TGF-β induces the expression of the adaptor Ndfip1 to silence IL-4 production during iTreg cell differentiation.
TGF-β induces the expression of the adaptor Ndfip1 to silence IL-4 production during iTreg cell differentiation.
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DOI：
10.1038/ni.2154
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发表时间：
2011-11-13
影响因子：
30.5
通讯作者：
Oliver, Paula M.
中科院分区：
文献类型：
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作者：
Beal, Allison M.;Ramos-Hernandez, Natalia;Riling, Chris R.;Nowelsky, Erin A.;Oliver, Paula M.
Mice deficient for the adaptor Ndfip1 develop inflammation at sites of environmental antigen exposure. We show here that these animals contain fewer inducible regulatory (iTreg) cells. In vitro, Ndfip1-deficient T cells express normal levels of the transcription factor Foxp3 during the first 48 hours of iTreg cell differentiation, however this cannot be sustained. Abortive Foxp3 expression is because Ndfip1–/– cells produce interleukin 4 (IL-4). We demonstrate that Ndfip1 is transiently unregulated during iTreg cell differentiation in a transforming growth factor-β (TGF-β) dependent manner. Once expressed Ndfip1 promotes Itch-mediated degradation of the transcription factor JunB, thus preventing IL-4 production. Based on these data, we propose that TGF-β signaling induces Ndfip1 expression to silence IL-4 production, thus permitting iTreg cell differentiation.
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影响因子：
15.3
作者：
Apostolou, I;von Boehmer, H
通讯作者：
von Boehmer, H
影响因子：
32.4
作者：
Oliver, Paula M.;Cao, Xiao;Yang, Baoli
通讯作者：
Yang, Baoli
GATA3驱动的Th2响应抑制TGF-BETA1诱导的FOXP3表达和调节T细胞的形成。
影响因子：
9.8
作者：
Mantel PY;Kuipers H;Boyman O;Rhyner C;Ouaked N;Rückert B;Karagiannidis C;Lambrecht BN;Hendriks RW;Crameri R;Akdis CA;Blaser K;Schmidt-Weber CB
通讯作者：
Schmidt-Weber CB
影响因子：
30.5
作者：
Dardalhon, Valerie;Awasthi, Amit;Kwon, Hyoung;Galileos, George;Gao, Wenda;Sobel, Raymond A.;Mitsdoerffer, Meike;Strom, Terry B.;Elyaman, Wassim;Ho, I-Cheng;Khoury, Samia;Oukka, Mohamed;Kuchroo, Vijay K.
通讯作者：
Kuchroo, Vijay K.
DOI：
10.4049/jimmunol.1000690
发表时间：
2010-11-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Liang Q;Guo L;Gogate S;Karim Z;Hanifi A;Leung DY;Gorska MM;Alam R
通讯作者：
Alam R