2024
Chitinase 3-like-1 Inhibits Innate Antitumor and Tissue Remodeling Immune Responses by Regulating CD47-SIRPα- and CD24-Siglec10-Mediated Phagocytosis.
Ma B, Kamle S, Sadanaga T, Lee C, Lee J, Yee D, Zhu Z, Silverman E, DeMeo D, Choi A, Lee C, Elias J. Chitinase 3-like-1 Inhibits Innate Antitumor and Tissue Remodeling Immune Responses by Regulating CD47-SIRPα- and CD24-Siglec10-Mediated Phagocytosis. The Journal Of Immunology 2024, 213: 1279-1291. PMID: 39291933, DOI: 10.4049/jimmunol.2400035.Peer-Reviewed Original ResearchImmune checkpoint moleculesChronic obstructive pulmonary diseaseInhibit adaptive immune responsesAdaptive immune responsesInnate immune responseImmune responseInhibition of innate immune responsesInhibits T cell costimulationGeneration of adaptive immune responsesMacrophage phagocytosisInhibit innate immune responsesChitinase 3-like 1T cell costimulationEpithelial cell deathObstructive pulmonary diseaseCheckpoint moleculesPoor prognosisLung injuryInhibit macrophagesPulmonary diseaseCHI3L1Inflammation pathwaysCancerSHP-2 phosphataseCell deathRetraction: Chitinase 1 regulates pulmonary fibrosis by modulating TGF-β/SMAD7 pathway via TGFBRAP1 and FOXO3
Lee C, He C, Park J, Lee J, Kamle S, Ma B, Akosman B, Cortez R, Chen E, Zhou Y, Herzog E, Ryu C, Peng X, Rosas I, Poli S, Bostwick C, Choi A, Elias J, Lee C. Retraction: Chitinase 1 regulates pulmonary fibrosis by modulating TGF-β/SMAD7 pathway via TGFBRAP1 and FOXO3. Life Science Alliance 2024, 7: e202402987. PMID: 39209538, PMCID: PMC11361373, DOI: 10.26508/lsa.202402987.Peer-Reviewed Original ResearchChitinase 3-like-1 (CHI3L1) in the pathogenesis of epidermal growth factor receptor mutant non-small cell lung cancer
Kamle S, Ma B, Schor G, Bailey M, Pham B, Cho I, Khan H, Azzoli C, Hofstetter M, Sadanaga T, Herbst R, Politi K, Lee C, Elias J. Chitinase 3-like-1 (CHI3L1) in the pathogenesis of epidermal growth factor receptor mutant non-small cell lung cancer. Translational Oncology 2024, 49: 102108. PMID: 39178575, PMCID: PMC11388375, DOI: 10.1016/j.tranon.2024.102108.Peer-Reviewed Original ResearchNon-small cell lung cancerEpidermal growth factor receptorTyrosine kinase inhibitorsEpidermal growth factor receptor mutant non-small cell lung cancerMutant non-small cell lung cancerEpidermal growth factor receptor axisCell lung cancerLung cancerTherapeutic resistanceDownstream targets of EGFRResistance to TKI therapyEpithelial cellsStimulated epidermal growth factor receptorWild type epidermal growth factor receptorTargeting of epidermal growth factor receptorActivating EGFR mutationsChitinase 3-like 1Progression free survivalInduce tumor cell deathEpidermal growth factor receptor activationEffects of EGFR activationInhibited pulmonary metastasisTumor cell deathResponse to treatmentGrowth factor receptorSuccinate dehydrogenase–complex II regulates skeletal muscle cellular respiration and contractility but not muscle mass in genetically induced pulmonary emphysema
Balnis J, Tufts A, Jackson E, Drake L, Singer D, Lacomis D, Lee C, Elias J, Doles J, Maher L, Jen A, Coon J, Jourd’heuil D, Singer H, Vincent C, Jaitovich A. Succinate dehydrogenase–complex II regulates skeletal muscle cellular respiration and contractility but not muscle mass in genetically induced pulmonary emphysema. Science Advances 2024, 10: eado8549. PMID: 39167644, PMCID: PMC11338223, DOI: 10.1126/sciadv.ado8549.Peer-Reviewed Original ResearchConceptsPulmonary emphysemaMuscle massSuccinate dehydrogenaseReduced skeletal muscle massAssociated with high mortalityCellular respirationSkeletal muscle massReduced cellular respirationKnockout miceMuscle dysfunctionActivity of succinate dehydrogenaseComplex I respirationMitochondrial oxygen consumptionMyopathic changesTransgenic miceSubunit cMuscle atrophyProteomic effectsMyofiber contractilityRespirometry analysisSuccinate accumulationMuscle mitochondriaEmphysemaHigher mortalityAnimal dataAlveolar Type 2 Cells With Impaired Proteostasis Signal to Monocyte-derived Macrophages Via a MIF/DDT-CD74 Signaling Network to Promotes Pulmonary Fibrosis in IPF
