2022
Integrative analyses for the identification of idiopathic pulmonary fibrosis-associated genes and shared loci with other diseases
Chen M, Zhang Y, Adams T, Ji D, Jiang W, Wain LV, Cho M, Kaminski N, Zhao H. Integrative analyses for the identification of idiopathic pulmonary fibrosis-associated genes and shared loci with other diseases. Thorax 2022, 78: 792-798. PMID: 36216496, PMCID: PMC10083187, DOI: 10.1136/thorax-2021-217703.Peer-Reviewed Original ResearchMeSH KeywordsCase-Control StudiesGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansIdiopathic Pulmonary FibrosisLungTranscription FactorsConceptsTranscriptome-wide association analysisLocal genetic correlationsSingle-cell expression dataCandidate genesTranscription factorsIntegrative analysisGenomic regionsGenetic correlationsExpression dataTF target genesComplex genetic architectureTF binding sitesWide association studyPower of GWASSpecific DEGsGenetic architectureNew genesNovel genesCausal genesTarget genesGenetic basisEnrichment analysisAssociation studiesRegulatory roleAssociation analysisLung Microenvironments and Disease Progression in Fibrotic Hypersensitivity Pneumonitis.
De Sadeleer LJ, McDonough JE, Schupp JC, Yan X, Vanstapel A, Van Herck A, Everaerts S, Geudens V, Sacreas A, Goos T, Aelbrecht C, Nawrot TS, Martens DS, Schols D, Claes S, Verschakelen JA, Verbeken EK, Ackermann M, Decottignies A, Mahieu M, Hackett TL, Hogg JC, Vanaudenaerde BM, Verleden SE, Kaminski N, Wuyts WA. Lung Microenvironments and Disease Progression in Fibrotic Hypersensitivity Pneumonitis. American Journal Of Respiratory And Critical Care Medicine 2022, 205: 60-74. PMID: 34724391, PMCID: PMC8865586, DOI: 10.1164/rccm.202103-0569oc.Peer-Reviewed Original ResearchConceptsFibrotic hypersensitivity pneumonitisIdiopathic pulmonary fibrosisHypersensitivity pneumonitisLung zonesMolecular traitsUnused donor lungsInterstitial lung diseaseLocal disease extentProgression of fibrosisSevere fibrosis groupGene co-expression network analysisCo-expression network analysisExplant lungsDonor lungsLung involvementEndothelial functionLung findingsDisease extentPulmonary fibrosisLung diseaseFibrosis groupLung microenvironmentClinical behaviorDisease progressionBAL samples
2021
Machine learning implicates the IL-18 signaling axis in severe asthma
Camiolo MJ, Zhou X, Wei Q, Bittar H, Kaminski N, Ray A, Wenzel S. Machine learning implicates the IL-18 signaling axis in severe asthma. JCI Insight 2021, 6: e149945. PMID: 34591794, PMCID: PMC8663569, DOI: 10.1172/jci.insight.149945.Peer-Reviewed Original ResearchConceptsLung functionIL-18NF-κBTranscriptional hallmarksExacerbation-prone asthmaSevere asthma pathogenesisSubgroup of patientsVariable natural historySevere Asthma Research Program (SARP) cohortDownstream NF-κBMixed inflammatory processActivator protein-1 (AP-1) activationPathobiological underpinningsCorticosteroid exposureSevere asthmaAsthma clustersAsthma pathogenesisPatient morbidityInflammatory processProtein-1 activationExternal cohortLung tissuePatient clustersAP-1 activityNatural history
2020
Assessment of viral RNA in idiopathic pulmonary fibrosis using RNA-seq
