Guidance of regulatory T cell development by Satb1-dependent super-enhancer establishment.
Guidance of regulatory T cell development by Satb1-dependent super-enhancer establishment.
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DOI：
10.1038/ni.3646
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发表时间：
2017-03
影响因子：
30.5
通讯作者：
Sakaguchi S
中科院分区：
文献类型：
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作者：
Kitagawa Y;Ohkura N;Kidani Y;Vandenbon A;Hirota K;Kawakami R;Yasuda K;Motooka D;Nakamura S;Kondo M;Taniuchi I;Kohwi-Shigematsu T;Sakaguchi S
大多数Foxp 3+调节性T（Treg）细胞在胸腺中发育为专门用于免疫抑制的功能成熟T细胞亚群。它们的细胞命运似乎在Foxp 3表达之前就已经决定了;然而，引发Foxp 3 − Treg前体细胞的分子事件在很大程度上还不清楚。我们发现Treg细胞特异性超级增强子（Treg-SE），与Foxp 3和其他Treg细胞标记基因相关，开始在Treg前体细胞中被激活。基因组组织者Satb 1的T细胞特异性缺陷损害Treg-SE激活和随后的Treg标签基因的表达，导致由于Treg细胞缺陷引起的严重自身免疫。这些结果表明，Satb 1依赖性Treg-SE激活是至关重要的Treg细胞谱系特化的胸腺，其扰动是自身免疫性和其他免疫性疾病的原因。
Most Foxp3+ regulatory T (Treg) cells develop in the thymus as a functionally mature T cell subpopulation specialized for immune suppression. Their cell fate appears to be determined before Foxp3 expression; yet molecular events that prime Foxp3− Treg precursor cells are largely obscure. We found that Treg cell–specific super-enhancers (Treg-SEs), which were associated with Foxp3 and other Treg cell signature genes, began to be activated in Treg precursor cells. T cell–specific deficiency of the genome organizer Satb1 impaired Treg-SE activation and the subsequent expression of Treg signature genes, causing severe autoimmunity due to Treg cell deficiency. These results suggest that Satb1-dependent Treg-SE activation is crucial for Treg cell lineage specification in the thymus and that its perturbation is causative of autoimmune and other immunological diseases.
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影响因子：
64.5
作者：
Hnisz D;Abraham BJ;Lee TI;Lau A;Saint-André V;Sigova AA;Hoke HA;Young RA
通讯作者：
Young RA
影响因子：
32.4
作者：
Lio, Chan-Wang Joaquim;Hsieh, Chyi-Song
通讯作者：
Hsieh, Chyi-Song
影响因子：
64.8
作者：
Feng Y;van der Veeken J;Shugay M;Putintseva EV;Osmanbeyoglu HU;Dikiy S;Hoyos BE;Moltedo B;Hemmers S;Treuting P;Leslie CS;Chudakov DM;Rudensky AY
通讯作者：
Rudensky AY
DOI：
10.1126/science.1259418
发表时间：
2015-02-27
期刊：
Science (New York, N.Y.)
影响因子：
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作者：
Arner E;Daub CO;Vitting-Seerup K;Andersson R;Lilje B;Drabløs F;Lennartsson A;Rönnerblad M;Hrydziuszko O;Vitezic M;Freeman TC;Alhendi AM;Arner P;Axton R;Baillie JK;Beckhouse A;Bodega B;Briggs J;Brombacher F;Davis M;Detmar M;Ehrlund A;Endoh M;Eslami A;Fagiolini M;Fairbairn L;Faulkner GJ;Ferrai C;Fisher ME;Forrester L;Goldowitz D;Guler R;Ha T;Hara M;Herlyn M;Ikawa T;Kai C;Kawamoto H;Khachigian LM;Klinken SP;Kojima S;Koseki H;Klein S;Mejhert N;Miyaguchi K;Mizuno Y;Morimoto M;Morris KJ;Mummery C;Nakachi Y;Ogishima S;Okada-Hatakeyama M;Okazaki Y;Orlando V;Ovchinnikov D;Passier R;Patrikakis M;Pombo A;Qin XY;Roy S;Sato H;Savvi S;Saxena A;Schwegmann A;Sugiyama D;Swoboda R;Tanaka H;Tomoiu A;Winteringham LN;Wolvetang E;Yanagi-Mizuochi C;Yoneda M;Zabierowski S;Zhang P;Abugessaisa I;Bertin N;Diehl AD;Fukuda S;Furuno M;Harshbarger J;Hasegawa A;Hori F;Ishikawa-Kato S;Ishizu Y;Itoh M;Kawashima T;Kojima M;Kondo N;Lizio M;Meehan TF;Mungall CJ;Murata M;Nishiyori-Sueki H;Sahin S;Nagao-Sato S;Severin J;de Hoon MJ;Kawai J;Kasukawa T;Lassmann T;Suzuki H;Kawaji H;Summers KM;Wells C;FANTOM Consortium;Hume DA;Forrest AR;Sandelin A;Carninci P;Hayashizaki Y
通讯作者：
Hayashizaki Y
影响因子：
64.8
作者：
通讯作者：
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