The interleukin 23 receptor is essential for the terminal differentiation of interleukin 17-producing effector T helper cells in vivo.

The interleukin 23 receptor is essential for the terminal differentiation of interleukin 17-producing effector T helper cells in vivo.
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DOI:
10.1038/ni.1698
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发表时间:
2009-03
期刊:
影响因子:
30.5
通讯作者:
--
中科院分区:
医学1区
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--
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白细胞介素23(IL-23)是由辅助性T细胞17型(TH-17细胞)介导的自身免疫炎症所必需的,并且与许多人类免疫疾病有关。在此,我们将IL-23受体(IL-23 R)缺陷限制在体内确定的细胞群中,以研究TH-17发育和自身免疫、炎症和感染中功能对IL-23信号传导的需求。在没有IL-23的情况下,TH-17发育在早期活化阶段“停滞”。TH-17细胞不能下调IL-2和肿瘤坏死因子受体超家族成员CD 27,维持IL-17的产生并上调IL-7 R α的表达。这些缺陷与增殖减少和离开淋巴结进入血流和组织的效应TH-17细胞数量减少有关。
Interleukin 23 (IL-23) is required for autoimmune inflammation mediated by T helper type 17 cells (TH-17 cells) and is implicated in a number of human immune disorders. Here we restricted IL-23 receptor (IL-23R) deficiency to defined cell populations in vivo to investigate the requirement for IL-23 signaling in TH-17 development and function in autoimmunity, inflammation, and infection. In the absence of IL-23, TH-17 development was ‘stalled’ at the early activation stage. TH-17 cells failed to downregulate IL-2 and the tumor necrosis factor receptor superfamily member CD27, to maintain IL-17 production and to upregulate IL-7Rα expression. These defects were associated with reduced proliferation and reduced numbers of effector TH-17 cells that exit lymph nodes destined for the bloodstream and tissues.
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期刊: CELL
影响因子: 64.5
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