2009
IFN-β Inhibits Human Th17 Cell Differentiation
Ramgolam V, Sha Y, Jin J, Zhang X, Markovic-Plese S. IFN-β Inhibits Human Th17 Cell Differentiation. The Journal Of Immunology 2009, 183: 5418-5427. PMID: 19783688, DOI: 10.4049/jimmunol.0803227.Peer-Reviewed Original ResearchMeSH KeywordsCD4-Positive T-LymphocytesCell DifferentiationCells, CulturedDendritic CellsDown-RegulationHumansInterferon beta-1aInterferon-betaInterleukin-10Interleukin-12 Subunit p35Interleukin-17Interleukin-1betaInterleukin-23 Subunit p19Multiple SclerosisNuclear Receptor Subfamily 1, Group F, Member 3PhosphorylationReceptors, CCR6Receptors, InterleukinReceptors, Retinoic AcidReceptors, Thyroid HormoneSTAT1 Transcription FactorSTAT3 Transcription FactorT-Lymphocytes, Helper-InducerUp-RegulationConceptsTh17 cell differentiationDendritic cellsMultiple sclerosisT cellsReceptor CIL-17AAutoimmune responseIL-1betaIFN beta-1a treatmentRelapsing-remitting multiple sclerosisIL-10 gene expressionTh17 cell markersUntreated MS patientsCNS inflammatory diseasesIL-10 secretionNaive T cellsTh17-polarizing conditionsEffect of IFNCell differentiationIL-27p28 expressionPrimary therapySuppressor of cytokineIL-17IL-23IL-23p19
2008
Interferon (IFN) beta ‐1a induces IL‐27 and IL‐12, and down‐regulates IL‐23 and IL‐1beta in dendritic cells (DCs), establishing inhibitory conditions for Th‐17 cell differentiation: Implications for treatment of multiple sclerosis (MS)
Ramgolam V, Speer D, Markovic‐Plese S. Interferon (IFN) beta ‐1a induces IL‐27 and IL‐12, and down‐regulates IL‐23 and IL‐1beta in dendritic cells (DCs), establishing inhibitory conditions for Th‐17 cell differentiation: Implications for treatment of multiple sclerosis (MS). The FASEB Journal 2008, 22: 1074.8-1074.8. DOI: 10.1096/fasebj.22.1_supplement.1074.8.Peer-Reviewed Original ResearchIFN beta-1aDendritic cellsIL-27Beta-1aMultiple sclerosisIL-23IL-1 betaIL-1betaPathogenesis of MSIL-23 promotesIL-27 expressionTh-17 cellsMature dendritic cellsInterferon beta-1aIL-1B expressionCytokines IL-6Cytokine gene expressionInduction of SOCS3Cell differentiationSTAT-1 activationExpression of SOCS3STAT-1 geneQuantitative RT-PCRMS patientsStandard therapy