2014
NLRP6 Expression By the Hosts Enhances the Severity of Experimental Graft-Versus-Host Disease (GVHD)
Toubai T, Tamaki H, Rossi C, Oravecz-Wilson K, Liu C, Mathewson N, Sun Y, Chen G, Reddy P. NLRP6 Expression By the Hosts Enhances the Severity of Experimental Graft-Versus-Host Disease (GVHD). Blood 2014, 124: 2421. DOI: 10.1182/blood.v124.21.2421.2421.Peer-Reviewed Original ResearchDonor T cellsT cellsGI tractGI GVHDWT B6GVHD severityImmune cellsCytokine secretionIntestinal epitheliumBALB/c donorsNOD-like receptor familyAlteration of microbiotaModel of GVHDGut microflora compositionBALB/c T cellsIL-18 secretionSplenic T cellsCertain immune cellsIntestinal epithelial cellsNon-hematopoietic cellsGVHD mortalityNLRP6 deficiencyAllogeneic recipientsDendritic cellsIntestinal inflammation
2013
c‐Rel is an essential transcription factor for the development of acute graft‐versus‐host disease in mice
Yu Y, Wang D, Kaosaard K, Liu C, Fu J, Haarberg K, Anasetti C, Beg A, Yu X. c‐Rel is an essential transcription factor for the development of acute graft‐versus‐host disease in mice. European Journal Of Immunology 2013, 43: 2327-2337. PMID: 23716202, PMCID: PMC3940138, DOI: 10.1002/eji.201243282.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Marrow TransplantationCell DifferentiationCell ProliferationForkhead Transcription FactorsGraft vs Host DiseaseImmune ToleranceLymphocyte ActivationMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutProto-Oncogene Proteins c-relTh1 CellsTh17 CellsT-Lymphocytes, RegulatoryTransplantation, HomologousConceptsT cellsAcute GVHDHost diseaseAllogeneic bone marrow transplantationAllogeneic hematopoietic cell transplantationC-RelGVHD target organsHematopoietic cell transplantationRegulatory T cellsBone marrow transplantationAcute graftLeukemia responseTransplant toleranceAllogeneic recipientsMarrow transplantationMinor histocompatibilityCell transplantationTh1 cellsLymphoid organsMurine modelTarget organsTherapeutic interventionsNF-κB familyGraftPotential target
2009
T helper17 Cells Are Sufficient But Not Necessary to Induce Acute Graft-Versus-Host Disease
Iclozan C, Yu Y, Liu C, Liang Y, Yi T, Anasetti C, Yu X. T helper17 Cells Are Sufficient But Not Necessary to Induce Acute Graft-Versus-Host Disease. Transplantation And Cellular Therapy 2009, 16: 170-178. PMID: 19804837, PMCID: PMC3876952, DOI: 10.1016/j.bbmt.2009.09.023.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalBody WeightBone Marrow TransplantationCD3 ComplexCells, CulturedGraft vs Host DiseaseGraft vs Host ReactionInterferon-gammaInterleukin-17MiceMice, Inbred StrainsMice, TransgenicNuclear Receptor Subfamily 1, Group F, Member 3Severity of Illness IndexSurvival AnalysisTh1 CellsTime FactorsT-Lymphocyte SubsetsT-Lymphocytes, Helper-InducerTumor Necrosis Factor-alphaWhole Body ImagingConceptsHost diseaseBALB/c recipientsBone marrow transplantation settingAcute Graft-VersusT helper17 cellsGVHD target organsInduction of graftPathogenesis of GVHDCD4 T cellsGraft-VersusGVHD developmentC recipientsT helperTh17 cellsAllogeneic recipientsAutoimmune diseasesC57BL/6 miceSyngeneic recipientsTransplantation settingGVHDT cellsIFN-gammaTarget organsSuperior expansionDisease
2007
Benzodiazepine-423, an Inhibitor of Mitochondrial Respiration, Causes Selective Apoptosis of Activated Lymphocytes and Reverses Experimental GVHD While Preserving GVL Effects.
Gatza E, Clouthier S, Reddy P, Liu C, Opipari A, Glick G, Ferrara J. Benzodiazepine-423, an Inhibitor of Mitochondrial Respiration, Causes Selective Apoptosis of Activated Lymphocytes and Reverses Experimental GVHD While Preserving GVL Effects. Blood 2007, 110: 68. DOI: 10.1182/blood.v110.11.68.68.Peer-Reviewed Original ResearchT cellsGVL effectExperimental GVHDDonor CD4T cell-mediated modelBeneficial GVL effectComplete donor engraftmentDay of BMTEvidence of lymphomaSpleen T cellsEL-4 lymphomaEL-4 lymphoma cellsMitochondrial membrane potentialSelective apoptosisB6 recipientsGVHD inductionSyngeneic BMTAllogeneic BMTHost diseaseDonor engraftmentAllogeneic recipientsImproved survivalClinical scoresMitochondrial respirationMembrane potential
2003
A critical role for CCR2/MCP-1 interactions in the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation
Hildebrandt G, Duffner U, Olkiewicz K, Corrion L, Willmarth N, Williams D, Clouthier S, Hogaboam C, Reddy P, Moore B, Kuziel W, Liu C, Yanik G, Cooke K. A critical role for CCR2/MCP-1 interactions in the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation. Blood 2003, 103: 2417-2426. PMID: 14615370, DOI: 10.1182/blood-2003-08-2708.Peer-Reviewed Original ResearchConceptsMonocyte chemoattractant protein-1Idiopathic pneumonia syndromeAllogeneic bone marrow transplantationBone marrow transplantationChemokine receptor 2CCR2/MCPAllo-BMTPneumonia syndromeMarrow transplantationBronchoalveolar lavage fluid cellularityExperimental Idiopathic Pneumonia SyndromeBAL fluid levelsMouse BMT modelSoluble p55 TNF receptorTime of diagnosisPreliminary clinical findingsChemoattractant protein-1P55 TNF receptorDonor leukocytesLung injuryMajor complicationsAllogeneic recipientsBAL fluidLethal complicationPulmonary expression