Adjunct Faculty
Adjunct faculty typically have an academic or research appointment at another institution and contribute or collaborate with one or more School of Medicine faculty members or programs.
Adjunct rank detailsJonas Christian Schupp, MD
Assistant Professor AdjunctAbout
Research
Publications
2026
Antibodies against Ro52 in idiopathic inflammatory myopathies are associated with objective sicca symptoms
Meinecke A, Seeliger B, Schupp J, Skripuletz T, Gödecke V, Holzer M, Ernst D, Witte T. Antibodies against Ro52 in idiopathic inflammatory myopathies are associated with objective sicca symptoms. Frontiers In Immunology 2026, 17: 1841969. PMID: 42344888, PMCID: PMC13286919, DOI: 10.3389/fimmu.2026.1841969.Peer-Reviewed Original ResearchConceptsIdiopathic inflammatory myopathiesInterstitial lung diseaseAnti-Ro52 antibodiesInflammatory myopathiesRetrospective data analysisSicca symptomsTear productionClinical associationsPresence of anti-Ro52 antibodiesLung diseaseIdiopathic inflammatory myopathy patientsOccurrence of interstitial lung diseaseAssociation of interstitial lung diseaseRetrospective data analysis of patientsSeverity of interstitial lung diseaseAssociated with interstitial lung diseaseData analysis of patientsInflammatory myopathy patientsAnalysis of patientsHannover Medical SchoolSSA antibodySchirmer testSjogren's diseaseClinical manifestationsMyopathy patientsTranscriptional landscape of pulmonary artery endothelium reveals subpopulation- and disease-specific remodeling signatures
Lins T, Valzano F, Fließer E, Borek I, Crnkovic S, Morley M, Basil M, Katzen J, Cantu E, Schupp J, Kneidinger N, Lindenmann J, Aigner C, Benazzo A, Morrisey E, Bartkuhn M, Marsh L, Birnhuber A, Kwapiszewska G. Transcriptional landscape of pulmonary artery endothelium reveals subpopulation- and disease-specific remodeling signatures. Communications Biology 2026 PMID: 42115292, DOI: 10.1038/s42003-026-10204-0.Peer-Reviewed Original ResearchPulmonary hypertensionEndothelial cellsPulmonary arterial hypertensionHuman pulmonary arteriesPulmonary artery endotheliumDisease-specific therapeutic targetsTranscriptional programsSubset compositionLipid metabolism dysfunctionPulmonary arteryArterial hypertensionHealthy donorsPulmonary fibrosisAntigen presentationDysregulated angiogenesisVascular toneTranscriptional landscapeMetabolic dysfunctionState of endothelial cellsAnatomical locationArterial endotheliumCoronary arteryArterial bedEndothelial phenotypeExpression signaturesThe pleuroparenchymal fibroelastosis atlas reveals aberrant cell states and their zonation as an alternate roadmap to lung fibrosis
Ruwisch J, Cazes A, Leiber L, Borie R, Neubert L, Christian L, de Montpréville V, Szmul A, Moussa F, Verleden S, Gaedcke S, Hegermann J, Fuge J, Ballmaier M, Kamp J, Greer M, Braubach P, Werlein C, Ius F, Graalmann T, Aburahma K, De Sadeleer L, Egashira R, Ackermann M, Yamada D, Hoeper M, Falk C, Gottlieb J, Schiller H, Vanaudenaerde B, Seeliger B, Debray M, Bernaudin J, Knudsen L, Bergot E, Jacob J, Mal H, Jonigk D, Dettmer S, Mordant P, Prasse A, Fadel E, Wuyts W, Crestani B, Kaminski N, Justet A, Schupp J. The pleuroparenchymal fibroelastosis atlas reveals aberrant cell states and their zonation as an alternate roadmap to lung fibrosis. Science Advances 2026, 12: eaeb5967. PMID: 42102198, PMCID: PMC13162212, DOI: 10.1126/sciadv.aeb5967.Peer-Reviewed Original ResearchConceptsInterstitial lung diseasePleuroparenchymal