2016
SH2 Domain–Containing Phosphatase-2 Is a Novel Antifibrotic Regulator in Pulmonary Fibrosis
Tzouvelekis A, Yu G, Lino Cardenas CL, Herazo-Maya JD, Wang R, Woolard T, Zhang Y, Sakamoto K, Lee H, Yi JS, DeIuliis G, Xylourgidis N, Ahangari F, Lee PJ, Aidinis V, Herzog EL, Homer R, Bennett AM, Kaminski N. SH2 Domain–Containing Phosphatase-2 Is a Novel Antifibrotic Regulator in Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2016, 195: 500-514. PMID: 27736153, PMCID: PMC5378419, DOI: 10.1164/rccm.201602-0329oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisProfibrotic stimuliLung fibroblastsChronic fatal lung diseaseMyofibroblast differentiationPrimary human lung fibroblastsFatal lung diseaseNovel therapeutic strategiesVivo therapeutic effectPotential therapeutic usefulnessHuman lung fibroblastsMouse lung fibroblastsDismal prognosisFibroblastic fociLung fibrosisLung diseaseBleomycin modelTherapeutic effectTherapeutic usefulnessTherapeutic strategiesTherapeutic targetTransgenic miceFibrosisSHP2 overexpression
2004
The C10/CCL6 Chemokine and CCR1 Play Critical Roles in the Pathogenesis of IL-13-Induced Inflammation and Remodeling
Ma B, Zhu Z, Homer RJ, Gerard C, Strieter R, Elias JA. The C10/CCL6 Chemokine and CCR1 Play Critical Roles in the Pathogenesis of IL-13-Induced Inflammation and Remodeling. The Journal Of Immunology 2004, 172: 1872-1881. PMID: 14734772, DOI: 10.4049/jimmunol.172.3.1872.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCathepsinsChemokine CCL2Chemokines, CCDown-RegulationImmune SeraInflammationInterleukin-13LungLung ComplianceLung Volume MeasurementsMatrix Metalloproteinase 2Matrix Metalloproteinase 9MiceMice, Inbred C57BLMice, KnockoutMice, TransgenicProtease InhibitorsPulmonary AlveoliReceptors, CCR1Receptors, ChemokineUp-RegulationConceptsIL-13-induced inflammationMatrix metalloproteinase-2IL-13Potent stimulatorMMP-9Alveolar remodelingMonocyte chemoattractant protein-1Transgenic IL-13Inflammatory protein-1alphaChemoattractant protein-1Wild-type miceIL-13 stimulationPulmonary phenotypeLevels of mRNAMetalloproteinase-4Murine lungMetalloproteinase-2Tissue inhibitorInflammationTargeted null mutationCompliance alterationsPathogenesisCCL6ChemokinesProtein 1
2001
IL-4 Promotes Airway Eosinophilia by Suppressing IFN-γ Production: Defining a Novel Role for IFN-γ in the Regulation of Allergic Airway Inflammation
Cohn L, Herrick C, Niu N, Homer R, Bottomly K. IL-4 Promotes Airway Eosinophilia by Suppressing IFN-γ Production: Defining a Novel Role for IFN-γ in the Regulation of Allergic Airway Inflammation. The Journal Of Immunology 2001, 166: 2760-2767. PMID: 11160342, DOI: 10.4049/jimmunol.166.4.2760.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, CutaneousAdministration, IntranasalAdoptive TransferAnimalsBone Marrow CellsBone Marrow TransplantationBronchiCell MovementDown-RegulationEosinophilsFemaleHematopoietic Stem CellsInflammationInterferon-gammaInterleukin-13Interleukin-4Interleukin-5MaleMiceMice, Inbred BALB CMice, KnockoutMice, TransgenicOvalbuminPulmonary EosinophiliaReceptors, InterferonRespiratory HypersensitivityTh2 CellsUp-RegulationConceptsAirway eosinophiliaIL-4IFN-gammaTh2 cellsAirway eosinophilsIL-5Allergic airway inflammationIFN-γ productionTh2 cell generationAirway inflammationEosinophilic inflammationLung eosinophiliaLung parenchymalTh2 cytokinesIntranasal administrationRespiratory tractLung tissueCounterregulatory effectsEosinophiliaCell transferEosinophilsHemopoietic cellsInflammationAirwayIFN