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dc.contributor.authorSun, Michaelen
dc.contributor.authorHa, Ngocen
dc.contributor.authorPham, Duc-Hungen
dc.contributor.authorFrederick, Meganen
dc.contributor.authorSharma, Bandanaen
dc.contributor.authorNaruse, Chieen
dc.contributor.authorAsano, Masahideen
dc.contributor.authorPipkin, Matthew E.en
dc.contributor.authorGeorge, Rani E.en
dc.contributor.authorThai, To-Haen
dc.contributor.alternative浅野, 雅秀ja
dc.date.accessioned2017-03-06T08:16:28Z-
dc.date.available2017-03-06T08:16:28Z-
dc.date.issued2017-02-21-
dc.identifier.issn2045-2322-
dc.identifier.urihttp://hdl.handle.net/2433/218632-
dc.descriptionCbx3/HP1γ is a histone reader whose function in the immune system is not completely understood. Here, we demonstrate that in CD8+ T cells, Cbx3/HP1γ insufficiency leads to chromatin remodeling accompanied by enhanced Prf1, Gzmb and Ifng expression. In tumors obtained from Cbx3/HP1γ- insufficient mice or wild type mice treated with Cbx3/HP1γ-insufficient CD8+ T cells, there is an increase of CD8+ effector T cells expressing the stimulatory receptor Klrk1/NKG2D, a decrease in CD4+ CD25+ FOXP3+ regulatory T cells (Treg cells) as well as CD25+ CD4+ T cells expressing the inhibitory receptor CTLA4. Together these changes in the tumor immune environment may have mitigated tumor burden in Cbx3/HP1γ-insufficient mice or wild type mice treated with Cbx3/HP1γ-insufficient CD8+ T cells. These findings suggest that targeting Cbx3/HP1γ can represent a rational therapeutic approach to control growth of solid tumors.en
dc.format.mimetypeapplication/pdf-
dc.language.isoeng-
dc.publisherSpringer Natureen
dc.rightsThis work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/en
dc.titleCbx3/HP1γ deficiency confers enhanced tumor-killing capacity on CD8+ T cellsen
dc.typejournal article-
dc.type.niitypeJournal Article-
dc.identifier.jtitleScientific Reportsen
dc.identifier.volume7-
dc.relation.doi10.1038/srep42888-
dc.textversionpublisher-
dc.identifier.artnum42888-
dc.addressInstitute of Laboratory Animals, Graduate School of Medicine, Kyoto Universityen
dc.identifier.pmid28220815-
dcterms.accessRightsopen access-
dc.identifier.eissn2045-2322-
出現コレクション:学術雑誌掲載論文等

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