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
1996
Targeted expression of IL-11 in the murine airway causes lymphocytic inflammation, bronchial remodeling, and airways obstruction.
Tang W, Geba GP, Zheng T, Ray P, Homer RJ, Kuhn C, Flavell RA, Elias JA. Targeted expression of IL-11 in the murine airway causes lymphocytic inflammation, bronchial remodeling, and airways obstruction. Journal Of Clinical Investigation 1996, 98: 2845-2853. PMID: 8981933, PMCID: PMC507752, DOI: 10.1172/jci119113.Peer-Reviewed Original ResearchMeSH KeywordsAirway ObstructionAirway ResistanceAnimalsBlotting, NorthernBlotting, SouthernCloning, MolecularDisease Models, AnimalGene Expression RegulationHistocytochemistryImmunohistochemistryInterleukin-11LungMethacholine ChlorideMiceMice, TransgenicMicroscopy, ElectronPromoter Regions, GeneticProteinsPulmonary FibrosisUteroglobinConceptsIL-11Fibrotic responseTransgene miceAlpha-smooth muscle actinMononuclear cell infiltratePotential effector functionsSmooth muscle actinTargeted expressionSmooth muscle cellsHuman airway disordersType IIILung stromal cellsAirway disordersLymphocytic inflammationCell infiltrateSubepithelial fibrosisAirway resistanceRespiratory virusesMouse airwaysMurine airwaysInflammatory fociPhysiologic evaluationInflammatory responseBronchial remodelingMHC class