Yin Q, Strong MJ, Zhuang Y, Flemington EK, Kaminski N, de Andrade JA, Lasky JA. Assessment of viral RNA in idiopathic pulmonary fibrosis using RNA-seq. BMC Pulmonary Medicine 2020, 20: 81. PMID: 32245461, PMCID: PMC7119082, DOI: 10.1186/s12890-020-1114-1.Peer-Reviewed Original ResearchMeSH KeywordsCase-Control StudiesHumansIdiopathic Pulmonary FibrosisLungReal-Time Polymerase Chain ReactionRNA, ViralRNA-SeqVirus DiseasesConceptsIdiopathic pulmonary fibrosisViral RNA expressionViral infectionPulmonary fibrosisPathogenesis of IPFLung biopsy samplesRNA expressionHerpes virus infectionLow-level evidenceReal-time RT-PCRAcute exacerbationControl lungsLung tissueVirus infectionBiopsy samplesSelect virusesPossible associationInfectionRT-PCRStatistical differenceNext-generation sequencingViral RNAFibrosisVirusRNA-seq resultsGenome-Wide Association Study of Susceptibility to Idiopathic Pulmonary Fibrosis
Allen RJ, Guillen-Guio B, Oldham JM, Ma SF, Dressen A, Paynton ML, Kraven LM, Obeidat M, Li X, Ng M, Braybrooke R, Molina-Molina M, Hobbs BD, Putman RK, Sakornsakolpat P, Booth HL, Fahy WA, Hart SP, Hill MR, Hirani N, Hubbard RB, McAnulty RJ, Millar AB, Navaratnam V, Oballa E, Parfrey H, Saini G, Whyte MKB, Zhang Y, Kaminski N, Adegunsoye A, Strek ME, Neighbors M, Sheng XR, Gudmundsson G, Gudnason V, Hatabu H, Lederer DJ, Manichaikul A, Newell JD, O’Connor G, Ortega VE, Xu H, Fingerlin TE, Bossé Y, Hao K, Joubert P, Nickle DC, Sin DD, Timens W, Furniss D, Morris AP, Zondervan KT, Hall IP, Sayers I, Tobin MD, Maher TM, Cho MH, Hunninghake GM, Schwartz DA, Yaspan BL, Molyneaux PL, Flores C, Noth I, Jenkins RG, Wain LV. Genome-Wide Association Study of Susceptibility to Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2020, 201: 564-574. PMID: 31710517, PMCID: PMC7047454, DOI: 10.1164/rccm.201905-1017oc.Peer-Reviewed Original ResearchMeSH KeywordsAgedCase-Control StudiesCell Cycle ProteinsFemaleGene ExpressionGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansIdiopathic Pulmonary FibrosisIntracellular Signaling Peptides and ProteinsKinesinsMaleMiddle AgedRisk AssessmentSignal TransductionSpindle ApparatusTOR Serine-Threonine KinasesConceptsGenome-wide association studiesAssociation studiesIPF susceptibilityNew genome-wide significant signalsGenome-wide significant signalsGenome-wide analysisCell-cell adhesionLarge genome-wide association studiesImportance of mTORPolygenic risk score analysisTelomere maintenanceCausal genesFunctional analysisSusceptibility variantsRisk score analysisMultiple pathwaysGenetic associationGenesHost defensePolygenic risk scoresIndependent studiesPossible roleExpression associatesSignificant signalRecent studies
2019
BAL Cell Gene Expression in Severe Asthma Reveals Mechanisms of Severe Disease and Influences of Medications
Weathington N, O’Brien M, Radder J, Whisenant TC, Bleecker ER, Busse WW, Erzurum SC, Gaston B, Hastie A, Jarjour N, Meyers D, Milosevic J, Moore W, Tedrow J, Trudeau J, Wong H, Wu W, Kaminski N, Wenzel S, Modena B. BAL Cell Gene Expression in Severe Asthma Reveals Mechanisms of Severe Disease and Influences of Medications. American Journal Of Respiratory And Critical Care Medicine 2019, 200: 837-856. PMID: 31161938, PMCID: PMC6812436, DOI: 10.1164/rccm.201811-2221oc.Peer-Reviewed Original ResearchMeSH KeywordsAdrenergic beta-AgonistsAdultAsthmaBronchoalveolar Lavage FluidCase-Control StudiesCyclic AMPEosinophilsEpithelial CellsFemaleGene ExpressionHumansIn Vitro TechniquesLymphocytesMacrophages, AlveolarMaleNeutrophilsSequence Analysis, RNASeverity of Illness IndexSignal TransductionTHP-1 CellsConceptsCell gene expressionGene expressionAirway epithelial cell gene expressionEpithelial cell gene expressionGlobal gene expressionCellular gene expressionCell expression profilesAsthma susceptibility lociProtein levelsSystem-wide analysisExpression networksImportant disease mechanismCoexpression networkCellular milieuExpression changesExpression profilesSusceptibility lociCellular modelDisease mechanismsBiomolecular mechanismsNew targetsRobust upregulationSample traitsGenesExpressionPlasma mitochondrial DNA is associated with extrapulmonary sarcoidosis
