Forced IFIT-2 expression represses LPS induced TNF-alpha expression at posttranscriptional levels

被引：51

作者：

Berchtold, Susanne ^{[1
]}

Manncke, Birgit ^{[1
]}

Klenk, Juliane ^{[1
]}

Geisel, Julia ^{[1
]}

Autenrieth, Ingo B. ^{[1
]}

Bohn, Erwin ^{[1
]}

机构：

[1] Univ Klinikum Tubingen, Inst Med Mikrobiol & Hyg, Tubingen, Germany

来源：

BMC IMMUNOLOGY | 2008年 / 9卷 / 1期

关键词：

D O I：

10.1186/1471-2172-9-75

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Background: Interferon induced tetratricopeptide repeat protein 2 (IFIT-2, P54) belongs to the type I interferon response genes and is highly induced after stimulation with LPS. The biological function of this protein is so far unclear. Previous studies indicated that IFIT-2 binds to the initiation factor subunit eIF-3c, affects translation initiation and inhibits protein synthesis. The aim of the study was to further characterize the function of IFIT-2. Results: Stimulation of RAW264.7 macrophages with LPS or IFN-gamma leads to the expression of IFIT-2 in a type I interferon dependent manner. By using stably transfected RAW264.7 macrophages overexpressing IFIT-2 we found that IFIT-2 inhibits selectively LPS induced expression of TNF-alpha, IL-6, and MIP-2 but not of IFIT-1 or EGR-1. In IFIT-2 overexpressing cells TNF-alpha mRNA expression was lower after LPS stimulation due to reduced mRNA stability. Further experiments suggest that characteristics of the 3'UTR of transcripts discriminate whether IFIT-2 has a strong impact on protein expression or not. Conclusion: Our data suggest that IFIT-2 may affect selectively LPS induced protein expression probably by regulation at different posttranscriptional levels.

引用

页数：12

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