2016
TGF-β1 modulates microglial phenotype and promotes recovery after intracerebral hemorrhage
Taylor RA, Chang CF, Goods BA, Hammond MD, Mac Grory B, Ai Y, Steinschneider AF, Renfroe SC, Askenase MH, McCullough LD, Kasner SE, Mullen MT, Hafler DA, Love JC, Sansing LH. TGF-β1 modulates microglial phenotype and promotes recovery after intracerebral hemorrhage. Journal Of Clinical Investigation 2016, 127: 280-292. PMID: 27893460, PMCID: PMC5199690, DOI: 10.1172/jci88647.Peer-Reviewed Original ResearchConceptsIntracerebral hemorrhageTGF-β1 treatmentTGF-β1Functional recoveryBrain injuryMurine modelPlasma TGF-β1 concentrationResolution phasePhenotype of microgliaTissue-resident microgliaAcute brain injuryBlood-derived macrophagesTGF-β1 concentrationsRapid inflammatory reactionIL6 gene expressionLongitudinal transcriptional profilingInflammatory profileMicroglial phenotypeFunctional outcomeBrain parenchymaInflammatory reactionPromotes recoveryMicrogliaTherapeutic targetDevastating form
2014
Treg Cells Expressing the Coinhibitory Molecule TIGIT Selectively Inhibit Proinflammatory Th1 and Th17 Cell Responses
Joller N, Lozano E, Burkett PR, Patel B, Xiao S, Zhu C, Xia J, Tan TG, Sefik E, Yajnik V, Sharpe AH, Quintana FJ, Mathis D, Benoist C, Hafler DA, Kuchroo VK. Treg Cells Expressing the Coinhibitory Molecule TIGIT Selectively Inhibit Proinflammatory Th1 and Th17 Cell Responses. Immunity 2014, 40: 569-581. PMID: 24745333, PMCID: PMC4070748, DOI: 10.1016/j.immuni.2014.02.012.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell ProliferationCells, CulturedCytokinesEosinophilsFibrinogenForkhead Transcription FactorsGene Expression ProfilingGene Expression RegulationImmunosuppression TherapyLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicReceptors, ImmunologicRespiratory HypersensitivityTh1-Th2 BalanceT-Lymphocyte SubsetsT-Lymphocytes, RegulatoryConceptsTreg cell subsetsTh2 cell responsesTreg cellsCell subsetsCell responsesProinflammatory T helper 1T effector cell proliferationTreg cell-mediated suppressionFibrinogen-like protein 2Allergic airway inflammationT regulatory (Treg) cellsTh2 cytokine productionSuppression of Th1T helper 1Effector cell proliferationTreg signature genesProinflammatory Th1TIGIT expressionAirway inflammationTh17 cellsRegulatory cellsHelper 1Cytokine productionT cellsImmune response
2005
High Incidence of Spontaneous Disease in an HLA-DR15 and TCR Transgenic Multiple Sclerosis Model
Ellmerich S, Mycko M, Takacs K, Waldner H, Wahid FN, Boyton RJ, King RH, Smith PA, Amor S, Herlihy AH, Hewitt RE, Jutton M, Price DA, Hafler DA, Kuchroo VK, Altmann DM. High Incidence of Spontaneous Disease in an HLA-DR15 and TCR Transgenic Multiple Sclerosis Model. The Journal Of Immunology 2005, 174: 1938-1946. PMID: 15699121, DOI: 10.4049/jimmunol.174.4.1938.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigen PresentationCell MovementCentral Nervous SystemDisease Models, AnimalDisease ProgressionDNA-Binding ProteinsEpitopes, T-LymphocyteHLA-DR AntigensHLA-DR Serological SubtypesMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMultiple SclerosisMyelin Basic ProteinParalysisPeptide FragmentsReceptors, Antigen, T-Cell, alpha-betaT-Lymphocyte SubsetsConceptsT cell responsesHLA-DR15Multiple sclerosisDeterminant spreadSpontaneous diseaseCell responsesCD4 T cell recognitionCNS tissue damageHuman multiple sclerosisMultiple sclerosis modelT cell reactivityExperimental allergic encephalomyelitisMyelin oligodendrocyte glycoproteinT cell recognitionMyelin basic proteinAllergic encephalomyelitisMyelin epitopesPeptide immunotherapyAxonal degenerationCell reactivityOligodendrocyte glycoproteinPathogenic roleT cellsHigh incidenceTransgenic mice
