2021
IL-10 Deficiency Accelerates Type 1 Diabetes Development via Modulation of Innate and Adaptive Immune Cells and Gut Microbiota in BDC2.5 NOD Mice
Huang J, Tan Q, Tai N, Pearson JA, Li Y, Chao C, Zhang L, Peng J, Xing Y, Zhang L, Hu Y, Zhou Z, Wong FS, Wen L. IL-10 Deficiency Accelerates Type 1 Diabetes Development via Modulation of Innate and Adaptive Immune Cells and Gut Microbiota in BDC2.5 NOD Mice. Frontiers In Immunology 2021, 12: 702955. PMID: 34394099, PMCID: PMC8362616, DOI: 10.3389/fimmu.2021.702955.Peer-Reviewed Original ResearchConceptsNOD miceProportion of neutrophilsT cellsGut microbiotaDiabetes developmentT cell-mediated destructionT cell receptor transgenicType 1 diabetes developmentAccelerated diabetes developmentInhibition of diabetesModulation of InnatePathogenicity of CD4Cell-mediated destructionAdaptive immune cellsObese diabetic miceT regulatory (Treg) cellsDevelopment of diabetesPrevention of diabetesActivation of CD4Modulation of neutrophilsType 1 diabetesGut microbiota compositionInsulin-producing β-cellsSevere insulitisSpontaneous diabetes
2018
TRIF deficiency protects non-obese diabetic mice from type 1 diabetes by modulating the gut microbiota and dendritic cells
Gülden E, Chao C, Tai N, Pearson JA, Peng J, Majewska-Szczepanik M, Zhou Z, Wong FS, Wen L. TRIF deficiency protects non-obese diabetic mice from type 1 diabetes by modulating the gut microbiota and dendritic cells. Journal Of Autoimmunity 2018, 93: 57-65. PMID: 29960834, PMCID: PMC6108920, DOI: 10.1016/j.jaut.2018.06.003.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Vesicular TransportAdoptive TransferAnimalsBacteroidetesBurkholderialesCell ProliferationDendritic CellsDiabetes Mellitus, ExperimentalDisease SusceptibilityFemaleFirmicutesGastrointestinal MicrobiomeGene Expression RegulationLymphocyte ActivationMiceMice, Inbred NODMice, KnockoutMyeloid Differentiation Factor 88Signal TransductionT-LymphocytesToll-Like Receptor 3Toll-Like Receptor 4ConceptsWT NOD miceNOD miceType 1 diabetesGut microbiotaDiabetes developmentDendritic cellsCell activationNon-obese diabetic (NOD) mouse modelMyeloid differentiation primary response gene 88Wild-type NOD miceNon-obese diabetic (NOD) miceToll-like receptor signalingDiabetes susceptibilityStrong inflammatory immune responseDevelopment of diabetesInflammatory immune responseDiabetic mouse modelAdapter-inducing interferonImmune cell activationT cell activationTRIF deficiencyAdaptor protein downstreamFurther immunological analysisHuman T1D.T1D development
2012
TLR4 regulates cardiac lipid accumulation and diabetic heart disease in the nonobese diabetic mouse model of type 1 diabetes
Dong B, Qi D, Yang L, Huang Y, Xiao X, Tai N, Wen L, Wong F. TLR4 regulates cardiac lipid accumulation and diabetic heart disease in the nonobese diabetic mouse model of type 1 diabetes. AJP Heart And Circulatory Physiology 2012, 303: h732-h742. PMID: 22842069, PMCID: PMC3468457, DOI: 10.1152/ajpheart.00948.2011.Peer-Reviewed Original ResearchMeSH KeywordsAMP-Activated Protein KinasesAnimalsBlood GlucoseCell LineDiabetes Mellitus, Type 1Diabetic CardiomyopathiesDisease Models, AnimalFatty Acids, NonesterifiedJNK Mitogen-Activated Protein KinasesLipid MetabolismLipoprotein LipaseMiceMice, Inbred C57BLMice, Inbred NODMice, KnockoutMyeloid Differentiation Factor 88MyocardiumMyocytes, CardiacOleic AcidP38 Mitogen-Activated Protein KinasesPhosphorylationRatsRNA InterferenceTime FactorsToll-Like Receptor 4TriglyceridesConceptsDiabetic heart diseaseType 1 diabetesHeart diseaseNOD animalsLipoprotein lipaseLipid accumulationNonobese diabetic (NOD) mouse modelLeft ventricular developed pressureCardiac fatty acid metabolismMyeloid differentiation primary response geneCardiac lipid accumulationControl nondiabetic miceGreater ejection fractionRole of TLR4Nonobese diabetic (NOD) miceOnset of diabetesVentricular developed pressureDevelopment of diabetesToll-like receptorsGreater fractional shorteningDiabetic mouse modelPlasma triglyceride levelsWild-type NODLower triglyceride accumulationCellular lipid accumulation