2017
Bile acids initiate cholestatic liver injury by triggering a hepatocyte-specific inflammatory response
Cai SY, Ouyang X, Chen Y, Soroka CJ, Wang J, Mennone A, Wang Y, Mehal WZ, Jain D, Boyer JL. Bile acids initiate cholestatic liver injury by triggering a hepatocyte-specific inflammatory response. JCI Insight 2017, 2: e90780. PMID: 28289714, PMCID: PMC5333973, DOI: 10.1172/jci.insight.90780.Peer-Reviewed Original ResearchConceptsLiver injuryInflammatory responseBile acid-induced liver injuryCholestatic liver injuryInflammatory liver injuryProinflammatory cytokine expressionCholestatic liver diseaseBile duct ligationVivo mouse modelHepatic infiltrationInflammatory injurySerum aminotransferasesLiver diseaseCholestatic patientsCytokine expressionChemokine inductionPathophysiologic concentrationsNeutrophil chemotaxisDuct ligationPathophysiologic levelsMouse modelNew therapiesInnate immunityInjuryPeriportal areas
2016
αvβ6 Integrin Promotes Castrate-Resistant Prostate Cancer through JNK1-Mediated Activation of Androgen Receptor
Lu H, Wang T, Li J, Fedele C, Liu Q, Zhang J, Jiang Z, Jain D, Iozzo RV, Violette SM, Weinreb PH, Davis RJ, Gioeli D, FitzGerald TJ, Altieri DC, Languino LR. αvβ6 Integrin Promotes Castrate-Resistant Prostate Cancer through JNK1-Mediated Activation of Androgen Receptor. Cancer Research 2016, 76: 5163-5174. PMID: 27450452, PMCID: PMC5012867, DOI: 10.1158/0008-5472.can-16-0543.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, NeoplasmCell Line, TumorDisease Models, AnimalFlow CytometryFluorescent Antibody TechniqueGene Knockdown TechniquesHumansImmunohistochemistryIntegrinsMaleMiceMice, KnockoutMitogen-Activated Protein Kinase 8Prostatic Neoplasms, Castration-ResistantReceptors, AndrogenSignal TransductionConceptsΑvβ6 expressionAndrogen receptorProstate cancerΑvβ6 integrinCastrate-resistant prostate cancerProstate cancer mouse modelAbsence of androgenFurther clinical developmentProstate cancer therapyCancer mouse modelNormal prostatic epitheliumProstate cancer progressionΑv-containing integrinsMajor therapeutic targetUpregulation of survivinActivation of JNK1Androgen ablationDownstream kinase activationMechanisms of resistanceProstatic adenocarcinomaInvolvement of p38Preclinical resultsMouse modelProstatic epitheliumClinical development
2012
Gaucher disease gene GBA functions in immune regulation
Liu J, Halene S, Yang M, Iqbal J, Yang R, Mehal WZ, Chuang WL, Jain D, Yuen T, Sun L, Zaidi M, Mistry PK. Gaucher disease gene GBA functions in immune regulation. Proceedings Of The National Academy Of Sciences Of The United States Of America 2012, 109: 10018-10023. PMID: 22665763, PMCID: PMC3382552, DOI: 10.1073/pnas.1200941109.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDGaucher DiseaseGlucosylceramidaseImmunophenotypingMiceMice, KnockoutConceptsGaucher diseaseHematopoietic stem cellsImmune regulationDisease severityGBA geneWidespread immune dysregulationB cell recruitmentPeripheral lymphoid organsT cell maturationLyso-GL1Immune dysregulationT helperImmune defectsTh2 cytokinesEarly thymic progenitorsLymphoid organsAntigen presentationGBA deficiencyGBA mutationsSevere diseaseClassic manifestationsClinical observationsGCase deficiencyBone marrowMature thymocytes
2011
Graft-versus-Host Disease Is Independent of Innate Signaling Pathways Triggered by Pathogens in Host Hematopoietic Cells
Li H, Matte-Martone C, Tan HS, Venkatesan S, McNiff J, Demetris AJ, Jain D, Lakkis F, Rothstein D, Shlomchik WD. Graft-versus-Host Disease Is Independent of Innate Signaling Pathways Triggered by Pathogens in Host Hematopoietic Cells. The Journal Of Immunology 2011, 186: 230-241. PMID: 21098219, PMCID: PMC5822434, DOI: 10.4049/jimmunol.1002965.Peer-Reviewed Original ResearchConceptsT cell responsesHost APCsHost diseaseAPC maturationT cellsAllogeneic hematopoietic stem cell transplantationAlloreactive donor T cellsCell responsesAdaptive T cell responsesHematopoietic stem cell transplantationHost hematopoietic cellsHost IL-12Donor T cellsAlloreactive T cellsStem cell transplantationT cell productionType I IFNInnate signaling pathwaysPattern recognition receptorsHematopoietic cellsMyD88/IL-12Cell transplantationIL-1βInflammatory cytokines
2008
CD8+ but not CD4+ T cells require cognate interactions with target tissues to mediate GVHD across only minor H antigens, whereas both CD4+ and CD8+ T cells require direct leukemic contact to mediate GVL
Matte-Martone C, Liu J, Jain D, McNiff J, Shlomchik WD. CD8+ but not CD4+ T cells require cognate interactions with target tissues to mediate GVHD across only minor H antigens, whereas both CD4+ and CD8+ T cells require direct leukemic contact to mediate GVL. Blood 2008, 111: 3884-3892. PMID: 18223170, PMCID: PMC2275040, DOI: 10.1182/blood-2007-11-125294.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesDisease Models, AnimalGraft vs Host DiseaseGraft vs Leukemia EffectHistocompatibility Antigens Class IHistocompatibility Antigens Class IIHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMiceMice, KnockoutMinor Histocompatibility AntigensReceptors, Antigen, T-CellStem Cell TransplantationTransplantation ChimeraTransplantation, HomologousConceptsCD4 cellsT cellsT cell antigen receptorAllogeneic stem cell transplantationMajor histocompatibility complex class IDirect cytolytic actionDistinct effector mechanismsDonor CD4 cellsDonor T cellsStem cell transplantationHistocompatibility complex class IMinor H antigensClass II moleculesComplex class IHost diseaseBCR-ABL cDNAGVHDEffector mechanismsMouse modelCML cellsBone marrowCognate interactionNoncytolytic pathwaysCD8Cytolytic action