2023
Lung endothelium, tau, and amyloids in health and disease
Balczon R, Lin M, Voth S, Nelson A, Schupp J, Wagener B, Pittet J, Stevens T. Lung endothelium, tau, and amyloids in health and disease. Physiological Reviews 2023, 104: 533-587. PMID: 37561137, PMCID: PMC11281824, DOI: 10.1152/physrev.00006.2023.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsEnd-organ dysfunctionLung endotheliumLower respiratory tract infectionsRespiratory tract infectionsAlveolar-capillary barrierLung capillary endotheliumTract infectionsImmune responseNeurocognitive dysfunctionBarrier integrityProtein tauLung capillariesInfectionCapillary endotheliumDysfunctionEpithelial cellsEndotheliumTau variantsVascular nicheTauHost-pathogen interactionsType ICytotoxic activityCytotoxicAmyloid variants
2022
FK506-Binding Protein 11 Is a Novel Plasma Cell-Specific Antibody Folding Catalyst with Increased Expression in Idiopathic Pulmonary Fibrosis
Preisendörfer S, Ishikawa Y, Hennen E, Winklmeier S, Schupp JC, Knüppel L, Fernandez IE, Binzenhöfer L, Flatley A, Juan-Guardela BM, Ruppert C, Guenther A, Frankenberger M, Hatz RA, Kneidinger N, Behr J, Feederle R, Schepers A, Hilgendorff A, Kaminski N, Meinl E, Bächinger HP, Eickelberg O, Staab-Weijnitz CA. FK506-Binding Protein 11 Is a Novel Plasma Cell-Specific Antibody Folding Catalyst with Increased Expression in Idiopathic Pulmonary Fibrosis. Cells 2022, 11: 1341. PMID: 35456020, PMCID: PMC9027113, DOI: 10.3390/cells11081341.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPlasma cellsPulmonary fibrosisIgG antibodiesFatal chronic lung diseaseCell linesAntibody-producing plasma cellsChronic lung diseaseAdaptive immune responsesHybridoma cell linesAlveolar epithelial cell lineCell-specific antibodiesCell deathAntibody-producing hybridoma cellsAutoimmune featuresX-box-binding protein 1IPF lungsLung diseaseEpithelial cell lineImmune responseLymphatic tissueB cellsStress-mediated cell deathAntibody secretionER stress-mediated cell deathSingle-cell multi-omics reveals dyssynchrony of the innate and adaptive immune system in progressive COVID-19
Unterman A, Sumida TS, Nouri N, Yan X, Zhao AY, Gasque V, Schupp JC, Asashima H, Liu Y, Cosme C, Deng W, Chen M, Raredon MSB, Hoehn KB, Wang G, Wang Z, DeIuliis G, Ravindra NG, Li N, Castaldi C, Wong P, Fournier J, Bermejo S, Sharma L, Casanovas-Massana A, Vogels CBF, Wyllie AL, Grubaugh ND, Melillo A, Meng H, Stein Y, Minasyan M, Mohanty S, Ruff WE, Cohen I, Raddassi K, Niklason L, Ko A, Montgomery R, Farhadian S, Iwasaki A, Shaw A, van Dijk D, Zhao H, Kleinstein S, Hafler D, Kaminski N, Dela Cruz C. Single-cell multi-omics reveals dyssynchrony of the innate and adaptive immune system in progressive COVID-19. Nature Communications 2022, 13: 440. PMID: 35064122, PMCID: PMC8782894, DOI: 10.1038/s41467-021-27716-4.Peer-Reviewed Original ResearchMeSH KeywordsAdaptive ImmunityAgedAntibodies, Monoclonal, HumanizedCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCells, CulturedCOVID-19COVID-19 Drug TreatmentFemaleGene Expression ProfilingGene Expression RegulationHumansImmunity, InnateMaleReceptors, Antigen, B-CellReceptors, Antigen, T-CellRNA-SeqSARS-CoV-2Single-Cell AnalysisConceptsProgressive COVID-19B cell clonesSingle-cell analysisT cellsImmune responseMulti-omics single-cell analysisCOVID-19Cell clonesAdaptive immune interactionsSevere COVID-19Dynamic immune responsesGene expressionSARS-CoV-2 virusAdaptive immune systemSomatic hypermutation frequenciesCellular effectsProtein markersEffector CD8Immune signaturesProgressive diseaseHypermutation frequencyProgressive courseClassical monocytesClonesImmune interactions