Kim S, Nouws J, Cooley J, Ahangari F, Leng L, Elias J, Kaminski N, Lee P, Redente E, Kang M, Sun H, Herzog E, Bucala R, Prasse A, Sauler M. Alveolar Type 2 Cells With Impaired Proteostasis Signal to Monocyte-derived Macrophages Via a MIF/DDT-CD74 Signaling Network to Promotes Pulmonary Fibrosis in IPF. 2024, a3001-a3001. DOI: 10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a3001.Peer-Reviewed Original Research
2023
The tumor-derived cytokine Chi3l1 induces neutrophil extracellular traps that promote T cell exclusion in triple-negative breast cancer
Taifour T, Attalla S, Zuo D, Gu Y, Sanguin-Gendreau V, Proud H, Solymoss E, Bui T, Kuasne H, Papavasiliou V, Lee C, Kamle S, Siegel P, Elias J, Park M, Muller W. The tumor-derived cytokine Chi3l1 induces neutrophil extracellular traps that promote T cell exclusion in triple-negative breast cancer. Immunity 2023, 56: 2755-2772.e8. PMID: 38039967, DOI: 10.1016/j.immuni.2023.11.002.Peer-Reviewed Original ResearchTriple-negative breast cancerImmune checkpoint blockadeBreast cancerAnti-tumor immune responseHuman triple-negative breast cancerNeutrophil extracellular trap formationT cell exclusionAnti-tumor immunityPoor clinical outcomeImmunosuppressive tumor microenvironmentMammary tumor onsetNeutrophil extracellular trapsExtracellular trap formationBreast cancer modelMurine breast tumorsClinical outcomesNeutrophil recruitmentCell infiltrationCHI3L1 expressionTumor infiltrationExtracellular trapsTranscription factor STAT3Immune responseLack of responsivenessSolid tumors
2009
Role of breast regression protein 39 (BRP-39)/chitinase 3-like-1 in Th2 and IL-13–induced tissue responses and apoptosis
Lee CG, Hartl D, Lee GR, Koller B, Matsuura H, Da Silva CA, Sohn MH, Cohn L, Homer RJ, Kozhich AA, Humbles A, Kearley J, Coyle A, Chupp G, Reed J, Flavell RA, Elias JA. Role of breast regression protein 39 (BRP-39)/chitinase 3-like-1 in Th2 and IL-13–induced tissue responses and apoptosis. Journal Of Experimental Medicine 2009, 206: 1149-1166. PMID: 19414556, PMCID: PMC2715037, DOI: 10.1084/jem.20081271.Peer-Reviewed Original ResearchConceptsBRP-39/YKLBreast regression protein 39YKL-40BRP-39Th2 responsesIL-13-induced tissue responsesDendritic cell accumulationAlternative macrophage activationApoptosis/cell deathProtein 39Protein kinase B/AktTh2 inflammationDisease activityAntigen sensitizationEffector phaseTissue inflammationExaggerated quantitiesPulmonary epitheliumTherapeutic targetMacrophage activationTransgenic miceCell accumulationFas expressionNovel regulatory roleMiceAcidic Mammalian Chitinase Regulates Epithelial Cell Apoptosis via a Chitinolytic-Independent Mechanism
Hartl D, He CH, Koller B, Da Silva CA, Kobayashi Y, Lee CG, Flavell RA, Elias JA. Acidic Mammalian Chitinase Regulates Epithelial Cell Apoptosis via a Chitinolytic-Independent Mechanism. The Journal Of Immunology 2009, 182: 5098-5106. PMID: 19342690, PMCID: PMC2666938, DOI: 10.4049/jimmunol.0803446.Peer-Reviewed Original ResearchConceptsAcidic mammalian chitinaseTh2-mediated diseasesEpithelial cellsMammalian chitinasePI3K/Akt pathwayPulmonary epithelial cellsEpithelial cell apoptosisApoptosis-inhibiting effectsComparable cytoprotectionGrowth factor withdrawal-induced apoptosisChitinolytic activityEffector responsesParacrine mannerFas ligand-induced apoptosisAntiparasite responsesGrowth factor withdrawalWithdrawal-induced apoptosisLigand-induced apoptosisFas ligandAkt pathwayCell apoptosisAkt phosphorylationAMCaseBiologic propertiesCytoprotection
2008
Cigarette smoke selectively enhances viral PAMP– and virus-induced pulmonary innate immune and remodeling responses in mice
