| Autor: |
Yi Wang, Hong-Xin Zhang, Yue-Ping Sun, Zi-Xing Liu, Xue-Song Liu, Long Wang, Shun-Yuan Lu, Hui Kong, Qiao-Ling Liu, Xi-Hua Li, Zhen-Yu Lu, Sai-Juan Chen, Zhu Chen, Shi-San Bao, Wei Dai, Zhu-Gang Wang |
| Předmět: |
|
| Zdroj: |
Cell Research; Oct2007, Vol. 17 Issue 10, p858-868, 11p, 1 Black and White Photograph, 5 Graphs |
| Abstrakt: |
RIG-I (retinoid acid-inducible gene-I), a putative RNA helicase with a cytoplasmic caspase-recruitment domain (CARD), was identified as a pattern-recognition receptor (PRR) that mediates antiviral immunity by inducing type I interferon production. To further study the biological function of RIG-I, we generated Rig-I−/− mice through homologous recombination, taking a different strategy to the previously reported strategy. Our Rig-I−/− mice are viable and fertile. Histological analysis shows that Rig-I−/− mice develop a colitis-like phenotype and increased susceptibility to dextran sulfate sodium-induced colitis. Accordingly, the size and number of Peyer's patches dramatically decreased in mutant mice. The peripheral T-cell subsets in mutant mice are characterized by an increase in effector T cells and a decrease in naïve T cells, indicating an important role for Rig-I in the regulation of T-cell activation. It was further found that Rig-I deficiency leads to the downregulation of G protein αi2 subunit (Gαi2) in various tissues, including T and B lymphocytes. By contrast, upregulation of Rig-I in NB4 cells that are treated with ATRA is accompanied by elevated Gαi2 expression. Moreover, Gαi2 promoter activity is increased in co-transfected NIH3T3 cells in a Rig-I dose-dependent manner. All these findings suggest that Rig-I has crucial roles in the regulation of Gαi2 expression and T-cell activation. The development of colitis may be, at least in part, associated with downregulation of Gαi2 and disturbed T-cell homeostasis.Cell Research (2007) 17:858–868. doi: 10.1038/cr.2007.81; published online 25 September 2007 [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
