期刊
NATURE IMMUNOLOGY
卷 15, 期 5, 页码 439-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2864
关键词
-
类别
资金
- Vienna Science and Technology Fund [LS09-031]
- Austrian Science Fund (FWF)
- MedUni Vienna doctoral program [DK W1212]
- FWF projects [P19930, P23641, I00698, P25807, W1220, P24265, P23669]
- Genome Research in Austria project Epigenetic Regulation of Cell Fate Decisions
- Innovative Medicines Initiative Joint Undertaking [115142]
- European Union
- European Federation of Pharmaceutical Industries and Associations companies
- NIH [AI097244]
- Austrian Science Fund (FWF) [P23669, P25807, W1212] Funding Source: Austrian Science Fund (FWF)
- Grants-in-Aid for Scientific Research [26293109, 21229008, 26114720] Funding Source: KAKEN
- Austrian Science Fund (FWF) [I 698, P 25807, P 23641, P 24321, P 23669] Funding Source: researchfish
Molecular mechanisms that maintain lineage integrity of helper T cells are largely unknown. Here we show histone deacetylases 1 and 2 (HDAC1 and HDAC2) as crucial regulators of this process. Loss of HDAC1 and HDAC2 during late T cell development led to the appearance of major histocompatibility complex (MHC) class II-selected CD4(+) helper T cells that expressed CD8-lineage genes such as Cd8a and Cd8b1. HDAC1 and HDAC2-deficient T helper type 0 (T(H)0) and T(H)1 cells further upregulated CD8-lineage genes and acquired a CD8(+) effector T cell program in a manner dependent on Runx-CBFb complexes, whereas T(H)2 cells repressed features of the CD8(+) lineage independently of HDAC1 and HDAC2. These results demonstrate that HDAC1 and HDAC2 maintain integrity of the CD4 lineage by repressing Runx-CBFb complexes that otherwise induce a CD8(+) effector T cell-like program in CD4(+) T cells.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据