2021
DNA glycosylase deficiency leads to decreased severity of lupus in the Polb-Y265C mouse model
Paluri SL, Burak M, Senejani AG, Levinson M, Rahim T, Clairmont K, Kashgarian M, Alvarado-Cruz I, Meas R, Cardó-Vila M, Zeiss C, Maher S, Bothwell ALM, Coskun E, Kant M, Jaruga P, Dizdaroglu M, Lloyd R, Sweasy JB. DNA glycosylase deficiency leads to decreased severity of lupus in the Polb-Y265C mouse model. DNA Repair 2021, 105: 103152. PMID: 34186496, PMCID: PMC8635285, DOI: 10.1016/j.dnarep.2021.103152.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDisease Models, AnimalDNADNA GlycosylasesDNA Polymerase betaDNA RepairGene DeletionLupus Erythematosus, SystemicMiceMutationOxidative Stress
2020
B cell-intrinsic TLR9 expression is protective in murine lupus
Tilstra JS, John S, Gordon RA, Leibler C, Kashgarian M, Bastacky S, Nickerson KM, Shlomchik MJ. B cell-intrinsic TLR9 expression is protective in murine lupus. Journal Of Clinical Investigation 2020, 130: 3172-3187. PMID: 32191633, PMCID: PMC7260024, DOI: 10.1172/jci132328.Peer-Reviewed Original ResearchConceptsToll-like receptor 9Systemic lupus erythematosusTLR9 deficiencyTLR9 expressionDendritic cellsB cellsPlasmacytoid dendritic cellsAnti-nucleosome antibodiesLupus erythematosusAutoantibody productionMurine lupusSLE pathogenesisTLR9 signalsReceptor 9Cell type-specific effectsType-specific effectsDisease pathogenesisTherapeutic potentialSelective deletionDiseaseNonredundant roleNephritisLupusPathogenesisDeficiency
2010
Dendritic Cells in Lupus Are Not Required for Activation of T and B Cells but Promote Their Expansion, Resulting in Tissue Damage
Teichmann LL, Ols ML, Kashgarian M, Reizis B, Kaplan DH, Shlomchik MJ. Dendritic Cells in Lupus Are Not Required for Activation of T and B Cells but Promote Their Expansion, Resulting in Tissue Damage. Immunity 2010, 33: 967-978. PMID: 21167752, PMCID: PMC3010763, DOI: 10.1016/j.immuni.2010.11.025.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutoantibodiesBlood Component RemovalB-LymphocytesCell DifferentiationCell MovementDendritic CellsDisease Models, AnimalHumansImmunoglobulin Class SwitchingInterferon-gammaLupus Erythematosus, SystemicLymphocyte ActivationMiceMice, Inbred C57BLMice, Inbred MRL lprT-Lymphocyte SubsetsT-Lymphocytes, RegulatoryConceptsDendritic cellsAdaptive immune responsesMurine lupusImmune responseAbsence of DCsEffects of DCsSystemic lupus erythematosusSerum immunoglobulin concentrationsPotential therapeutic targetLupus erythematosusInterstitial infiltratesAutoimmune disordersHumoral responseAutoantibody concentrationsPlasmablast numbersImmunoglobulin concentrationsTherapeutic targetB cellsTissue damageLupusCell numberCellsInitial activationComplex roleActivation
1987
Animal model of primary hyperparathyroidism
Jaeger P, Jones W, Kashgarian M, Baron R, Clemens T, Segre G, Hayslett J. Animal model of primary hyperparathyroidism. American Journal Of Physiology 1987, 252: e790-e798. PMID: 3591940, DOI: 10.1152/ajpendo.1987.252.6.e790.Peer-Reviewed Original ResearchConceptsTheoretical renal thresholdPrimary hyperparathyroidismPlasma levelsRenal thresholdAnimal modelsD plasma levelsPTH plasma levelsPlasma calcium levelsSynthetic parathyroid hormonePTH levelsDihydroxyvitamin DParathyroid hormoneParathyroidectomized animalsBovine PTHChronic hyperparathyroidismSustained elevationNormal limitsPlasma calciumHyperparathyroidismCalcium levelsOrgan systemsEpithelial functionControl valuesBasal levelsExperimental model
1986
Mechanism of Nephrocalcinosis in Primary Hyperparathyroidism
Jaeger P, Jones W, Hayslett J, Kashgarian M, Segre G. Mechanism of Nephrocalcinosis in Primary Hyperparathyroidism. Advances In Experimental Medicine And Biology 1986, 208: 379-382. PMID: 3565154, DOI: 10.1007/978-1-4684-5206-8_47.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalciumDisease Models, AnimalHyperparathyroidismKidney CortexKidney MedullaMaleNephrocalcinosisPhosphorusRatsRats, Inbred Strains
1975
Diffuse glomerulonephritis in rabbits with Streptococcus viridans endocarditis.
Arnold S, Valone J, Askenase P, Kashgarian M, Freedman L. Diffuse glomerulonephritis in rabbits with Streptococcus viridans endocarditis. Laboratory Investigation 1975, 32: 681-9. PMID: 125360.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, BacterialComplement C3Disease Models, AnimalEndocarditis, BacterialFluorescent Antibody TechniqueGlomerulonephritisHistological TechniquesImmune Complex DiseasesImmunizationImmunoglobulin GKidneyMaleMicroscopy, ElectronMicroscopy, FluorescenceRabbitsRheumatoid FactorSplenomegalyStreptococcal InfectionsConceptsInfective endocarditisDiffuse glomerulonephritisSubendothelial electron-dense depositsStreptococcus viridans endocarditisDeposition of IgGDiffuse proliferative glomerulonephritisSerum complement levelsAcute diffuse proliferative glomerulonephritisPositive blood culturesElectron microscopic findingsElectron-dense depositsComplement levelsGlomerular changesValvular vegetationsRheumatoid factorLeukocytic infiltrationMesangial proliferationProliferative glomerulonephritisBlood culturesImmune mechanismsCapillary occlusionMorphologic findingsIntravenous administrationMicroscopic findingsEndocarditis