2016
BBB-permeable peptide conjugated cytoplasmic domain of CTLA-4 inhibits Th1 and Th17 responses and pathogenesis of multiple sclerosis
Lim S, Kim W, Kim Y, Lee S, Koo J, Lee J, Kim H, Park H, Kim D, Lee H, Yoon H, Kim J, Shin J, Kim L, Doh J, Kim H, Bothwell A, Lee S, Suh M, Choi J. BBB-permeable peptide conjugated cytoplasmic domain of CTLA-4 inhibits Th1 and Th17 responses and pathogenesis of multiple sclerosis. The Journal Of Immunology 2016, 196: 139.7-139.7. DOI: 10.4049/jimmunol.196.supp.139.7.Peer-Reviewed Original ResearchCentral nervous systemBlood-brain barrierExperimental autoimmune encephalomyelitisMultiple sclerosisT cellsCytotoxic T-lymphocyte antigen-4T-lymphocyte antigen-4T helper 17 (Th17) cellsAbstract Multiple sclerosisCNS inflammatory diseasesInfiltrated T cellsEffector T cellsHelper 17 cellsSevere autoimmune diseaseT helper 1Activated T cellsMOG35-55Autoimmune encephalomyelitisTh17 responsesHelper 1Autoimmune diseasesCytokine productionSevere inflammationAntigen-4Model mice
2006
The mutant leucine-zipper domain impairs both dimerization and suppressive function of Foxp3 in T cells
Chae WJ, Henegariu O, Lee SK, Bothwell AL. The mutant leucine-zipper domain impairs both dimerization and suppressive function of Foxp3 in T cells. Proceedings Of The National Academy Of Sciences Of The United States Of America 2006, 103: 9631-9636. PMID: 16769892, PMCID: PMC1480458, DOI: 10.1073/pnas.0600225103.Peer-Reviewed Original ResearchConceptsWild-type FOXP3Regulatory T cellsCD4 T cellsT cellsAutoimmune diseasesTh2-type cytokine secretionScurfy mutant mouseSevere autoimmune diseaseFoxp3 transcription factorAntigenic stimulationCytokine secretionFoxp3Suppressive functionMutant miceAdhesion moleculesSuppressor activityDiseaseGlutamic acidImportant roleCellsCD103HyporesponsivenessTh1Leucine zipper domainTranscription factors
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