fibroelastosisProgressive interstitial lung diseaseCellular landscapeTertiary lymphoid structuresAberrant cell statesIdiopathic pulmonary fibrosisRNA in situ hybridizationIntra-alveolar fibrosisCellular disease processesCellular machineryLymphoid structuresSeptal elastosisImmune cellsPulmonary fibrosisBasaloid cellsFibrotic remodelingLung fibrosisInflammatory microenvironmentLung diseaseCell statesTherapeutic strategiesCollagen depositionMolecular rationaleFibrosisD18-09 The Multiorgan Multicenter Spatial Transcriptomics Atlas Reveals Layered Granuloma Architecture and Cellular Programs Driving Sarcoidosis
Ruwisch J, Christian L, Traidl S, Dietrich J, Kamp J, Casper J, Giercke L, Seeliger B, Ius F, Greer M, Werlein C, Gottlieb J, Hoeper M, Justet A, Falk C, Li Y, Teichmann S, Kaminski N, Jeny F, Schmidt-Ott K, Schacht V, Schefzyk M, Jonigk D, Neubert L, Schupp J. D18-09 The Multiorgan Multicenter Spatial Transcriptomics Atlas Reveals Layered Granuloma Architecture and Cellular Programs Driving Sarcoidosis. American Journal Of Respiratory And Critical Care Medicine 2026, 212: aamag162.2835. DOI: 10.1093/ajrccm/aamag162.2835.Peer-Reviewed Original ResearchMultinucleated giant cellsGranuloma biologySarcoidosis granulomasGiant cellsMultiplex immunofluorescence stainingImmune cell aggregatesGranuloma architectureTranscriptional programsCellular blueprintLigand-receptor analysisSarcoidosis diagnosisStromal zonesMonocyte stateTissue-specific programsLymph nodesMyeloid cellsBone marrowStress adaptation pathwaysMacrophage programmingPulmonary granulomasSarcoidosisInflammatory fibroblastsInflammatory diseasesTherapeutic strategiesOrgan-specific featuresC103-24 Effect of Nerandomilast in Patients With Progressive Pulmonary Fibrosis (PPF) by Gap Stage: Subgroup Analysis of the FIBRONEER-ILD Trial
Podolanczuk A, Kuwana M, Li F, Wolters P, Schupp J, Song J, Hofmann P, Rohr K, Wachtlin D, Valenzuela C. C103-24 Effect of Nerandomilast in Patients With Progressive Pulmonary Fibrosis (PPF) by Gap Stage: Subgroup Analysis of the FIBRONEER-ILD Trial. American Journal Of Respiratory And Critical Care Medicine 2026, 212: aamag162.2818. DOI: 10.1093/ajrccm/aamag162.2818.Peer-Reviewed Original ResearchGAP stage IGAP stage IIProgressive pulmonary fibrosisAcute exacerbation of ILDAcute exacerbationGAP stageStage IStage IIIStage IIHazard ratioHigh riskDatabase lockHigher risk of mortalityRisk of mortalityRespiratory causesPost Hoc AnalysisTrial medicationAbstract Rationale:Pulmonary fibrosisSubgroup analysisPlaceboDisease progressionPatientsEvidence of heterogeneityBoehringer IngelheimLung fibroblasts contribute to release of Serum Amyloid A as potential biomarker of exacerbation of lung fibrosis in mice
Steinmetz L, Seeliger B, Schupp J, Röpke T, Aschenbrenner F, Maus R, DeLuca D, Gaedcke S, Pich A, Knudsen L, Neubert L, Ius F, Prasse A, Kolb M, Maus U. Lung fibroblasts contribute to release of Serum Amyloid A as potential biomarker of exacerbation of lung fibrosis in mice. ERJ Open Research 2026, 01320-2025. DOI: 10.1183/23120541.01320-2025.Peer-Reviewed Original ResearchInterstitial lung diseaseAcute exacerbation of interstitial lung diseaseExacerbation of interstitial lung diseaseIdiopathic pulmonary fibrosisAcute exacerbationPlasma of miceSerum amyloid A levelsLung fibrosisSerum amyloid ALung fibroblastsLung diseasePlatelet-derived growth factor receptor ABleomycin-induced lung fibrosisPotential biomarkersPlasma of patientsAmyloid AProtein levels in vitroAE-ILDAntibiotic therapyLevels in vitroClinical stagePulmonary fibrosisInflammatory phenotypePneumococcal challengeReceptor A(1216) Pilot Study of the Auto-Antibody Profile Against Nuclear, Cytoplasmic and Cytokine Auto-Antigens in Lung Transplant Recipients
