IL-21 induces IL-22 production in CD4+ T cells.

IL-21 induces IL-22 production in CD4+ T cells.
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DOI:
10.1038/ncomms4753
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发表时间:
2014-05-06
影响因子:
16.6
通讯作者:
Quintana, Francisco J.
Quintana, Francisco J.
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Yeste, Ada;Mascanfroni, Ivan D.;Nadeau, Meghan;Burns, Evan J.;Tukpah, Ann-Marcia;Santiago, Andrezza;Wu, Chuan;Patel, Bonny;Kumar, Deepak;Quintana, Francisco J.

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IL-22是由先天性淋巴细胞(inatelymphocyte,ILC)和CD 4 + T细胞产生的,在机体防御和黏膜内环境稳定中起重要作用,因此研究IL-22产生的调控机制具有重要意义。我们研究了CD 4 + T细胞产生IL-22的调节。在这里,我们表明,IL-21触发IL-22,但不是IL-17的CD 4 + T细胞的生产。由IL-21激活的STAT 3控制il 22启动子的表观遗传状态及其与芳烃受体(AhR)的相互作用。此外,T细胞中的IL-21和AhR信号传导控制IL-22产生和ILC缺陷小鼠中葡聚糖硫酸钠诱导的结肠炎的发展。因此,我们已经确定了IL-21作为诱导剂的IL-22生产的CD 4 + T细胞在体外和体内。
IL-22 produced by innate lymphoid cells (ILCs) and CD4+ T cells plays an important role in host defense and mucosal homeostasis, thus it is important to investigate the mechanisms that regulate IL-22 production. We investigated the regulation IL-22 production by CD4+ T cells. Here we show that IL-21 triggers IL-22, but not IL-17 production by CD4+ T cells. STAT3, activated by IL-21, controls the epigenetic status of the il22 promoter and its interaction with the aryl hydrocarbon receptor (AhR). Moreover, IL-21 and AhR signaling in T cells control IL-22 production and the development of dextran sodium sulfate-induced colitis in ILC-deficient mice. Thus, we have identified IL-21 as an inducer of IL-22 production in CD4+ T cells in vitro and in vivo.
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