2021
Tet2 Controls the Responses of β cells to Inflammation in Autoimmune Diabetes
Rui J, Deng S, Perdigoto AL, Ponath G, Kursawe R, Lawlor N, Sumida T, Levine-Ritterman M, Stitzel ML, Pitt D, Lu J, Herold KC. Tet2 Controls the Responses of β cells to Inflammation in Autoimmune Diabetes. Nature Communications 2021, 12: 5074. PMID: 34417463, PMCID: PMC8379260, DOI: 10.1038/s41467-021-25367-z.Peer-Reviewed Original ResearchConceptsImmune cellsΒ-cellsNOD/SCID recipientsDiabetogenic immune cellsDiabetogenic T cellsBone marrow transplantType 1 diabetesExpression of TET2Human β-cellsIslet infiltratesSCID recipientsMarrow transplantInflammatory pathwaysTransfer of diseaseT cellsInflammatory genesImmune killingPathologic interactionsReduced expressionDiabetesInflammationTET2MiceRecipientsCells
2018
Myeloid cell plasticity in the evolution of central nervous system autoimmunity
Giles DA, Washnock‐Schmid J, Duncker PC, Dahlawi S, Ponath G, Pitt D, Segal BM. Myeloid cell plasticity in the evolution of central nervous system autoimmunity. Annals Of Neurology 2018, 83: 131-141. PMID: 29283442, PMCID: PMC5876132, DOI: 10.1002/ana.25128.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArginaseAutoimmune Diseases of the Nervous SystemBone Marrow CellsCell PlasticityChimeraDisease ProgressionEncephalomyelitis, Autoimmune, ExperimentalHumansImmunohistochemistryLectins, C-TypeMannose ReceptorMannose-Binding LectinsMiceMice, Inbred C57BLMultiple SclerosisMyeloid CellsNitric Oxide Synthase Type IIPhenotypeReceptors, Cell SurfaceConceptsInducible nitric oxide synthaseExperimental autoimmune encephalomyelitisCNS myeloid cellsCentral nervous systemCentral nervous system autoimmunityChronic active MS lesionsActive MS lesionsMultiple sclerosisMyeloid cellsMS lesionsAnimal model experimental autoimmune encephalomyelitisRemission of EAEModel experimental autoimmune encephalomyelitisMyeloid cell plasticityEncephalitogenic T cellsNitric oxide synthaseMyeloid cell phenotypeFuture therapeutic strategiesHuman myeloid cellsAnn NeurolNoninflammatory phenotypePolarized subsetsClinical remissionAutoimmune encephalomyelitisProinflammatory markers
2009
Dysmyelinated axons in shiverer mice are highly vulnerable to α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor-mediated toxicity
Pitt D, Gonzales E, Cross AH, Goldberg MP. Dysmyelinated axons in shiverer mice are highly vulnerable to α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor-mediated toxicity. Brain Research 2009, 1309: 146-154. PMID: 19896473, PMCID: PMC7343376, DOI: 10.1016/j.brainres.2009.10.066.Peer-Reviewed Original ResearchMeSH KeywordsAlpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAnimalsBiomarkersBrainDisease Models, AnimalExcitatory Amino Acid AgonistsFemaleHereditary Central Nervous System Demyelinating DiseasesLuminescent ProteinsMiceMice, Inbred C57BLMice, Neurologic MutantsMovement DisordersMyelin Basic ProteinNerve DegenerationNerve Fibers, MyelinatedNeurotoxinsN-MethylaspartateReceptors, AMPAConceptsNMDA receptorsShiverer miceAMPA/kainate receptorsLumbar dorsal columnWhite matter injuryWidespread axonal degenerationSpinal cord axonsActivation of receptorsReceptor-mediated toxicitySubset of axonsMyelin basic proteinAxonal vulnerabilityNeuroprotective therapiesGlutamate excitotoxicityNMDA injectionAxonal degenerationAxonal injuryDorsal columnsRotarod performanceAxon damageGlutamate toxicityCentral axonsGlial cellsS-AMPAAxonal toxicity
2003
Experimental Autoimmune Encephalomyelitis (EAE) in CCR2−/− Mice Susceptibility in Multiple Strains
Gaupp S, Pitt D, Kuziel WA, Cannella B, Raine CS. Experimental Autoimmune Encephalomyelitis (EAE) in CCR2−/− Mice Susceptibility in Multiple Strains. American Journal Of Pathology 2003, 162: 139-150. PMID: 12507897, PMCID: PMC1851120, DOI: 10.1016/s0002-9440(10)63805-9.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DivisionCrosses, GeneticDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalGenetic Predisposition to DiseaseGlycoproteinsImmunity, InnateImmunohistochemistryIn Situ HybridizationLymphocytesMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred StrainsMice, KnockoutMyelin SheathMyelin-Oligodendrocyte GlycoproteinNuclease Protection AssaysPeptide FragmentsReceptors, CCR2Receptors, ChemokineRNA, MessengerSpecies SpecificityConceptsExperimental autoimmune encephalomyelitisCentral nervous systemAutoimmune encephalomyelitisLow molecular weight cytokinesLack of CCR2Deletion of CCR2Sites of inflammationWild-type animalsDifferent mouse strainsCCR2 deletionCNS lesionsMultiple sclerosisWeight cytokinesAutoimmune diseasesMouse susceptibilityNervous systemImmune systemCompensatory mechanismsBalb CCCR2Mouse strainsChemokinesMonocytesEncephalomyelitisAppropriate receptors