Activation of the Jak-Stat pathway in cells that exhibit selective sensitivity to the antiviral effects of IFN-β compared with IFN-α

被引:28
作者
Grumbach, IM
Fish, EN
Uddin, S
Majchrzak, B
Colamonici, OR
Figulla, HR
Heim, A
Platanias, LC
机构
[1] Univ Illinois, Hematol Oncol Sect, Chicago, IL 60607 USA
[2] W Side VA Hosp, Chicago, IL 60607 USA
[3] Univ Toronto, Dept Med Genet & Microbiol, Toronto, ON M5S 3E2, Canada
[4] Univ Tennessee, Dept Pathol, Memphis, TN 38163 USA
[5] Univ Gottingen, Abt Kardiol, Gottingen, Germany
[6] Med Hsch Hannover, Inst Virol & Seuchen Hyg, Hannover, Germany
关键词
D O I
10.1089/107999099313659
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We determined whether selective activation of components of the Jak-Stat pathway by different type I interferons (IFN) occurs in human myocardial fibroblasts that exhibit much higher sensitivity to the antiviral effects of IFN-beta than of IFN-alpha. Similar levels of activation of the Tyk2 kinase and the Stat3 transcription factor were induced in response to either IFN-beta or IFN-alpha treatment. However, activation of the Jak1 tyrosine kinase was detectable only in IFN-beta-treated but not IFN-alpha-treated cells. Consistent with this, tyrosine phosphorylation of Stat1 and Stat2 and formation of the IFN-stimulated gene factor 3 (ISGF3) complex occurred to a much higher degree in response to IFN-beta stimulation. These findings demonstrate that differential activation of distinct components of the Jak-Stat pathway by different type I IFN can occur. Furthermore, they strongly suggest that such selective activation accounts for the occurrence of differences in the antiviral properties of distinct type I IFN in certain cell types.
引用
收藏
页码:797 / 801
页数:5
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