Ryu C, Brandsdorfer C, Adams T, Hu B, Kelleher DW, Yaggi M, Manning EP, Walia A, Reeves B, Pan H, Winkler J, Minasyan M, Dela Cruz CS, Kaminski N, Gulati M, Herzog EL. Plasma mitochondrial DNA is associated with extrapulmonary sarcoidosis. European Respiratory Journal 2019, 54: 1801762. PMID: 31273041, PMCID: PMC8088542, DOI: 10.1183/13993003.01762-2018.Peer-Reviewed Original ResearchConceptsExtrapulmonary diseaseMitochondrial DNAExtracellular mtDNABAL fluidAlpha-1 antitrypsin deficiencyPlasma mitochondrial DNAPlasma of patientsAfrican AmericansExtrapulmonary sarcoidosisSarcoidosis cohortSarcoidosis subjectsScadding stageAfrican American descentClinical featuresClinical findingsGranulomatous diseaseHealthy controlsAntitrypsin deficiencyGenomic researchHigher oddsSarcoidosisAggressive phenotypeMechanistic basisDiseaseTherapeutic insights
2018
S100A12 as a marker of worse cardiac output and mortality in pulmonary hypertension
Tzouvelekis A, Herazo‐Maya J, Ryu C, Chu J, Zhang Y, Gibson KF, Adonteng‐Boateng P, Li Q, Pan H, Cherry B, Ahmad F, Ford HJ, Herzog EL, Kaminski N, Fares WH. S100A12 as a marker of worse cardiac output and mortality in pulmonary hypertension. Respirology 2018, 23: 771-779. PMID: 29611244, PMCID: PMC6047907, DOI: 10.1111/resp.13302.Peer-Reviewed Original ResearchConceptsPeripheral blood mononuclear cellsPH patientsPH cohortCardiac outputWorld Health Organization group 1Idiopathic pulmonary fibrosis patientsPulmonary hypertension patientsPulmonary fibrosis patientsBlood mononuclear cellsProtein serum concentrationsHigher S100A12Pulmonary hypertensionS100A12 levelsOverall mortalityHypertension patientsPrognostic valueValidation cohortMononuclear cellsPeripheral bloodSerum concentrationsInflammatory diseasesGroup 1PatientsFibrosis patientsS100A12
2017
Identification and validation of differentially expressed transcripts by RNA-sequencing of formalin-fixed, paraffin-embedded (FFPE) lung tissue from patients with Idiopathic Pulmonary Fibrosis
Vukmirovic M, Herazo-Maya JD, Blackmon J, Skodric-Trifunovic V, Jovanovic D, Pavlovic S, Stojsic J, Zeljkovic V, Yan X, Homer R, Stefanovic B, Kaminski N. Identification and validation of differentially expressed transcripts by RNA-sequencing of formalin-fixed, paraffin-embedded (FFPE) lung tissue from patients with Idiopathic Pulmonary Fibrosis. BMC Pulmonary Medicine 2017, 17: 15. PMID: 28081703, PMCID: PMC5228096, DOI: 10.1186/s12890-016-0356-4.Peer-Reviewed Original ResearchConceptsPaired-end sequencingTranscript profilingHuman genomeRNA sequencingTranscriptomic profilingFFPE lung tissuesSequencing readsLung tissueTotal RNABackgroundIdiopathic pulmonary fibrosisLethal lung diseaseSequencingReadsProfilingPulmonary fibrosisLung diseaseUnknown etiologyIPF tissueGenomeHiSeqTissueTopHat2GenesIPFRNA
2016
Validation of the prognostic value of MMP‐7 in idiopathic pulmonary fibrosis
Tzouvelekis A, Herazo‐Maya J, Slade M, Chu J, Deiuliis G, Ryu C, Li Q, Sakamoto K, Ibarra G, Pan H, Gulati M, Antin‐Ozerkis D, Herzog EL, Kaminski N. Validation of the prognostic value of MMP‐7 in idiopathic pulmonary fibrosis. Respirology 2016, 22: 486-493. PMID: 27761978, PMCID: PMC5352520, DOI: 10.1111/resp.12920.Peer-Reviewed Original ResearchConceptsTransplant-free survivalIdiopathic pulmonary fibrosisMMP-7 concentrationsMatrix metalloproteinase-7IPF patientsCause mortalityPulmonary fibrosisHealthy controlsMultivariate Cox proportional hazards modelCox proportional hazards modelPulmonary function parametersVariable clinical courseBaseline pulmonary function parametersProportional hazards modelIPF biomarkersProgressive diseaseClinical coursePoor prognosisPrognostic valueVital capacityIndependent biomarkerLung capacityPrognostic thresholdPlasma concentrationsMortality risk
