Yeste Ada, Mascanfroni Ivan D, Nadeau Meghan, Burns Evan J, Tukpah Ann-Marcia, Santiago Andrezza, Wu Chuan, Patel Bonny, Kumar Deepak, Quintana Francisco J
1] Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA [2].
Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA.
Nat Commun. 2014 May 6;5:3753. doi: 10.1038/ncomms4753.
Interleukin (IL)-22 produced by innate lymphoid cells (ILCs) and CD4+ T cells plays an important role in host defence 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 signalling in T cells control IL-22 production and the development of dextran sodium sulphate-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.
由固有淋巴细胞（ILC）和CD4 + T细胞产生的白细胞介素（IL）-22在宿主防御和粘膜稳态中起重要作用，因此研究调节IL-22产生的机制非常重要。我们研究了CD4 + T细胞对IL-22产生的调节作用。在此我们表明，IL-21触发CD4 + T细胞产生IL-22，但不触发其产生IL-17。由IL-21激活的STAT3控制il22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的产生以及ILC缺陷小鼠中葡聚糖硫酸钠诱导的结肠炎的发展。因此，我们已确定IL-21在体外和体内均为CD4 + T细胞中IL-22产生的诱导剂。
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