2019
Tumor regression mediated by oncogene withdrawal or erlotinib stimulates infiltration of inflammatory immune cells in EGFR mutant lung tumors
Ayeni D, Miller B, Kuhlmann A, Ho PC, Robles-Oteiza C, Gaefele M, Levy S, de Miguel FJ, Perry C, Guan T, Krystal G, Lockwood W, Zelterman D, Homer R, Liu Z, Kaech S, Politi K. Tumor regression mediated by oncogene withdrawal or erlotinib stimulates infiltration of inflammatory immune cells in EGFR mutant lung tumors. Journal For ImmunoTherapy Of Cancer 2019, 7: 172. PMID: 31291990, PMCID: PMC6617639, DOI: 10.1186/s40425-019-0643-8.Peer-Reviewed Original ResearchConceptsTyrosine kinase inhibitorsEGFR-mutant lung cancerMutant lung cancerTumor regressionErlotinib treatmentLung cancerImmune cellsLung tumorsMouse modelEffects of TKIsGrowth factor receptor tyrosine kinase inhibitorsTumor-infiltrating immune cellsDrug resistanceReceptor tyrosine kinase inhibitorsInflammatory immune cellsInflammatory T cellsEffect of erlotinibEGFR mutant lung tumorsInflammatory cellsImmunological profileT cellsCD40 agonistsImmunostimulatory effectsAlveolar macrophagesErlotinib
2014
IL-6 Receptor α Defines Effector Memory CD8+ T Cells Producing Th2 Cytokines and Expanding in Asthma
Lee N, You S, Shin MS, Lee WW, Kang KS, Kim SH, Kim WU, Homer RJ, Kang MJ, Montgomery RR, Dela Cruz CS, Shaw AC, Lee PJ, Chupp GL, Hwang D, Kang I. IL-6 Receptor α Defines Effector Memory CD8+ T Cells Producing Th2 Cytokines and Expanding in Asthma. American Journal Of Respiratory And Critical Care Medicine 2014, 190: 1383-1394. PMID: 25390970, PMCID: PMC4299645, DOI: 10.1164/rccm.201403-0601oc.Peer-Reviewed Original ResearchConceptsEffector memory CD8EM CD8T cellsPeripheral bloodMemory CD8IL-13IL-5IL-6RαTh2-type cytokine IL-5Different T cell subsetsLevels of GATA3Frequency of ILT cell subsetsTh2-type cytokinesHealthy control subjectsRespiratory syncytial virusT cell populationsCytokines IL-5IL-6 receptor αIL-6Rα expressionHuman peripheral bloodEffector CD8Syncytial virusTh2 cytokinesCell subsetsAn ENU-induced splicing mutation reveals a role for Unc93b1 in early immune cell activation following influenza A H1N1 infection
Lafferty EI, Flaczyk A, Angers I, Homer R, d'Hennezel E, Malo D, Piccirillo CA, Vidal SM, Qureshi ST. An ENU-induced splicing mutation reveals a role for Unc93b1 in early immune cell activation following influenza A H1N1 infection. Genes & Immunity 2014, 15: 320-332. PMID: 24848930, PMCID: PMC4978536, DOI: 10.1038/gene.2014.22.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingAnimalsCD8-Positive T-LymphocytesChemokine CXCL10EndosomesEthylnitrosoureaImmunity, InnateInfluenza A Virus, H1N1 SubtypeInterferon Type IInterferon-gammaL-SelectinLungLymphocyte ActivationMacrophage ActivationMembrane Transport ProteinsMiceMice, Inbred C57BLMutationOrthomyxoviridae InfectionsToll-Like ReceptorsConceptsEndosomal TLRsImmune responseEndosomal Toll-like receptorsInfluenza A/PR/8/34Expression of CXCL10Toll-like receptorsImmune cell activationCD69 activation markerInnate immune responseHuman infectious diseasesViral clearanceActivation markersInfected lungsRespiratory pathogensTLR responsesT cellsLymphoid cellsCell activationTissue pathologyInfectious diseasesMouse strainsInfectionExudate macrophagesReduced expressionUNC93B1CD4+CD25+FoxP3+ Regulatory Tregs inhibit fibrocyte recruitment and fibrosis via suppression of FGF-9 production in the TGF-β1 exposed murine lung