2015
FK506-Binding Protein 10, a Potential Novel Drug Target for Idiopathic Pulmonary Fibrosis
Staab-Weijnitz CA, Fernandez IE, Knüppel L, Maul J, Heinzelmann K, Juan-Guardela BM, Hennen E, Preissler G, Winter H, Neurohr C, Hatz R, Lindner M, Behr J, Kaminski N, Eickelberg O. FK506-Binding Protein 10, a Potential Novel Drug Target for Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2015, 192: 455-467. PMID: 26039104, PMCID: PMC4595665, DOI: 10.1164/rccm.201412-2233oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPrimary human lung fibroblastsGrowth factor-β1Endoplasmic reticulum stressPulmonary fibrosisFKBP10 expressionLung fibrosisNovel drug targetsControl subjectsFactor-β1Protein 10Immunofluorescent stainingReticulum stressReverse transcriptase-polymerase chain reactionQuantitative reverse transcriptase-polymerase chain reactionTranscriptase-polymerase chain reactionSmooth muscle actinPotential novel drug targetsHuman lung fibroblastsCollagen secretionDrug targetsWestern blot analysisProfibrotic mediatorsU.S. cohortGerman cohorteQTL of bronchial epithelial cells and bronchial alveolar lavage deciphers GWAS‐identified asthma genes
Li X, Hastie AT, Hawkins GA, Moore WC, Ampleford EJ, Milosevic J, Li H, Busse WW, Erzurum SC, Kaminski N, Wenzel SE, Meyers DA, Bleecker ER. eQTL of bronchial epithelial cells and bronchial alveolar lavage deciphers GWAS‐identified asthma genes. Allergy 2015, 70: 1309-1318. PMID: 26119467, PMCID: PMC4583797, DOI: 10.1111/all.12683.Peer-Reviewed Original ResearchMeSH KeywordsAllelesAsthmaBronchoalveolar Lavage FluidCase-Control StudiesChromosome MappingEpithelial CellsFemaleGenetic Association StudiesGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansImmunoglobulin EMaleOrgan SpecificityPolymorphism, Single NucleotideQuantitative Trait LociRespiratory Function TestsRespiratory MucosaConceptsExpression quantitative trait lociGenome-wide association studiesSingle nucleotide polymorphismsAsthma genesQuantitative trait lociGenes/single-nucleotide polymorphismsCis-eQTL analysisFurther functional studiesDisease-relevant tissuesDecreased expressionTrait lociCausal genesTranscription analysisGene expressionPromoter regionAsthma-related genesAssociation studiesBronchial epithelial cellsProtein secretionGenesFunctional studiesNucleotide polymorphismsSpecific regulationExpression levelsExpression of IL33
2014
Gene Expression in Relation to Exhaled Nitric Oxide Identifies Novel Asthma Phenotypes with Unique Biomolecular Pathways
Modena BD, Tedrow JR, Milosevic J, Bleecker ER, Meyers DA, Wu W, Bar-Joseph Z, Erzurum SC, Gaston BM, Busse WW, Jarjour NN, Kaminski N, Wenzel SE. Gene Expression in Relation to Exhaled Nitric Oxide Identifies Novel Asthma Phenotypes with Unique Biomolecular Pathways. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 1363-1372. PMID: 25338189, PMCID: PMC4294630, DOI: 10.1164/rccm.201406-1099oc.Peer-Reviewed Original ResearchConceptsEpithelial cell gene expressionCell gene expressionGene expressionAirway epithelial cell gene expressionGene expression patternsSevere Asthma Research ProgramActin cytoskeletonGene clusterGenomic studiesGene transcriptionGene pathwaysMolecular basisExpression patternsAsthma phenotypesWnt pathwayMicroarray platformGenesNovel pathwayPhenotypeBiomolecular pathwaysNeuronal functionPathwayUnadjusted p-valuesExpressionBiological characteristicsRelationship of DNA Methylation and Gene Expression in Idiopathic Pulmonary Fibrosis
