2022
A Human MSH6 Germline Variant Associated With Systemic Lupus Erythematosus Induces Lupus‐like Disease in Mice
Meas R, Nititham J, Taylor KE, Maher S, Clairmont K, Carufe KEW, Kashgarian M, Nottoli T, Cheong A, Nagel ZD, Gaffney PM, Criswell LA, Sweasy JB. A Human MSH6 Germline Variant Associated With Systemic Lupus Erythematosus Induces Lupus‐like Disease in Mice. ACR Open Rheumatology 2022, 4: 760-770. PMID: 35708944, PMCID: PMC9469486, DOI: 10.1002/acr2.11471.Peer-Reviewed Original ResearchSystemic lupus erythematosusAntinuclear antibodiesMSH6 variantsLupus erythematosusMSH6 mutationsMouse modelSingle nucleotide polymorphismsDevelopment of SLELevel of ANAInfiltration of CD68Lupus-like diseaseInflammatory lung diseasesLung alveolar spacesRepair genesMismatch repair genesLung diseaseHealthy controlsPeyer's patchesWildtype miceAlveolar spaceCRISPR/Cas9 gene targetingSomatic hypermutation frequenciesAutoimmune phenotypeMiceDifferent mismatch repair genes
2001
Molecular mechanisms of TGF‐β antagonism by interferon γ and cyclosporine A in lung fibroblasts
EICKELBERG O, PANSKY A, KOEHLER E, BIHL M, TAMM M, HILDEBRAND P, PERRUCHOUD A, KASHGARIAN M, ROTH M. Molecular mechanisms of TGF‐β antagonism by interferon γ and cyclosporine A in lung fibroblasts. The FASEB Journal 2001, 15: 797-806. PMID: 11259398, DOI: 10.1096/fj.00-0233com.Peer-Reviewed Original ResearchMeSH KeywordsCells, CulturedCollagenCyclosporineDNA-Binding ProteinsExtracellular MatrixFibroblastsGenes, ReporterHumansInterferon-gammaLungModels, BiologicalOligonucleotides, AntisenseProto-Oncogene Proteins c-junPulmonary FibrosisSignal TransductionSTAT1 Transcription FactorTrans-ActivatorsTranscription Factor AP-1Transforming Growth Factor betaConceptsCollagen depositionLung fibroblastsIFN-gammaExcess extracellular matrix depositionGrowth factor-beta activityPrimary human lung fibroblastsFibrotic lung diseaseHuman lung fibroblastsTGF-beta antagonismAP-1IFN-gamma treatmentExtracellular matrix depositionLung fibrosisFatal conditionLung diseaseMolecular mechanismsPathological featuresInterferon γTranscription factor AP-1Future therapiesPharmacological agentsJunD homodimersFactor AP-1Novel targetDirect inhibition