Abstract:
:Secretion of type I interferon (IFN) is the first cellular reaction to invading pathogens. Despite the protective function of these cytokines, an excessive response to their action can contribute to serious pathologies, such as autoimmune diseases. Transcripts of most cytokines contain adenylate-uridylate (A/U)-rich elements (AREs) that make them highly unstable. RNA-binding proteins (RBPs) are mediators of the regulatory mechanisms that determine the fate of mRNAs containing AREs. Here, we applied an affinity proteomic approach and identified lethal, abnormal vision, drosophila-like 1 (ELAVL1)/Hu antigen R (HuR) as the predominant RBP of the IFN-β mRNA ARE. Reduced expression or chemical inhibition of HuR severely hampered the type I IFN response in various cell lines and fibroblast-like synoviocytes isolated from joints of rheumatoid arthritis patients. These results define a role for HuR as a potent modulator of the type I IFN response. Taken together, HuR could be used as therapeutic target for diseases where type I IFN production is exaggerated.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Herdy B,Karonitsch T,Vladimer GI,Tan CS,Stukalov A,Trefzer C,Bigenzahn JW,Theil T,Holinka J,Kiener HP,Colinge J,Bennett KL,Superti-Furga Gdoi
10.1002/eji.201444979subject
Has Abstractpub_date
2015-05-01 00:00:00pages
1500-11issue
5eissn
0014-2980issn
1521-4141journal_volume
45pub_type
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