2007
Functional inhibition related to structure of a highly potent insulin‐specific CD8 T cell clone using altered peptide ligands
de Marquesini L, Moustakas A, Thomas I, Wen L, Papadopoulos G, Wong F. Functional inhibition related to structure of a highly potent insulin‐specific CD8 T cell clone using altered peptide ligands. European Journal Of Immunology 2007, 38: 240-249. PMID: 18157812, PMCID: PMC2901522, DOI: 10.1002/eji.200737762.Peer-Reviewed Original ResearchConceptsCD8 T cellsT cellsCD8 T cell clonesAntagonist activityT cell functionT cell clonesProduction assaysMHC-peptide complexesTCR contact sitesNOD miceCD8 epitopesAgonist responsesTherapeutic useFunctional inhibitionCell clonesTCR stimulationCell functionPeptide ligandsNative peptideCellsPeptidesCytotoxicityAPLAssaysCD4
1999
Identification of an MHC class I-restricted autoantigen in type 1 diabetes by screening an organ-specific cDNA library
Wong F, Karttunen J, Dumont C, Wen L, Visintin I, Pilip I, Shastri N, Pamer E, Janeway C. Identification of an MHC class I-restricted autoantigen in type 1 diabetes by screening an organ-specific cDNA library. Nature Medicine 1999, 5: 1026-1031. PMID: 10470079, DOI: 10.1038/12465.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAutoantigensCD8-Positive T-LymphocytesClone CellsCloning, MolecularCOS CellsDiabetes Mellitus, Type 1Epitopes, T-LymphocyteGene LibraryHistocompatibility Antigens Class IInsulinInterferon-gammaIslets of LangerhansLymphocyte ActivationLymphocyte CountMiceMice, Inbred NODMice, Inbred StrainsOrgan SpecificityPeptidesConceptsType 1 diabetesAutoimmune diseasesT cellsPathogenic CD4 T cellsPathogenic CD8 T cellsNon-obese diabetic (NOD) miceCD8 T cell epitopesInsulin-producing pancreatic β-cellsAntigen-specific immunotherapyCD8 T lymphocytesCD8 T cellsCD4 T cellsT cell epitopesGood animal modelMHC class IIdentification of autoantigensPancreatic β-cellsDiabetic micePreventative therapyHuman diabetesT lymphocytesAnimal modelsImmune processesDiabetesΒ-cells
1998
The expression in vivo of a second isoform of pT alpha: implications for the mechanism of pT alpha action.
Barber D, Passoni L, Wen L, Geng L, Hayday A. The expression in vivo of a second isoform of pT alpha: implications for the mechanism of pT alpha action. The Journal Of Immunology 1998, 161: 11-6. PMID: 9647201, DOI: 10.4049/jimmunol.161.1.11.Peer-Reviewed Original ResearchPrimary gamma delta cell clones can be defined phenotypically and functionally as Th1/Th2 cells and illustrate the association of CD4 with Th2 differentiation.
Wen L, Barber D, Pao W, Wong F, Owen M, Hayday A. Primary gamma delta cell clones can be defined phenotypically and functionally as Th1/Th2 cells and illustrate the association of CD4 with Th2 differentiation. The Journal Of Immunology 1998, 160: 1965-74. PMID: 9469460, DOI: 10.4049/jimmunol.160.4.1965.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsApoptosisB-LymphocytesCD4 AntigensCell DifferentiationCells, CulturedClone CellsCytokinesFas Ligand ProteinFas ReceptorGene ExpressionImmunoglobulin Class SwitchingImmunoglobulin IsotypesImmunophenotypingMembrane GlycoproteinsMiceMice, KnockoutMice, SCIDMolecular Sequence DataReceptors, Antigen, T-Cell, alpha-betaTh1 CellsTh2 CellsConceptsAlpha beta T cellsBeta T cellsGamma delta cellsT cellsCell clonesTh1/Th2 cellsGamma delta T cellsCD8 alpha betaDelta cellsDelta T cellsDivision of CD4Association of CD4Autoimmune diseasesCytokine expressionImmunoregulatory roleTh2 phenotypeTh2 subsetsTh2 cellsAntigen presentationCD4 expressionTh2 differentiationCD4Clonal levelAlpha betaStrong association
1997
Inhibition of Diabetes by an Insulin-Reactive CD4 T-Cell Clone in the Nonobese Diabetic Mouse
Zekzer D, Wong F, Wen L, Altieri M, Gurlo T, von Grafenstein H, Sherwin R. Inhibition of Diabetes by an Insulin-Reactive CD4 T-Cell Clone in the Nonobese Diabetic Mouse. Diabetes 1997, 46: 1124-1132. PMID: 9200646, DOI: 10.2337/diab.46.7.1124.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnimalsCattleCD4 AntigensCell Adhesion MoleculesClone CellsCytokinesDiabetes Mellitus, Type 2Disease Models, AnimalDose-Response Relationship, DrugFemaleFlow CytometryInsulinMiceMice, Inbred NODPolymerase Chain ReactionRatsReceptors, Antigen, T-Cell, alpha-betaRNASpecific Pathogen-Free OrganismsTh1 CellsConceptsNOD miceDiabetic splenocytesIslet supernatantAdoptive transferDiabetic miceCD4 T-cell clonesInhibition of diabetesInjection of splenocytesPancreatic lymph nodesNonobese diabetic (NOD) miceAnti-transforming growthT cell clonesTh1 cell linesT cell receptorNOD isletsNOD splenocytesSpontaneous diabetesInsulin therapyLymph nodesAntibody treatmentTh1 cellsProtective effectDiabetesB chain peptideSplenocytes
1996
Germinal center formation, immunoglobulin class switching, and autoantibody production driven by "non alpha/beta" T cells.