Kang MJ, Lee CG, Lee JY, Dela Cruz CS, Chen ZJ, Enelow R, Elias JA. Cigarette smoke selectively enhances viral PAMP– and virus-induced pulmonary innate immune and remodeling responses in mice. Journal Of Clinical Investigation 2008, 118: 2771-2784. PMID: 18654661, PMCID: PMC2483678, DOI: 10.1172/jci32709.Peer-Reviewed Original ResearchConceptsChronic obstructive pulmonary diseaseMitochondrial antiviral signaling proteinCigarette smokeDisease exacerbationIFN-gammaInnate immunityViral PAMPsEffects of CSIL-12/ILSevere disease exacerbationsObstructive pulmonary diseaseEffects of influenzaType I IFNAirway fibrosisAirway inflammationLung functionPulmonary diseasePulmonary inflammationIL-18IL-18RalphaI IFNMurine lungViral infectionInflammationRNA-dependent protein kinase
2007
A Chitinase-like Protein in the Lung and Circulation of Patients with Severe Asthma
Chupp GL, Lee CG, Jarjour N, Shim YM, Holm CT, He S, Dziura JD, Reed J, Coyle AJ, Kiener P, Cullen M, Grandsaigne M, Dombret MC, Aubier M, Pretolani M, Elias JA. A Chitinase-like Protein in the Lung and Circulation of Patients with Severe Asthma. New England Journal Of Medicine 2007, 357: 2016-2027. PMID: 18003958, DOI: 10.1056/nejmoa073600.Peer-Reviewed Original ResearchConceptsSerum YKL-40 levelsYKL-40 levelsSeverity of asthmaYKL-40Chitinase-like proteinsParis cohortOral corticosteroid useCohort of patientsRescue inhaler useSubgroup of patientsCirculation of patientsCorticosteroid useSevere asthmaAirway remodelingClinical characteristicsExpiratory volumeAcidic mammalian chitinasePatient populationHigh serumAsthmaImmunohistochemical analysisPatientsAnimal modelsLocus of expressionMorphometric quantitationSemaphorin 7A plays a critical role in TGF-β1–induced pulmonary fibrosis
Kang HR, Lee CG, Homer RJ, Elias JA. Semaphorin 7A plays a critical role in TGF-β1–induced pulmonary fibrosis. Journal Of Experimental Medicine 2007, 204: 1083-1093. PMID: 17485510, PMCID: PMC2118575, DOI: 10.1084/jem.20061273.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsAntigens, CDApoptosisCollagenDNA DamageImmunoblottingImmunohistochemistryIn Situ HybridizationIn Situ Nick-End LabelingIntegrin beta1MiceMice, TransgenicNerve Tissue ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPulmonary AlveoliPulmonary FibrosisReceptors, Cell SurfaceReverse Transcriptase Polymerase Chain ReactionSemaphorinsTransforming Growth Factor beta1ConceptsProtein kinase BSEMA 7APKB/Akt inhibitionAkt-dependent pathwayCritical roleSemaphorin 7ACCN proteinsFibroblast growth factor-2Kinase BCritical regulatorApoptosis regulatorMatrix proteinsGrowth factor 2Akt inhibitionBeta1 integrinReceptor componentsTissue remodelingFactor 2Fibrotic stimuliSmad 2/3Myofibroblast hyperplasiaGrowth factorRegulatorCentral roleProtein
2003
Adenosine mediates IL-13–induced inflammation and remodeling in the lung and interacts in an IL-13–adenosine amplification pathway
Blackburn MR, Lee CG, Young HW, Zhu Z, Chunn JL, Kang MJ, Banerjee SK, Elias JA. Adenosine mediates IL-13–induced inflammation and remodeling in the lung and interacts in an IL-13–adenosine amplification pathway. Journal Of Clinical Investigation 2003, 112: 332-344. PMID: 12897202, PMCID: PMC166289, DOI: 10.1172/jci16815.Peer-Reviewed Original ResearchConceptsIL-13-induced inflammationIL-13Adenosine receptorsAdenosine accumulationIL-13-induced tissue responsesADA enzyme therapyIL-13 overexpressionTh2-mediated disordersIL-13-induced increaseAmplification pathwayAdenosine deaminase activityLevels of adenosineA2A adenosine receptorsAlveolar destructionRespiratory failureMurine lungEnzyme therapyADA activityRemodeling responseImportant mediatorInflammationLungReceptorsProgressive increaseTissue responseCytokine regulation of IL-13Rα2 and IL-13Rα1 in vivo and in vitro
Zheng T, Zhu Z, Liu W, Lee CG, Chen Q, Homer RJ, Elias JA. Cytokine regulation of IL-13Rα2 and IL-13Rα1 in vivo and in vitro. Journal Of Allergy And Clinical Immunology 2003, 111: 720-728. PMID: 12704349, DOI: 10.1067/mai.2003.1383.Peer-Reviewed Original ResearchConceptsIL-13Ralpha1 mRNAIL-13IL-13Ralpha2IL-13Ralpha1IL-4IFN-gammaRegulatory eventsTransgenic IL-13Epithelial cellsIL-13 responsesMRNA accumulationAirway epithelial cellsSites of inflammationIL-13 signalsIL-13 stimulationHigh-affinity receptorIL-10Lung fragmentsControl miceOverexpression miceIL-13Rα2Cytokine regulationIL-4RalphaIL-13Rα1Receptor subunits