2011
RIG-like Helicase Innate Immunity Inhibits Vascular Endothelial Growth Factor Tissue Responses via a Type I IFN–dependent Mechanism
Ma B, Dela Cruz CS, Hartl D, Kang MJ, Takyar S, Homer RJ, Lee CG, Elias JA. RIG-like Helicase Innate Immunity Inhibits Vascular Endothelial Growth Factor Tissue Responses via a Type I IFN–dependent Mechanism. American Journal Of Respiratory And Critical Care Medicine 2011, 183: 1322-1335. PMID: 21278304, PMCID: PMC3114061, DOI: 10.1164/rccm.201008-1276oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDEAD Box Protein 58DEAD-box RNA HelicasesDisease Models, AnimalEdemaFocal Adhesion Protein-Tyrosine KinasesImmunity, InnateInflammationInterferon Type IMiceMice, TransgenicMitogen-Activated Protein KinasesNitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasePoly I-CPulmonary Disease, Chronic ObstructiveToll-Like Receptor 3Vascular Endothelial Growth Factor AConceptsVascular endothelial growth factorType 2 inflammationChronic obstructive pulmonary disease exacerbationsObstructive pulmonary disease exacerbationsChronic obstructive pulmonary diseaseViral pathogen-associated molecular patternsEndothelial nitric oxide synthaseRIG-like helicasePulmonary disease exacerbationsObstructive pulmonary diseasePathogenesis of asthmaRespiratory syncytial virusNormal pulmonary physiologyNitric oxide synthaseAntiviral innate immunityPathogen-associated molecular patternsReceptor-dependent pathwayTissue responseEndothelial growth factorVEGF receptor 1Ability of VEGFDisease exacerbationPulmonary diseaseRespiratory virusesControl mice
2010
Transgenic modelling of cytokine polarization in the lung
Dela Cruz CS, Kang M, Cho W, Lee CG. Transgenic modelling of cytokine polarization in the lung. Immunology 2010, 132: 9-17. PMID: 21091906, PMCID: PMC3015070, DOI: 10.1111/j.1365-2567.2010.03376.x.Peer-Reviewed Original ResearchConceptsCytokine polarizationT helper type 17 cytokinesT helper type 2T helper type 1Type 1Type 17 cytokinesHelper type 2Type 2 cytokinesHelper type 1Human lung diseasesVariety of cytokinesCytokine milieuPulmonary inflammationEnvironmental allergensLung diseaseTissue phenotypeInjury modelT-betCommon siteCertain cytokinesEffector functionsTransgenic miceIndividual cytokinesPathophysiological consequencesType 2Role of Breast Regression Protein–39 in the Pathogenesis of Cigarette Smoke–Induced Inflammation and Emphysema
Matsuura H, Hartl D, Kang MJ, Dela Cruz CS, Koller B, Chupp GL, Homer RJ, Zhou Y, Cho WK, Elias JA, Lee CG. Role of Breast Regression Protein–39 in the Pathogenesis of Cigarette Smoke–Induced Inflammation and Emphysema. American Journal Of Respiratory Cell And Molecular Biology 2010, 44: 777-786. PMID: 20656949, PMCID: PMC3135840, DOI: 10.1165/rcmb.2010-0081oc.Peer-Reviewed Original ResearchConceptsChronic obstructive pulmonary diseaseBRP-39/YKLBreast regression protein 39YKL-40BRP-39Alveolar destructionCigarette smokeChitinase-like protein YKL-40Emphysematous alveolar destructionLungs of CSObstructive pulmonary diseaseProtein YKL-40Excessive inflammatory responseAirway epithelial cellsAlveolar type II cellsNull mutant miceProtein 39Epithelial cell apoptosisType II cellsCurrent smokersPulmonary diseaseBronchoalveolar lavageTissue inflammationEmphysematous destructionSerum concentrations