Notch receptors and Smad3 signaling cooperate in the induction of interleukin-9-producing T cells.
Notch receptors and Smad3 signaling cooperate in the induction of interleukin-9-producing T cells.
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DOI：
10.1016/j.immuni.2012.01.020
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发表时间：
2012-04-20
期刊：
影响因子：
32.4
通讯作者：
Khoury SJ
中科院分区：
文献类型：
--
作者：
Elyaman W;Bassil R;Bradshaw EM;Orent W;Lahoud Y;Zhu B;Radtke F;Yagita H;Khoury SJ
Interleukin 9 (IL-9) is a pleiotropic cytokine that can regulate autoimmune responses by enhancing regulatory CD4+FoxP3+ T regulatory (Treg) cell survival and T helper 17 (Th17) cell proliferation. Here, we analyzed the costimulatory requirements for the induction of Th9 cells, and demonstrated that Notch pathway cooperated with TGF-β signaling to induce IL-9. Conditional ablation of Notch1 and Notch2 receptors inhibited the development of Th9 cells. Notch1 intracellular domain (NICD1) recruited Smad3, downstream of TGF-β cytokine signaling, and together with recombining binding protein (RBP)-Jκ bound the Il9 promoter and induced its transactivation. In experimental autoimmune encephalomyelitis (EAE), Jagged2 ligation regulated clinical disease in an IL-9-dependent fashion. Signaling through Jagged2 expanded Treg cells and suppressed EAE when administered before antigen immunization, but worsened EAE when administered concurrently with immunization by favoring Th17 cell expansion. We propose that Notch and Smad3 cooperate to induce IL-9 and participate in regulating the immune response.
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影响因子：
64.8
作者：
Bettelli, E;Carrier, YJ;Kuchroo, VK
通讯作者：
Kuchroo, VK
影响因子：
4.4
作者：
Fukushima, Atsuki;Sumi, Tamaki;Yagita, Hideo
通讯作者：
Yagita, Hideo
DOI：
10.1084/jem.20091442
发表时间：
2009-08-03
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Locksley RM
通讯作者：
Locksley RM
影响因子：
82.9
作者：
Korn, Thomas;Reddy, Jayagopala;Kuchroo, Vijay K.
通讯作者：
Kuchroo, Vijay K.
影响因子：
64.8
作者：
JARRIAULT, S;BROU, C;ISRAEL, A
通讯作者：
ISRAEL, A