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维甲酸诱导基因-I在肠道上皮细胞中组成性表达,并参与干扰素-γ刺激的CXCL9-11生成。

Retinoic acid-inducible gene-I is constitutively expressed and involved in IFN-gamma-stimulated CXCL9-11 production in intestinal epithelial cells.

作者信息

Kawaguchi Shogo, Ishiguro Yoh, Imaizumi Tadaatsu, Mori Fumiaki, Matsumiya Tomoh, Yoshida Hidemi, Ota Ken, Sakuraba Hirotake, Yamagata Kazufumi, Sato Yuki, Tanji Kunikazu, Haga Toshihiro, Wakabayashi Koichi, Fukuda Shinsaku, Satoh Kei

机构信息

Department of Gastroenterology and Hematology, Institute of Brain Science, Hirosaki University Graduate School of Medicine, 5 Zaifu-cho, Hirosaki, 036-8562, Japan.

出版信息

Immunol Lett. 2009 Mar 24;123(1):9-13. doi: 10.1016/j.imlet.2009.01.008. Epub 2009 Feb 6.

DOI:10.1016/j.imlet.2009.01.008
PMID:19201382
Abstract

Retinoic acid-inducible gene-I (RIG-I) is a member of the DExH/D family proteins, and plays an important role in antiviral response via interferon-stimulated genes (ISGs) and type 1 IFN. In this study, the roles of RIG-I in the epithelial cells in the cross-talk between type 2 IFN and inducible chemokines production are high-lighted. The results showed that RIG-I was constitutively expressed in normal surface epithelia lining the colonic mucosa. RIG-I was constitutively expressed in the epithelial cell lines HT-29, and IFN-gamma and TNF-alpha enhanced the RIG-I expression in a dose-dependent manner. IFN-gamma was shown to stimulate CXCL9-11 production, and RNA interference against RIG-I resulted in significant decrease of IFN-gamma-induced CXCL9-11 productions. These results suggest that RIG-I play an important role in the cross-talk between inflammatory cytokines and immune cell trafficking. In conclusion, RIG-I might regulate the gut barrier function in homeostatic and inflammatory conditions.

摘要

维甲酸诱导基因I(RIG-I)是DExH/D家族蛋白的成员之一,通过干扰素刺激基因(ISG)和1型干扰素在抗病毒反应中发挥重要作用。在本研究中,着重探讨了RIG-I在2型干扰素与诱导性趋化因子产生之间的相互作用中在上皮细胞中的作用。结果显示,RIG-I在结肠黏膜的正常表面上皮中组成性表达。RIG-I在HT-29上皮细胞系中组成性表达,并且干扰素-γ和肿瘤坏死因子-α以剂量依赖性方式增强RIG-I的表达。已表明干扰素-γ可刺激CXCL9 - 11的产生,针对RIG-I的RNA干扰导致干扰素-γ诱导的CXCL9 - 11产生显著降低。这些结果表明,RIG-I在炎性细胞因子与免疫细胞迁移之间的相互作用中发挥重要作用。总之,RIG-I可能在稳态和炎症条件下调节肠道屏障功能。

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