2009
Expression of Diabetes-Associated Genes by Dendritic Cells and CD4 T Cells Drives the Loss of Tolerance in Nonobese Diabetic Mice
Hamilton-Williams EE, Martinez X, Clark J, Howlett S, Hunter KM, Rainbow DB, Wen L, Shlomchik MJ, Katz JD, Beilhack GF, Wicker LS, Sherman LA. Expression of Diabetes-Associated Genes by Dendritic Cells and CD4 T Cells Drives the Loss of Tolerance in Nonobese Diabetic Mice. The Journal Of Immunology 2009, 183: 1533-1541. PMID: 19592648, PMCID: PMC2733871, DOI: 10.4049/jimmunol.0900428.Peer-Reviewed Original ResearchConceptsRegulatory T cellsT cellsDendritic cellsNOD miceProtective allelesCD4 T-cell expressionTolerance defectsImmune tolerance resultsPancreatic lymph nodesCD8 T cellsNonobese diabetic (NOD) miceCD4 T cellsT cell expressionLoss of toleranceIL-2 productionDiabetes 3Lymph nodesDiabetic miceIslet AgsNOD alleleCell expressionMiceSpontaneous developmentIdd3Tolerance results
2008
Toll‐Like Receptors and Diabetes
Wong F, Wen L. Toll‐Like Receptors and Diabetes. Annals Of The New York Academy Of Sciences 2008, 1150: 123-132. PMID: 19120280, DOI: 10.1196/annals.1447.063.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutoimmunityDiabetes MellitusHumansImmunity, InnateInfectionsModels, BiologicalT-Lymphocytes, RegulatoryToll-Like ReceptorsConceptsToll-like receptorsAntigen-presenting cellsType 1 interferonAdaptive immune systemRegulatory cellsAutoimmune responseInflammatory cytokinesMore specific responsesIFN-alphaImmune responseEndogenous ligandImmune systemMolecular patternsInfectionMicrobial infectionsReceptorsInterferonEndogenous stimuliDirect effectCellular stressSpecific responsesCellsResponseAutoimmunityDiabetes
2007
CD86 Has Sustained Costimulatory Effects on CD8 T Cells
Thomas IJ, de Marquesini L, Ravanan R, Smith RM, Guerder S, Flavell RA, Wraith DC, Wen L, Wong FS. CD86 Has Sustained Costimulatory Effects on CD8 T Cells. The Journal Of Immunology 2007, 179: 5936-5946. PMID: 17947667, PMCID: PMC2629533, DOI: 10.4049/jimmunol.179.9.5936.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsB7-1 AntigenB7-2 AntigenCD8-Positive T-LymphocytesCell DifferentiationCell ProliferationCells, CulturedCytokinesDiabetes MellitusGene Expression RegulationHealthHumansIslets of Langerhans TransplantationMiceMice, TransgenicPromoter Regions, GeneticRatsReceptor, InsulinSurvival RateTime FactorsTransgenesConceptsCD8 T cellsT cellsT cell activationCD86 costimulationCell activationCytotoxic T-cell activationTransfer of diabetesOld NOD miceInhibitory molecule expressionRat insulin promoterGreater sustained activityNOD isletsRecurrent diabetesNOD miceDiabetes onsetDiabetic miceCostimulatory moleculesCTLA-4Cytokine secretionMolecule expressionCostimulatory effectImmune responseCD80CD86CD80 costimulation
2006
Age-dependent loss of tolerance to an immunodominant epitope of glutamic acid decarboxylase in diabetic-prone RIP-B7/DR4 mice
Gebe J, Unrath K, Falk B, Ito K, Wen L, Daniels T, Lernmark Å, Nepom G. Age-dependent loss of tolerance to an immunodominant epitope of glutamic acid decarboxylase in diabetic-prone RIP-B7/DR4 mice. Clinical Immunology 2006, 121: 294-304. PMID: 16979383, PMCID: PMC1850983, DOI: 10.1016/j.clim.2006.08.002.Peer-Reviewed Original ResearchConceptsGlial fibrillary acidic proteinNon-diabetic miceGlutamic acid decarboxylaseImmunodominant epitopesAcid decarboxylaseIslet-specific glucose-6-phosphatase catalytic subunit-related proteinHLA transgenic miceMean onset ageFibrillary acidic proteinAge-dependent lossIslet infiltratesOvert diabetesDiabetic miceFemale miceHistological evidenceMale miceDR4 miceYoung miceOnset ageProliferative responseDiabetic diseaseTransgenic miceImmunogenic epitopesAcidic proteinMice