Yang IV, Pedersen BS, Rabinovich E, Hennessy CE, Davidson EJ, Murphy E, Guardela BJ, Tedrow JR, Zhang Y, Singh MK, Correll M, Schwarz MI, Geraci M, Sciurba FC, Quackenbush J, Spira A, Kaminski N, Schwartz DA. Relationship of DNA Methylation and Gene Expression in Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 1263-1272. PMID: 25333685, PMCID: PMC4315819, DOI: 10.1164/rccm.201408-1452oc.Peer-Reviewed Original ResearchConceptsGene expressionDNA methylationMethylation marksMethylation changesQuantitative trait lociTrans-gene expressionIntegrative genomic analysisTrait lociEpigenetic mechanismsTranscriptional changesGenomic analysisTranscription factorsCASZ1 expressionTarget genesFunctional validationExpression relationshipsMethylationGenesDMRsExpressionEnvironmental factorsTargeted analysisPathogenesis of IPFComplex interactionsTranscriptomeBlockade of the Programmed Death-1 Pathway Restores Sarcoidosis CD4+ T-Cell Proliferative Capacity
Braun NA, Celada LJ, Herazo-Maya JD, Abraham S, Shaginurova G, Sevin CM, Grutters J, Culver DA, Dworski R, Sheller J, Massion PP, Polosukhin VV, Johnson JE, Kaminski N, Wilkes DS, Oswald-Richter KA, Drake WP. Blockade of the Programmed Death-1 Pathway Restores Sarcoidosis CD4+ T-Cell Proliferative Capacity. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 560-571. PMID: 25073001, PMCID: PMC4214083, DOI: 10.1164/rccm.201401-0188oc.Peer-Reviewed Original ResearchConceptsPD-1 pathway blockadeT cell proliferative capacityPeripheral blood mononuclear cellsPD-L1 expressionPD-1 pathwayBlood mononuclear cellsT cell functionPathway blockadePD-L1Clinical outcomesLung diseaseMononuclear cellsControl subjectsProliferative capacityT cellsImmunohistochemistry analysisPD-1/PD-L1 expressionControl peripheral blood mononuclear cellsHealthy control peripheral blood mononuclear cellsHealthy control lungsIdiopathic lung diseaseSpontaneous clinical resolutionChronic lung diseaseHealthy control subjectsEffective therapeutic interventionsC-X-C Motif Chemokine 13 (CXCL13) Is a Prognostic Biomarker of Idiopathic Pulmonary Fibrosis
Vuga LJ, Tedrow JR, Pandit KV, Tan J, Kass DJ, Xue J, Chandra D, Leader JK, Gibson KF, Kaminski N, Sciurba FC, Duncan SR. C-X-C Motif Chemokine 13 (CXCL13) Is a Prognostic Biomarker of Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2014, 189: 966-974. PMID: 24628285, PMCID: PMC4098096, DOI: 10.1164/rccm.201309-1592oc.Peer-Reviewed Original ResearchMeSH KeywordsAgedAged, 80 and overBiomarkersCase-Control StudiesChemokine CXCL13Disease ProgressionEnzyme-Linked Immunosorbent AssayFemaleHumansIdiopathic Pulmonary FibrosisImmunohistochemistryMaleMiddle AgedOligonucleotide Array Sequence AnalysisPredictive Value of TestsPrognosisPulmonary Disease, Chronic ObstructiveRisk FactorsSensitivity and SpecificitySeverity of Illness IndexConceptsChronic obstructive pulmonary diseaseC motif chemokine 13IPF lungsPrognostic biomarkerB cellsIdiopathic pulmonary fibrosis (IPF) pathogenesisB cell-targeted therapiesAntibody-mediated syndromeDysregulated B cellsPulmonary fibrosis pathogenesisPulmonary artery hypertensionObstructive pulmonary diseaseIdiopathic pulmonary fibrosisSix-month survivalB-cell traffickingAcute exacerbationArtery hypertensionCXCL13 mRNAPlasma CXCL13IPF pathogenesisRespiratory failureLung injuryCXCL13 concentrationsPulmonary diseaseRadiographic emphysema
2013