Peng X, Moore MW, Peng H, Sun H, Gan Y, Homer RJ, Herzog EL. CD4+CD25+FoxP3+ Regulatory Tregs inhibit fibrocyte recruitment and fibrosis via suppression of FGF-9 production in the TGF-β1 exposed murine lung. Frontiers In Pharmacology 2014, 5: 80. PMID: 24904415, PMCID: PMC4032896, DOI: 10.3389/fphar.2014.00080.Peer-Reviewed Original ResearchTGF-β1Lung fibrosisDepletion of TregsRole of TregsRegulatory T cellsMurine lung fibrosisHuman TGF-β1 geneFibroblast growth factor 9TGF-β1 signalingTGF-β1 geneGrowth factor 9Model of fibrosisRegulatory TregTreg quantityCD25 antibodyDoxycycline-inducible overexpressionPulmonary fibrosisNaïve CD4Fibrocyte recruitmentIL-1αFGF-9 expressionLung parenchymaT cellsTregsFibrocyte accumulation
2012
Semaphorin 7a+ Regulatory T Cells Are Associated with Progressive Idiopathic Pulmonary Fibrosis and Are Implicated in Transforming Growth Factor-β1–induced Pulmonary Fibrosis
Reilkoff RA, Peng H, Murray LA, Peng X, Russell T, Montgomery R, Feghali-Bostwick C, Shaw A, Homer RJ, Gulati M, Mathur A, Elias JA, Herzog EL. Semaphorin 7a+ Regulatory T Cells Are Associated with Progressive Idiopathic Pulmonary Fibrosis and Are Implicated in Transforming Growth Factor-β1–induced Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2012, 187: 180-188. PMID: 23220917, PMCID: PMC3570653, DOI: 10.1164/rccm.201206-1109oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisRegulatory T cellsProgressive idiopathic pulmonary fibrosisSEMA 7ATGF-β1Pulmonary fibrosisLung fibrosisT cellsMurine lungIL-10Bone marrow-derived cellsAdoptive transfer approachT-cell mediatorsMarrow-derived cellsTransforming Growth Factor-β1Murine lung fibrosisGrowth factor-β1Lung CD4Adoptive transferIL-17AIL-4Disease progressionSemaphorin 7ACD4Mouse model
2008
Cutting Edge: Engagement of NKG2A on CD8+ Effector T Cells Limits Immunopathology in Influenza Pneumonia
Zhou J, Matsuoka M, Cantor H, Homer R, Enelow RI. Cutting Edge: Engagement of NKG2A on CD8+ Effector T Cells Limits Immunopathology in Influenza Pneumonia. The Journal Of Immunology 2008, 180: 25-29. PMID: 18096998, DOI: 10.4049/jimmunol.180.1.25.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigensCD8-Positive T-LymphocytesHistocompatibility Antigens Class IInfluenza A virusMiceMice, Inbred BALB CMice, Inbred C57BLNK Cell Lectin-Like Receptor Subfamily CNK Cell Lectin-Like Receptor Subfamily DOrthomyxoviridae InfectionsPneumonia, ViralReceptors, ImmunologicReceptors, Natural Killer CellConceptsInfluenza pneumoniaT cellsLung injuryTNF productionT cell-mediated clearanceQa-1bAg-specific CD8Considerable lung injurySevere influenza infectionCD94/NKG2AT cell Ag recognitionEffector cell recognitionLimit immunopathologyNKG2A blockadeAntiviral CD8Distal airwaysInfluenza infectionPulmonary pathologyTNF-alphaCD8Infectious virusAg recognitionImmunopathologyPneumoniaCell recognition
2006
IL9 leads to airway inflammation by inducing IL13 expression in airway epithelial cells
Temann UA, Laouar Y, Eynon EE, Homer R, Flavell RA. IL9 leads to airway inflammation by inducing IL13 expression in airway epithelial cells. International Immunology 2006, 19: 1-10. PMID: 17101709, DOI: 10.1093/intimm/dxl117.Peer-Reviewed Original ResearchConceptsAirway epithelial cellsLung inflammationTg miceEnhanced lung inflammationEosinophilic lung inflammationEpithelial cellsMast cell hyperplasiaAsthma-like phenotypeRecombinase-activating genes 1IL13 levelsMucus hypersecretionCell hyperplasiaInflammatory cytokinesLung pathologyLung sectionsT cellsMast cellsMucus productionIL13 expressionB cellsLung epitheliumTransgenic miceInflammationIL13Lung