Klass D, Beushausen K, Keil J, Chichelnitskiy E, Schupp J, Gottlieb J, Hoeper M, Greer M, Ruhparwar A, Salman J, Ius F, Kuehne J, Falk C. (1216) Pilot Study of the Auto-Antibody Profile Against Nuclear, Cytoplasmic and Cytokine Auto-Antigens in Lung Transplant Recipients. The Journal Of Heart And Lung Transplantation 2026, 45: 565. DOI: 10.1016/j.healun.2026.02.1229.Peer-Reviewed Original ResearchManagement von SARD-ILD im Wandel
Witte T, Schupp J. Management von SARD-ILD im Wandel. Zeitschrift Für Rheumatologie 2026, 85: 382-389. PMID: 41879828, PMCID: PMC13234071, DOI: 10.1007/s00393-026-01807-3.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsProgressive pulmonary fibrosisSystematic PubMed searchWell-tolerated treatment optionInterstitial lung diseaseInhaled treprostinilCTD-ILDUnfavourable prognosisAnti-inflammatory propertiesPulmonary fibrosisAdverse eventsTreatment optionsAntifibrotic agentsLung function lossLung diseaseClinical studiesPubMed searchClinical investigationTherapeutic strategiesTherapeutic approachesLung functionRheumatic diseasesRespiratory symptomsObjectivesThis reviewTherapeutic perspectivesMethodsA systematic PubMed searchExtent of alveolar collapse in expiratory CT as a prognostic marker in idiopathic pulmonary fibrosis
Scharm S, Schaefer-Prokop C, Schreuder A, Ehmig J, Hunkemöller A, Fuge J, Seeliger B, Schupp J, Wacker F, Shin H. Extent of alveolar collapse in expiratory CT as a prognostic marker in idiopathic pulmonary fibrosis. PLOS ONE 2026, 21: e0345308. PMID: 41843601, PMCID: PMC12994813, DOI: 10.1371/journal.pone.0345308.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisAlveolar collapseCT scanPulmonary fibrosisAttenuation histogramPrognostic imaging markerBaseline forced vital capacityMann-Whitney U testRetrospective longitudinal studyBaseline FVC%Baseline CTExpiratory CTIPF patientsHistogram measuresPredictive markerPrognostic markerLogistic regression modelsPatient subgroupsPatient populationMann-WhitneyPatientsU testVital capacityImaging markersOutcome predictionAltered cholesterol immunometabolism activates the macrophage NLRP3-inflammasome in lung fibrosis.
Vaso M, Dukic M, Pennitz P, Manukyan A, Collum S, Lin W, Winder C, Dunn W, Schupp J, Braubach P, Wygrecka M, Ren D, Suarez E, Huang H, Hussain R, Patel B, Karmouty-Quintana H, Akalin A, Landthaler M, Nouailles G, Ochs M, Lopez-Rodriguez E, Giambelluca S. Altered cholesterol immunometabolism activates the macrophage NLRP3-inflammasome in lung fibrosis. American Journal Of Respiratory Cell And Molecular Biology 2026 PMID: 41738296, DOI: 10.1093/ajrcmb/aanag029.Peer-Reviewed Original ResearchBronchoalveolar lavage fluidBronchoalveolar lavage fluid cellsMurine modelLung fibrosisFibrosis patientsNLRP3 inflammasome activationNLRP3 inflammasomeBALF cellsInflammasome activationMurine model of lung fibrosisWild-type (WT) miceCholesterol metabolismModel of lung fibrosisLipidomic analysisIL-18 levelsHuman macrophage modelLung fibrosis progressionIPF patientsNLRP3 inflammasome componentsPatient cohortPulmonary fibrosisFibrosis progressionLavage fluidFibrosis markersMacrophage NLRP3 inflammasome