Abstract：
:Flavivirus-mediated inflammation causes neuronal death, but whether the infected neurons can evoke an innate immune response to elicit their own protection, is unknown. In an earlier study we have shown that neuronal RIG-I, play a significant role in inducing production and release of molecules that are related to inflammation. In this study, using a neuronal cell line, we show that RIG-I acts with STING in a concerted manner following its interaction with Japanese encephalitis viral RNA to induce a type 1 interferon response. Knock-down of STING showed that the expressions of various inflammatory signaling molecules were down-regulated along with increased intracellular viral load. Alternatively, over-expressing STING decreased intracellular viral load. Our results indicate that at the sub-cellular level, interaction between the pattern recognition receptor RIG-I and the adapter molecule STING, is a major contributor to elicit immunological responses involving the type 1 interferons in neurons following JEV infections.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Nazmi A,Mukhopadhyay R,Dutta K,Basu Adoi
10.1038/srep00347subject
Has Abstractpub_date
2012-01-01 00:00:00pages
347issn
2045-2322journal_volume
2pub_type
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journal_title：Scientific reports
pub_type： 杂志文章,meta分析
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abstract：:Copy Number Variants (CNVs) are a class of structural variations of DNA. Germline CNVs are known to confer disease susceptibility, but their role in breast cancer warrants further investigations. We hypothesized that breast cancer associated germline CNVs contribute to disease risk through gene dosage or other post-tr...
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pub_type： 杂志文章
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pub_type： 杂志文章
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pub_type： 杂志文章
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pub_type： 杂志文章
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pub_type： 杂志文章
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pub_type： 杂志文章
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journal_title：Scientific reports
pub_type： 杂志文章
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更新日期：2013-01-01 00:00:00
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更新日期：2016-03-22 00:00:00
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pub_type： 杂志文章
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更新日期：2014-07-18 00:00:00
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