2020
Kras mutation correlating with circulating regulatory T cells predicts the prognosis of advanced pancreatic cancer patients
Cheng H, Luo G, Jin K, Fan Z, Huang Q, Gong Y, Xu J, Yu X, Liu C. Kras mutation correlating with circulating regulatory T cells predicts the prognosis of advanced pancreatic cancer patients. Cancer Medicine 2020, 9: 2153-2159. PMID: 32017404, PMCID: PMC7064028, DOI: 10.1002/cam4.2895.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedBiomarkers, TumorCD4 Lymphocyte CountCirculating Tumor DNADNA Mutational AnalysisFemaleFollow-Up StudiesHumansKaplan-Meier EstimateMaleMiddle AgedMutationNeoplasm StagingPancreatic NeoplasmsPolymerase Chain ReactionPrognosisProto-Oncogene Proteins p21(ras)Retrospective StudiesT-Lymphocytes, RegulatoryTime FactorsConceptsCell-free circulating tumor DNAAdvanced pancreatic cancer patientsPancreatic cancer patientsCirculating regulatory T cellsCirculating T-cell subsetsCA19-9 levelsRegulatory T cellsKRAS mutation statusT cell subsetsTumor-node-metastasisCancer patientsMutation statusTumor DNAKRAS mutationsT cellsAssociated with extremely poor survivalRegulatory T cell levelsAdvanced pancreatic cancerLevels of TregsProportion of TregsAbnormal immune statusCirculating tumor DNAT cell levelsPredicted worse prognosisTumor-node-metastasis stage
2007
Lymphopenia-induced proliferation of donor T cells reduces their capacity for causing acute graft-versus-host disease
Maeda Y, Tawara I, Teshima T, Liu C, Hashimoto D, Matsuoka K, Tanimoto M, Reddy P. Lymphopenia-induced proliferation of donor T cells reduces their capacity for causing acute graft-versus-host disease. Experimental Hematology 2007, 35: 274-286. PMID: 17258076, DOI: 10.1016/j.exphem.2006.10.010.Peer-Reviewed Original ResearchConceptsAllogeneic bone marrow transplantationDonor T cellsBone marrow transplantationLymphopenia-induced proliferationNaïve T cellsT cellsHost diseaseAcute GVHD severityAnti-tumor immunityT cell subsetsPhenotype T cellsMurine experimental modelAnti-tumor functionAcute graftGVHD mortalitySevere GVHDGVHD severityAllograft rejectionMarrow transplantationCell depletionCell subsetsGVHDBiochemical parametersExperimental modelGraft
2004
Blockade of CXCR3 Receptor:Ligand Interactions Reduces Leukocyte Recruitment to the Lung and the Severity of Experimental Idiopathic Pneumonia Syndrome
Hildebrandt G, Corrion L, Olkiewicz K, Lu B, Lowler K, Duffner U, Moore B, Kuziel W, Liu C, Cooke K. Blockade of CXCR3 Receptor:Ligand Interactions Reduces Leukocyte Recruitment to the Lung and the Severity of Experimental Idiopathic Pneumonia Syndrome. The Journal Of Immunology 2004, 173: 2050-2059. PMID: 15265940, DOI: 10.4049/jimmunol.173.3.2050.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Marrow CellsBronchoalveolar Lavage FluidCells, CulturedChemokine CXCL10Chemokine CXCL9Chemokines, CXCChemotaxis, LeukocyteCrosses, GeneticFemaleHematopoietic Stem Cell TransplantationInterferon-gammaLigandsLungLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutPneumoniaReceptors, CCR5Receptors, ChemokineReceptors, CXCR3SpleenT-Lymphocytes, CytotoxicTransplantation, HomologousTumor Necrosis Factor-alphaConceptsIdiopathic pneumonia syndromeDonor T cellsPneumonia syndromeIP-10TNF-alphaT cellsIFN-gammaCXCR3 receptorDevelopment of IPSExperimental Idiopathic Pneumonia SyndromeIP-10 protein levelsAllogeneic stem cell transplantationAllo-SCT recipientsInfiltration of IFNStandard immunosuppressive therapyT cell subsetsBronchoalveolar lavage fluidStem cell transplantationT cell recruitmentControl-treated animalsImmunosuppressive therapyLigand MigAllo-SCTFatal complicationLung injuryParadoxical effects of interleukin-18 on the severity of acute graft-versus-host disease mediated by CD4+ and CD8+ T-cell subsets after experimental allogeneic bone marrow transplantation
Min C, Maeda Y, Lowler K, Liu C, Clouthier S, Lofthus D, Weisiger E, Ferrara J, Reddy P. Paradoxical effects of interleukin-18 on the severity of acute graft-versus-host disease mediated by CD4+ and CD8+ T-cell subsets after experimental allogeneic bone marrow transplantation. Blood 2004, 104: 3393-3399. PMID: 15280194, DOI: 10.1182/blood-2004-02-0763.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsAntibodies, MonoclonalApoptosisBone Marrow TransplantationCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCytokinesDisease Models, AnimalFemaleGraft vs Host DiseaseHistocompatibility Antigens Class IHistocompatibility Antigens Class IIInterleukin-18Interleukin-18 Receptor alpha SubunitMiceMice, Inbred C57BLReceptors, InterleukinReceptors, Interleukin-18Severity of Illness IndexT-Lymphocytes, CytotoxicTransplantation, HomologousConceptsAllogeneic bone marrow transplantationBone marrow transplantationExperimental allogeneic bone marrow transplantationDonor T cellsIL-18T cellsAcute GVHDAcute graftHost diseaseInterleukin-18Marrow transplantationClinical allogeneic bone marrow transplantationMajor histocompatibility complex class IIHistocompatibility complex class IIEndogenous IL-18Experimental acute graftT cell subsetsParadoxical effectFas-dependent mannerLess GVHDCytotoxic functionHistopathologic parametersGVHDClass IIFas expression