基因沉默
FOXP3型
转录因子
效应器
染色质
免疫系统
生物
心理压抑
细胞生物学
调解人
基因
基因表达调控
免疫耐受
遗传学
基因表达
作者
Ping Fan,Hong‐Ren Yu,Eric V. Dang,Joseph Barbi,Xiaoyu Pan,Joseph F. Grosso,Dinili Jinasena,Sudarshana M. Sharma,Erin McCadden,Derese Getnet,Charles G. Drake,Jun O. Liu,Michael C. Ostrowski,Drew M. Pardoll
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2009-08-28
卷期号:325 (5944): 1142-1146
被引量:286
标识
DOI:10.1126/science.1176077
摘要
CD4+ regulatory T cells (Tregs) maintain immunological self-tolerance and immune homeostasis by suppressing aberrant or excessive immune responses. The core genetic program of Tregs and their ability to suppress pathologic immune responses depends on the transcription factor Foxp3. Despite progress in understanding mechanisms of Foxp3-dependent gene activation, the molecular mechanism of Foxp3-dependent gene repression remains largely unknown. We identified Eos, a zinc-finger transcription factor of the Ikaros family, as a critical mediator of Foxp3-dependent gene silencing in Tregs. Eos interacts directly with Foxp3 and induces chromatin modifications that result in gene silencing in Tregs. Silencing of Eos in Tregs abrogates their ability to suppress immune responses and endows them with partial effector function, thus demonstrating the critical role that Eos plays in Treg programming.
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