2002
Interleukin-13 Mediates a Fundamental Pathway for Airway Epithelial Mucus Induced by CD4 T Cells and Interleukin-9
Whittaker L, Niu N, Temann U, Stoddard A, Flavell RA, Ray A, Homer RJ, Cohn L. Interleukin-13 Mediates a Fundamental Pathway for Airway Epithelial Mucus Induced by CD4 T Cells and Interleukin-9. American Journal Of Respiratory Cell And Molecular Biology 2002, 27: 593-602. PMID: 12397019, DOI: 10.1165/rcmb.4838.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD4-Positive T-LymphocytesCells, CulturedGene Expression RegulationInterferon-gammaInterleukin-13Interleukin-9LungMiceMice, Inbred BALB CMice, Mutant StrainsMice, TransgenicMucin 5ACMucinsNF-kappa BReceptors, InterferonReceptors, Interleukin-4Recombinant ProteinsRespiratory MucosaSignal TransductionTh2 CellsConceptsIL-13Th2 cellsTh2-induced airway inflammationEpithelial mucusCD4 Th cellsCD4 T cellsAbsence of interleukinIL-13 actsNuclear factor-kappaBAsthma resultsTh2 effectsAirway inflammationMucus hyperproductionNegative infectionsTh cytokinesInflammatory cellsRecipient miceTh cellsIL-4IL-5Respiratory tractAirway epitheliumIL-9T cellsComplete blockade
1997
Induction of Airway Mucus Production By T Helper 2 (Th2) Cells: A Critical Role For Interleukin 4 In Cell Recruitment But Not Mucus Production
Cohn L, Homer R, Marinov A, Rankin J, Bottomly K. Induction of Airway Mucus Production By T Helper 2 (Th2) Cells: A Critical Role For Interleukin 4 In Cell Recruitment But Not Mucus Production. Journal Of Experimental Medicine 1997, 186: 1737-1747. PMID: 9362533, PMCID: PMC2199146, DOI: 10.1084/jem.186.10.1737.Peer-Reviewed Original ResearchConceptsTh2 cellsMucus productionAirway inflammationIL-4Asthmatic patientsCell recruitmentOVA-specific Th2 cellsT helper 2 cellsIL-4-deficient miceAirway mucus productionOVA-specific TCRRole of Th1CD4 T cellsImportant clinical symptomInduction of inflammationTh2 cell recruitmentCD4 Th1Airway biopsiesClinical symptomsTh1 cellsTNF-alphaT cellsInterleukin-4Effector functionsMucus secretionAirway isocyanate-adducts in asthma induced by exposure to hexamethylene diisocyanate.
Redlich CA, Karol MH, Graham C, Homer RJ, Holm CT, Wirth JA, Cullen MR. Airway isocyanate-adducts in asthma induced by exposure to hexamethylene diisocyanate. Scandinavian Journal Of Work, Environment & Health 1997, 23: 227-31. PMID: 9243734, DOI: 10.5271/sjweh.203.Peer-Reviewed Original ResearchConceptsHuman bronchial biopsiesHuman lung tissueExposure-disease relationshipsAirway eosinophilsAirway histologyEpithelial exposureMethacholine challengeBronchial biopsiesEndobronchial biopsyInflammatory changesClinical featuresAirway biopsiesIsocyanate asthmaLung tissueT cellsImmunohistochemical stainingAsthmaBiopsyExposure patternsBronchoscopyExposureAirwayPatientsEosinophilsHistology
1993
T cell unresponsiveness correlates with quantitative TCR levels in a transgenic model
Homer R, Mamalaki C, Kioussis D, Flavell R. T cell unresponsiveness correlates with quantitative TCR levels in a transgenic model. International Immunology 1993, 5: 1495-1500. PMID: 7906139, DOI: 10.1093/intimm/5.12.1495.Peer-Reviewed Original Research
1987
Qc-1, a novel Q-region-controlled CTL determinant expressed on B lymphocytes.
Homer RJ, Murphy DB. Qc-1, a novel Q-region-controlled CTL determinant expressed on B lymphocytes. The Journal Of Immunology 1987, 138: 4322-8. PMID: 2438340, DOI: 10.4049/jimmunol.138.12.4322.Peer-Reviewed Original Research