2021
Chronic lung diseases are associated with gene expression programs favoring SARS-CoV-2 entry and severity
Bui LT, Winters NI, Chung MI, Joseph C, Gutierrez AJ, Habermann AC, Adams TS, Schupp JC, Poli S, Peter LM, Taylor CJ, Blackburn JB, Richmond BW, Nicholson AG, Rassl D, Wallace WA, Rosas IO, Jenkins RG, Kaminski N, Kropski JA, Banovich NE. Chronic lung diseases are associated with gene expression programs favoring SARS-CoV-2 entry and severity. Nature Communications 2021, 12: 4314. PMID: 34262047, PMCID: PMC8280215, DOI: 10.1038/s41467-021-24467-0.Peer-Reviewed Original ResearchConceptsChronic lung diseaseLung diseaseImmune responseSARS-CoV-2 entry factorsSevere coronavirus disease-19SARS-CoV-2 infectionWorse COVID-19 outcomesSARS-CoV-2 entryAdaptive immune responsesCoronavirus disease-19COVID-19 outcomesInnate immune responseInflammatory gene expression programSimilar cellular distributionPoor outcomePeripheral lungViral exposureDisease-19Inflammatory microenvironmentEntry factorsLung epitheliumLung cellsViral replicationAT2 cellsBasal differences
2017
Transcriptome profiles in sarcoidosis and their potential role in disease prediction
Schupp JC, Vukmirovic M, Kaminski N, Prasse A. Transcriptome profiles in sarcoidosis and their potential role in disease prediction. Current Opinion In Pulmonary Medicine 2017, 23: 487-492. PMID: 28590292, PMCID: PMC5637542, DOI: 10.1097/mcp.0000000000000403.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsGenome-wide expression studiesWide expression studiesTranscriptome profilesTranscriptomic dataRNA sequencingExpression studiesGene expressionMolecular mechanismsLarge prospective followTh1 immune responseTranscriptomeNonnecrotizing granulomasProspective followSystemic diseaseDisease progressionTreatment outcomesImmune responseSarcoidosisPotential roleControl tissuesProgressive sarcoidosisKey roleDiseaseTranscriptomicsGranulomas
2015
Immune response to Propionibacterium acnes in patients with sarcoidosis – in vivo and in vitro
Schupp J, Tchaptchet S, Lützen N, Engelhard P, Müller-Quernheim J, Freudenberg M, Prasse A. Immune response to Propionibacterium acnes in patients with sarcoidosis – in vivo and in vitro. BMC Pulmonary Medicine 2015, 15: 75. PMID: 26204953, PMCID: PMC4513400, DOI: 10.1186/s12890-015-0070-7.Peer-Reviewed Original ResearchConceptsHeat-killed P. acnesSarcoid patientsP. acnesBAL cellsBAL fluidTotal IgGImmune responseHealthy volunteersPathogenesis of sarcoidosisSpecific antibodiesGM-CSF productionIgA titresIgA levelsLymph nodesInflammatory cytokinesGranuloma formationMore TNFSarcoidosisPatientsPropionibacterium acnesAcneGM-CSFElevated levelsAntibodiesIgG
2013
Lung Collagens Perpetuate Pulmonary Fibrosis via CD204 and M2 Macrophage Activation
Stahl M, Schupp J, Jäger B, Schmid M, Zissel G, Müller-Quernheim J, Prasse A. Lung Collagens Perpetuate Pulmonary Fibrosis via CD204 and M2 Macrophage Activation. PLOS ONE 2013, 8: e81382. PMID: 24278429, PMCID: PMC3835428, DOI: 10.1371/journal.pone.0081382.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisAlveolar macrophagesCollagen type IHealthy donorsInterleukin-1 receptor antagonistType IM2 macrophage activationExpression of CCL2Lower respiratory tractIL-1ra productionAbundant collagen productionInnate immune responsePhospho-Akt expressionType I effectsExpression of CD204Collagen breakdown productsBronchoalveolar lavageReceptor antagonistCD204 expressionRespiratory tractLung collagenImmune responseM2 typeMacrophage activation