Genome-wide association study identifies multiple susceptibility loci for pulmonary fibrosis
Fingerlin TE, Murphy E, Zhang W, Peljto AL, Brown KK, Steele MP, Loyd JE, Cosgrove GP, Lynch D, Groshong S, Collard HR, Wolters PJ, Bradford WZ, Kossen K, Seiwert SD, du Bois RM, Garcia CK, Devine MS, Gudmundsson G, Isaksson HJ, Kaminski N, Zhang Y, Gibson KF, Lancaster LH, Cogan JD, Mason WR, Maher TM, Molyneaux PL, Wells AU, Moffatt MF, Selman M, Pardo A, Kim DS, Crapo JD, Make BJ, Regan EA, Walek DS, Daniel JJ, Kamatani Y, Zelenika D, Smith K, McKean D, Pedersen BS, Talbert J, Kidd RN, Markin CR, Beckman KB, Lathrop M, Schwarz MI, Schwartz DA. Genome-wide association study identifies multiple susceptibility loci for pulmonary fibrosis. Nature Genetics 2013, 45: 613-620. PMID: 23583980, PMCID: PMC3677861, DOI: 10.1038/ng.2609.Peer-Reviewed Original Research
2012
Profibrotic Role of miR-154 in Pulmonary Fibrosis
Milosevic J, Pandit K, Magister M, Rabinovich E, Ellwanger DC, Yu G, Vuga LJ, Weksler B, Benos PV, Gibson KF, McMillan M, Kahn M, Kaminski N. Profibrotic Role of miR-154 in Pulmonary Fibrosis. American Journal Of Respiratory Cell And Molecular Biology 2012, 47: 879-887. PMID: 23043088, PMCID: PMC3547095, DOI: 10.1165/rcmb.2011-0377oc.Peer-Reviewed Original ResearchMeSH KeywordsCase-Control StudiesCell MovementCell ProliferationCells, CulturedChromosomes, Human, Pair 14Cyclin-Dependent Kinase Inhibitor p15FibroblastsGene ExpressionHumansLungMicroRNAsMultigene FamilyOligonucleotide Array Sequence AnalysisPulmonary FibrosisRNA InterferenceTranscriptomeTransforming Growth Factor beta1Wnt Signaling PathwayConceptsIdiopathic pulmonary fibrosisNormal human lung fibroblastsMiR-154IPF lungsPulmonary fibrosisIPF fibroblastsProgressive interstitial lung diseaseInterstitial lung diseaseWnt/β-catenin pathwayHuman lung fibroblastsΒ-catenin pathwayTGF-β1 stimulationBinding of Smad3Quantitative RT-PCRLung diseaseProfibrotic roleExpression of microRNAsICG-001MiR-134Unknown originMiR-382MiR-487bProliferative effectLung fibroblastsMiR-410
2011
A Variant in the Promoter of MUC5B and Idiopathic Pulmonary Fibrosis
Zhang Y, Noth I, Garcia JG, Kaminski N. A Variant in the Promoter of MUC5B and Idiopathic Pulmonary Fibrosis. New England Journal Of Medicine 2011, 364: 1576-1577. PMID: 21506748, PMCID: PMC4327944, DOI: 10.1056/nejmc1013504.Peer-Reviewed Original ResearchMeSH KeywordsAgedCase-Control StudiesFemaleHumansIdiopathic Pulmonary FibrosisMaleMiddle AgedMucin-5BPolymorphism, Single NucleotideThe HLA Class II Allele DRB1*1501 Is Over-Represented in Patients with Idiopathic Pulmonary Fibrosis
Xue J, Gochuico BR, Alawad AS, Feghali-Bostwick CA, Noth I, Nathan SD, Rosen GD, Rosas IO, Dacic S, Ocak I, Fuhrman CR, Cuenco KT, Smith MA, Jacobs SS, Zeevi A, Morel PA, Pilewski JM, Valentine VG, Gibson KF, Kaminski N, Sciurba FC, Zhang Y, Duncan SR. The HLA Class II Allele DRB1*1501 Is Over-Represented in Patients with Idiopathic Pulmonary Fibrosis. PLOS ONE 2011, 6: e14715. PMID: 21373184, PMCID: PMC3044131, DOI: 10.1371/journal.pone.0014715.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisIPF patientsIPF subjectsAmbulatory patientsPulmonary fibrosisLung diseaseHLA-DRB1Normal subjectsEtiology of IPFHuman leukocyte antigen (HLA) allele frequenciesManifestations of IPFAbnormal adaptive immune responsesLung transplantation recipientsHLA class IIAdaptive immune responsesU.S. medical centersHLA-DR locusNormal reference populationDistinct clinical phenotypesRefractory lung diseaseSpecific HLA-DRB1Lung transplantationTransplant recipientsTransplantation recipientsGrim prognosis