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dc.contributor.authorOhkura, Naganari
dc.contributor.authorHamaguchi, Masahide
dc.contributor.authorMorikawa, Hiromasa
dc.contributor.authorSugimura, Kyoko
dc.contributor.authorTanaka, Atsushi
dc.contributor.authorIto, Yoshinaga
dc.contributor.authorOsaki, Motonao
dc.contributor.authorTanaka, Yoshiaki
dc.contributor.authorYamashita, Riu
dc.contributor.authorNakano, Naoko
dc.contributor.authorHuehn, Jochen
dc.contributor.authorFehling, Hans Joerg
dc.contributor.authorSparwasser, Tim
dc.contributor.authorNakai, Kenta
dc.contributor.authorSakaguchi, Shimon
dc.date.accessioned2013-02-11T10:31:47Z
dc.date.available2013-02-11T10:31:47Z
dc.date.issued2012-11-16
dc.identifier.citationT cell receptor stimulation-induced epigenetic changes and Foxp3 expression are independent and complementary events required for Treg cell development. 2012, 37 (5):785-99 Immunityen_GB
dc.identifier.issn1097-4180
dc.identifier.pmid23123060
dc.identifier.doi10.1016/j.immuni.2012.09.010
dc.identifier.urihttp://hdl.handle.net/10033/268892
dc.description.abstractThe transcription factor Foxp3 is essential for the development of regulatory T (Treg) cells, yet its expression is insufficient for establishing the Treg cell lineage. Here we showed that Treg cell development was achieved by the combination of two independent processes, i.e., the expression of Foxp3 and the establishment of Treg cell-specific CpG hypomethylation pattern. Both events were induced by T cell receptor stimulation. The Treg cell-type CpG hypomethylation began in the thymus and continued to proceed in the periphery and could be fully established without Foxp3. The hypomethylation was required for Foxp3(+) T cells to acquire Treg cell-type gene expression, lineage stability, and full suppressive activity. Thus, those T cells in which the two events have concurrently occurred are developmentally set into the Treg cell lineage. This model explains how Treg cell fate and plasticity is controlled and can be exploited to generate functionally stable Treg cells.
dc.language.isoenen
dc.rightsArchived with thanks to Immunityen_GB
dc.subject.meshAnimalsen_GB
dc.subject.meshDNA Methylationen_GB
dc.subject.meshEpigenesis, Geneticen_GB
dc.subject.meshForkhead Transcription Factorsen_GB
dc.subject.meshGene Expressionen_GB
dc.subject.meshHistonesen_GB
dc.subject.meshMaleen_GB
dc.subject.meshMiceen_GB
dc.subject.meshMice, Inbred BALB Cen_GB
dc.subject.meshMice, Inbred C57BLen_GB
dc.subject.meshReceptors, Antigen, T-Cellen_GB
dc.subject.meshT-Lymphocytes, Regulatoryen_GB
dc.subject.meshThymus Glanden_GB
dc.titleT cell receptor stimulation-induced epigenetic changes and Foxp3 expression are independent and complementary events required for Treg cell development.en
dc.typeArticleen
dc.contributor.departmentDepartment of Experimental Immunology, World Premier International Immunology Frontier Research Center, Osaka University, Suita, Japan.en_GB
dc.identifier.journalImmunityen_GB
refterms.dateFOA2018-06-13T09:16:01Z
html.description.abstractThe transcription factor Foxp3 is essential for the development of regulatory T (Treg) cells, yet its expression is insufficient for establishing the Treg cell lineage. Here we showed that Treg cell development was achieved by the combination of two independent processes, i.e., the expression of Foxp3 and the establishment of Treg cell-specific CpG hypomethylation pattern. Both events were induced by T cell receptor stimulation. The Treg cell-type CpG hypomethylation began in the thymus and continued to proceed in the periphery and could be fully established without Foxp3. The hypomethylation was required for Foxp3(+) T cells to acquire Treg cell-type gene expression, lineage stability, and full suppressive activity. Thus, those T cells in which the two events have concurrently occurred are developmentally set into the Treg cell lineage. This model explains how Treg cell fate and plasticity is controlled and can be exploited to generate functionally stable Treg cells.


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