Wen L, Pao W, Wong FS, Peng Q, Craft J, Zheng B, Kelsoe G, Dianda L, Owen MJ, Hayday AC. Germinal center formation, immunoglobulin class switching, and autoantibody production driven by "non alpha/beta" T cells. Journal Of Experimental Medicine 1996, 183: 2271-2282. PMID: 8642336, PMCID: PMC2192585, DOI: 10.1084/jem.183.5.2271.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutoantibodiesClone CellsFlow CytometryGerminal CenterHumansImmunoglobulin Class SwitchingImmunoglobulin EImmunoglobulin GLupus Erythematosus, SystemicLymphocyte DepletionMiceMice, Inbred NODMice, Inbred StrainsMice, KnockoutMice, SCIDReceptors, Antigen, T-Cell, alpha-betaSpleenT-LymphocytesConceptsSystemic lupus erythematosusBeta T cellsAlpha/beta T cellsGamma/delta T cellsDelta T cellsT cell helpT cellsT cell receptorCell helpT cell-mediated conditionsHuman systemic lupus erythematosusSevere combined immunodeficient (SCID) miceDevelopment of autoantibodiesCombined Immunodeficient MiceT-cell immunodeficiencyClass-switched antibodiesB cell collaborationGerminal center formationLupus erythematosusAutoantibody productionLymphoid folliclesImmunoglobulin class switchingIgE synthesisAlpha/betaCell immunodeficiencyCD8 T cell clones from young nonobese diabetic (NOD) islets can transfer rapid onset of diabetes in NOD mice in the absence of CD4 cells.
Wong FS, Visintin I, Wen L, Flavell RA, Janeway CA. CD8 T cell clones from young nonobese diabetic (NOD) islets can transfer rapid onset of diabetes in NOD mice in the absence of CD4 cells. Journal Of Experimental Medicine 1996, 183: 67-76. PMID: 8551245, PMCID: PMC2192404, DOI: 10.1084/jem.183.1.67.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsB7-1 AntigenBase SequenceCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesClone CellsCytokinesDiabetes Mellitus, Type 2FemaleImmunohistochemistryImmunotherapy, AdoptiveInsulinIslets of LangerhansLymphocyte ActivationMembrane GlycoproteinsMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred NODMice, SCIDMolecular Sequence DataPancreasPerforinPore Forming Cytotoxic ProteinsPromoter Regions, GeneticConceptsT cell linesNOD miceT cellsCD8 T cell linesCD8 T cell clonesNonobese diabetic (NOD) miceCB17 SCID miceCD4 T cellsPathogenesis of diabetesT cell clonesCell linesIslets of LangerhansT cell antigen receptorNOD isletsCD4 cellsLymphocytic infiltrateNOD-SCIDDiabetic miceDiabetic isletsFemale NODRapid onsetCell antigen receptorH-2KdAntigen receptorMice
1994
T Cell Clones Generated from Patients with Type 1 Diabetes Using Interleukin-2 Proliferate to Human Islet Antigens
Peakman M, Wen L, McNab G, Watkins P, Tan K, Vergani D. T Cell Clones Generated from Patients with Type 1 Diabetes Using Interleukin-2 Proliferate to Human Islet Antigens. Autoimmunity 1994, 17: 31-39. PMID: 8025212, DOI: 10.3109/08916939409014656.Peer-Reviewed Original ResearchMeSH KeywordsAdultAutoantigensAutoimmune DiseasesCD4 AntigensCD8 AntigensChildChild, PreschoolClone CellsDiabetes Mellitus, Type 1FemaleHumansInterleukin-2Islets of LangerhansLymphocyte ActivationMaleReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-Cell, gamma-deltaReceptors, Interleukin-2T-Lymphocyte SubsetsConceptsT cell clonesT lymphocytesIslet antigensControl subjectsAntigen specificityType 1Cell clonesT cell populationsPeripheral blood lymphocytesIL-2 receptorActivated T lymphocytesDose-dependent fashionPrediabetic periodLiver membrane preparationsPeripheral bloodAutologous APCIL-2Blood lymphocytesPatientsHuman isletsLymphocytesMembrane preparationsProliferation assaysPathogenesisAntigen
1990
T-cell-directed hepatocyte damage in autoimmune chronic active hepatitis
Wen L, Peakman M, Lobo-Yeo A, Vergani D, Mowat A, Mieli-Vergani, McFarlane B. T-cell-directed hepatocyte damage in autoimmune chronic active hepatitis. The Lancet 1990, 336: 1527-1530. PMID: 1979365, DOI: 10.1016/0140-6736(90)93306-a.Peer-Reviewed Original ResearchConceptsAutoimmune chronic active hepatitisChronic active hepatitisActive hepatitisPeripheral bloodT lymphocytesAutologous B lymphocytesLiver membrane antigensT cell clonesAsialoglycoprotein receptorActivated T lymphocytesLiver cell membraneSpecific autoantibodiesAutoimmune attackImmune attackHepatocyte damageHepatitisB lymphocytesLymphocytesBloodLipoprotein complexAutoantibodiesPatientsCell membraneAntigenClones