2022
Type I interferon transcriptional network regulates expression of coinhibitory receptors in human T cells
Sumida TS, Dulberg S, Schupp JC, Lincoln MR, Stillwell HA, Axisa PP, Comi M, Unterman A, Kaminski N, Madi A, Kuchroo VK, Hafler DA. Type I interferon transcriptional network regulates expression of coinhibitory receptors in human T cells. Nature Immunology 2022, 23: 632-642. PMID: 35301508, PMCID: PMC8989655, DOI: 10.1038/s41590-022-01152-y.Peer-Reviewed Original ResearchConceptsCoinhibitory receptor expressionHuman T cellsIFN-I responsesCoinhibitory receptorsT cellsTIGIT expressionReceptor expressionAcute SARS-CoV-2 infectionPD-1/TimSARS-CoV-2 infectionEnhancement of immunotherapyType 1 interferonT-cell featuresLAG-3Infectious diseasesDifferent temporal kineticsTranscription factorsCancer therapyReceptorsCell featuresKey transcription factorIFNPresent studyMRNA profilingKey regulator
2018
Activated β-catenin in Foxp3+ regulatory T cells links inflammatory environments to autoimmunity
Sumida T, Lincoln MR, Ukeje CM, Rodriguez DM, Akazawa H, Noda T, Naito AT, Komuro I, Dominguez-Villar M, Hafler DA. Activated β-catenin in Foxp3+ regulatory T cells links inflammatory environments to autoimmunity. Nature Immunology 2018, 19: 1391-1402. PMID: 30374130, PMCID: PMC6240373, DOI: 10.1038/s41590-018-0236-6.Peer-Reviewed Original ResearchConceptsProstaglandin E receptor 2Regulatory T cellsTreg cellsT cellsAnti-inflammatory cytokine productionIL-10 productionPeripheral immune toleranceIL-10 expressionΒ-cateninE receptor 2Treg subpopulationsTreg phenotypeIL-10Cytokines IFNImmune toleranceTreg signatureCytokine signatureMultiple sclerosisAutoimmune diseasesCytokine productionInflammatory environmentLethal autoimmunityReceptor 2Activated β-cateninIFN
2015
Multiple sclerosis—a quiet revolution
Ransohoff RM, Hafler DA, Lucchinetti CF. Multiple sclerosis—a quiet revolution. Nature Reviews Neurology 2015, 11: 134-142. PMID: 25686758, PMCID: PMC4556342, DOI: 10.1038/nrneurol.2015.14.Peer-Reviewed Original ResearchConceptsTreatment optionsMajor unmet medical needMultiple sclerosis susceptibilityUnmet medical needNeural tissue injuryGenetic variantsMS therapeuticsAcetate therapyMS riskInflammatory aspectsMultiple sclerosisAutoimmune diseasesTreatable diseaseTissue injuryIndividual patientsDisease evolutionClinical phenotypeMedical needPatientsDisease susceptibilityDiseaseGenetic componentSclerosisIFNOptions
2014
TLR‐mediated STAT3 and ERK activation controls IL‐10 secretion by human B cells
Liu B, Cao Y, Huizinga TW, Hafler DA, Toes RE. TLR‐mediated STAT3 and ERK activation controls IL‐10 secretion by human B cells. European Journal Of Immunology 2014, 44: 2121-2129. PMID: 24737107, DOI: 10.1002/eji.201344341.Peer-Reviewed Original ResearchConceptsIL-10 productionIL-10-producing B cellsB cellsHuman B cellsIL-10IL-10 secretionPotent immunoregulatory cytokineType I IFNERK activationType I IFN familyInhibition of STAT3TLR-MyD88Activation of STAT3Immunoregulatory cytokinesTLR signalingPotent productionMouse modelI IFNCD40 ligationAntibody productionTLRSTAT3 pathwayIFNIFN familyPotential target
2011
Identification of T helper type 1–like, Foxp3+ regulatory T cells in human autoimmune disease
Dominguez-Villar M, Baecher-Allan CM, Hafler DA. Identification of T helper type 1–like, Foxp3+ regulatory T cells in human autoimmune disease. Nature Medicine 2011, 17: 673-675. PMID: 21540856, PMCID: PMC3675886, DOI: 10.1038/nm.2389.Peer-Reviewed Original ResearchConceptsTreg cellsT helper type 1Regulatory T cellsT regulatory (Treg) cellsHelper type 1T helper typeHuman autoimmune diseasesHuman Treg cellsRegulatory cellsIL-12Multiple sclerosisAutoimmune diseasesPeripheral bloodHelper typeT cellsSuppressive activityType 1Functional plasticityConsiderable phenotypicCellsSclerosisIFNDiseaseMiceBlood
1998
Extreme Th1 bias of invariant Vα24JαQ T cells in type 1 diabetes
Wilson S, Kent S, Patton K, Orban T, Jackson R, Exley M, Porcelli S, Schatz D, Atkinson M, Balk S, Strominger J, Hafler D. Extreme Th1 bias of invariant Vα24JαQ T cells in type 1 diabetes. Nature 1998, 391: 177-181. PMID: 9428763, DOI: 10.1038/34419.Peer-Reviewed Original ResearchConceptsType 1 diabetesT cellsMajor histocompatibility complexIL-4T cell-mediated destructionNon-diabetic siblingsAutoreactive T cellsHigher serum levelsTwins/tripletsType1 diabetic patientsDiabetic patientsSerum levelsTh1 biasDiabetic siblingsImmune systemTissue damageIncomplete concordanceDiabetesHistocompatibility complexIDDMIdentical twinsIFNDiseaseRiskCells