTubulointerstitial damageTubulointerstitial injuryInterleukin-2RRenal diseaseDTH reactionExpression of macrophage migration inhibitory factor in human glomerulonephritis
Lan H, Yang N, Nikolic-Paterson D, Yu X, Mu W, Isbel N, Metz C, Bucala R, Atkins R. Expression of macrophage migration inhibitory factor in human glomerulonephritis. Kidney International 2000, 57: 499-509. PMID: 10652026, DOI: 10.1046/j.1523-1755.2000.00869.x.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAgedAged, 80 and overBiopsyCohort StudiesEpithelial CellsFemaleGene ExpressionGlomerulonephritis, MembranoproliferativeGlomerulonephritis, MembranousHumansIn Situ HybridizationKidney GlomerulusMacrophage Migration-Inhibitory FactorsMacrophagesMaleMiddle AgedReference ValuesRNA, MessengerT-LymphocytesConceptsMacrophage migration inhibitory factorMIF expressionMigration inhibitory factorFocal segmental glomerulosclerosisHuman glomerulonephritisProliferative formsMIF mRNAPathogenic roleExperimental glomerulonephritisInhibitory factorProgressive formRenal MIF expressionRenal function impairmentT cell accumulationT-cell infiltratesEpithelial cellsMinimal change diseaseFocal segmental lesionsGlomerular endothelial cellsTubular epithelial cellsNormal human kidneyAttractive therapeutic targetCreatinine clearanceGlomerular epithelial cellsLupus nephritis