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Nazmi, A and Mukhopadhyay, R and Dutta, K and Basu, A (2012) STING Mediates Neuronal Innate Immune Response Following Japanese Encephalitis Virus Infection. Scientific Reports.

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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.

Item Type: Article
Subjects: Neurodegenerative Disorders
Neuro-Oncological Disorders
Neurocognitive Processes
Neuronal Development and Regeneration
Informatics and Imaging
Genetics and Molecular Biology
Depositing User: Dr. D.D. Lal
Date Deposited: 05 May 2017 04:26
Last Modified: 15 Jan 2018 09:26
URI: http://nbrc.sciencecentral.in/id/eprint/67

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