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

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 induc...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Immunology letters 2009-03, Vol.123 (1), p.9-13
Hauptverfasser: 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
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung: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-γ and TNF-α enhanced the RIG-I expression in a dose-dependent manner. IFN-γ was shown to stimulate CXCL9–11 production, and RNA interference against RIG-I resulted in significant decrease of IFN-γ-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.
ISSN:0165-2478
1879-0542
DOI:10.1016/j.imlet.2009.01.008