2016
NR1H3 p.Arg415Gln Is Not Associated to Multiple Sclerosis Risk
Consortium T, Antel J, Ban M, Baranzini S, Barcellos L, Barizzone N, Beecham A, Berge T, Bernardinelli L, Booth D, Bos S, Buck D, Butkiewicz M, Celius E, Comabella M, Compston A, Dedham K, Cotsapas C, Alfonso S, De Jager P, Dubois B, Duquette P, Fontaine B, Gasperi C, Gil E, Goris A, Gourraud P, Graetz C, Gyllenberg A, Hadjigeorgiou G, Hafler D, Hribko D, Haines J, Harbo H, Hauser S, Warto S, Hawkins C, Hemmer B, Henry R, Hintzen R, Horakova D, Ivinson A, Howard M, Jelcic I, Kaskow B, Kira J, Kleinova P, Kockum I, Kucerova K, Lill C, Luessi F, Malhotra S, Martin R, Martinelli F, Matsushita T, McCabe C, McCauley J, Mescheriakkova J, Mitrovic M, Moen S, Montalban X, Muhlau M, Nakmura Y, Oksenberg J, Olsson T, Oturai A, Palotie A, Patsopoulos N, Pavlicova J, Pericak-Vance P, Piehl F, Rebeix I, Rioux J, Saarela J, Sawcer S, Sellebjerg F, Sondergaard H, Sorensen P, Sospedra M, Spurkland A, Stewart G, Taylor B, Uitterlinden A, Van Duijn C, Zipp F. NR1H3 p.Arg415Gln Is Not Associated to Multiple Sclerosis Risk. Neuron 2016, 92: 333-335. PMID: 27764667, PMCID: PMC5641967, DOI: 10.1016/j.neuron.2016.09.052.Peer-Reviewed Original ResearchConceptsPrimary progressive diseaseMultiple sclerosis riskProgressive diseaseMultiple sclerosisPatient's likelihoodDisease subtypesPatient collectionInsufficient sample sizeCommon variant associationsLow-frequency associationMendelian formsAssociationRecent studiesCertain individualsSample sizeVariant associationsSclerosisSubtypesDiseaseNeurons
2009
IL-17–producing human peripheral regulatory T cells retain suppressive function
Beriou G, Costantino CM, Ashley CW, Yang L, Kuchroo VK, Baecher-Allan C, Hafler DA. IL-17–producing human peripheral regulatory T cells retain suppressive function. Blood 2009, 113: 4240-4249. PMID: 19171879, PMCID: PMC2676084, DOI: 10.1182/blood-2008-10-183251.Peer-Reviewed Original ResearchMeSH KeywordsAntigens, CDEnzyme-Linked Immunosorbent AssayFlow CytometryForkhead Transcription FactorsHLA-DR AntigensHumansImmune ToleranceInterleukin-17Interleukin-1betaInterleukin-6Lymphocyte ActivationReverse Transcriptase Polymerase Chain ReactionT-LymphocytesT-Lymphocytes, RegulatoryTransforming Growth Factor betaConceptsRegulatory T cellsIL-17Suppressive functionTreg clonesT cellsPeripheral regulatory T cellsProinflammatory cytokines IL-1betaSustained Foxp3 expressionIL-17 productionIL-17 secretionCytokines IL-1betaAutoimmune pathogenesisEffector cellsInterleukin-17Foxp3 expressionHuman TregsInflammatory milieuIL-6IL-1betaInflammatory conditionsImmune functionSuppressive activityTregsCellsRecent studies
1999
The B7–CD28/CTLA-4 costimulatory pathways in autoimmune disease of the central nervous system
Anderson D, Sharpe A, Hafler D. The B7–CD28/CTLA-4 costimulatory pathways in autoimmune disease of the central nervous system. Current Opinion In Immunology 1999, 11: 677-683. PMID: 10631554, DOI: 10.1016/s0952-7915(99)00036-9.Peer-Reviewed Original ResearchConceptsSelf-reactive T cellsB7-CD28/CTLAAutoimmune diseasesT cellsTh1/Th2 cell differentiationB7-CD28 costimulationHuman autoimmune diseasesCentral nervous systemTh2 cell differentiationCostimulatory pathwayEffector phaseCTLA-4Nervous systemCritical roleDiseaseCTLARecent studiesCell differentiationCellsPast yearPathwayAutoimmunityCD28InitiationCostimulation