2004
Disease‐related epitope spread in a humanized T cell receptor transgenic model of multiple sclerosis
Ellmerich S, Takacs K, Mycko M, Waldner H, Wahid F, Boyton RJ, Smith PA, Amor S, Baker D, Hafler DA, Kuchroo VK, Altmann DM. Disease‐related epitope spread in a humanized T cell receptor transgenic model of multiple sclerosis. European Journal Of Immunology 2004, 34: 1839-1848. PMID: 15214032, DOI: 10.1002/eji.200324044.Peer-Reviewed Original ResearchConceptsHLA-DR15Multiple sclerosisTransgenic modelT cell receptor transgenic modelHLA class II moleculesHuman T cell clonesInduction of paralysisPoverty of movementHLA class IIT cell clonesClass II moleculesHuman TCR specificMBP 85Specific immunotherapyTCR specificMyelin epitopesT cellsIFN-gammaRodent modelsDiseaseCell clonesEpitopesDisease phenotypeSclerosisImmunization
2001
Molecular Mimicry in Lyme Arthritis Demonstrated at the Single Cell Level: LFA-1αL Is a Partial Agonist for Outer Surface Protein A-Reactive T Cells
Trollmo C, Meyer A, Steere A, Hafler D, Huber B. Molecular Mimicry in Lyme Arthritis Demonstrated at the Single Cell Level: LFA-1αL Is a Partial Agonist for Outer Surface Protein A-Reactive T Cells. The Journal Of Immunology 2001, 166: 5286-5291. PMID: 11290815, DOI: 10.4049/jimmunol.166.8.5286.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, SurfaceBacterial Outer Membrane ProteinsBacterial VaccinesBorrelia burgdorferi GroupClone CellsHumansHybridomasLipoproteinsLyme DiseaseLyme Disease VaccinesLymphocyte ActivationLymphocyte Function-Associated Antigen-1MiceMice, TransgenicMolecular MimicryPeptide FragmentsT-Lymphocyte SubsetsConceptsIL-13Antibiotic treatment-resistant Lyme arthritisPartial agonistTreatment-resistant Lyme arthritisChronic inflammatory joint diseaseT cell hybridsDR4 transgenic miceHuman T cell clonesClass II tetramersInflammatory joint diseaseSymptoms of arthritisT cell responsesT cell levelsEpisodes of arthritisT cell clonesSurface protein AAutoimmune mechanismsOuter surface protein ALyme arthritisJoint diseaseT cellsIFN-gammaImmunodominant epitopesCell levelTransgenic mice
1994
T cell receptor (TCR) usage determines disease susceptibility in experimental autoimmune encephalomyelitis: studies with TCR V beta 8.2 transgenic mice.
Kuchroo VK, Collins M, al-Sabbagh A, Sobel RA, Whitters MJ, Zamvil SS, Dorf ME, Hafler DA, Seidman JG, Weiner HL. T cell receptor (TCR) usage determines disease susceptibility in experimental autoimmune encephalomyelitis: studies with TCR V beta 8.2 transgenic mice. Journal Of Experimental Medicine 1994, 179: 1659-1664. PMID: 8163944, PMCID: PMC2191471, DOI: 10.1084/jem.179.5.1659.Peer-Reviewed Original ResearchConceptsExperimental allergic encephalomyelitisMyelin basic proteinAutoimmune diseasesEncephalitogenic epitopeTCR repertoireTCR VProteolipid proteinTransgenic miceT cell receptor usageDiverse T cell repertoireT cell receptor repertoireExperimental autoimmune encephalomyelitisAutoreactive T cellsCell receptor repertoireT cell repertoireT cell clonesAutoimmune encephalomyelitisAllergic encephalomyelitisSJL miceT cellsCell repertoirePLP epitopesReceptor usageReceptor repertoireImmunization