小鼠成纤维细胞的转化改变了病毒感染后I型干扰素的诱导模式。

Transformation of mouse fibroblasts alters the induction pattern of type I IFNs after virus infection.

作者信息

Samuelsson Christofer V, Lienenklaus Stefan, Müller Peter P, Zawatzky Rainer, Hauser Hansjörg, Weiss Siegfried

机构信息

Molecular Immunology, GBF, German Research Centre for Biotechnology, Braunschweig, Germany.

出版信息

Biochem Biophys Res Commun. 2005 Sep 23;335(2):584-9. doi: 10.1016/j.bbrc.2005.07.124.

DOI:10.1016/j.bbrc.2005.07.124

PMID:16091286

Abstract

Type I interferons (IFNs) have been shown to be involved in many immune defence and inflammatory responses. We here show that IFN-beta plays an absolute essential role in the efficient induction of all type I IFNs after infection of primary embryonic as well as primary adult fibroblasts with Sendai virus. In contrast, after immortalization of such fibroblasts with SV40 large T antigen, IFN-alpha4 can be induced independently of IFN-beta. However, efficient secretion of type I IFNs even in immortalized fibroblasts is only found when the complete signalling loop is induced by IFN-beta.

摘要

I型干扰素（IFNs）已被证明参与多种免疫防御和炎症反应。我们在此表明，在用仙台病毒感染原代胚胎和成体原代成纤维细胞后，IFN-β在所有I型干扰素的有效诱导中起着绝对关键的作用。相比之下，在用SV40大T抗原使此类成纤维细胞永生化后，IFN-α4可以独立于IFN-β被诱导。然而，只有当IFN-β诱导完整的信号传导回路时，才会在永生化的成纤维细胞中发现I型干扰素的有效分泌。