TLR3 Sensing of Viral Infection
F. Dunlevy, N. G. McElvaney, C. M. Greene*
Identifiers and Pagination:Year: 2010
First Page: 1
Last Page: 10
Publisher Id: TOIDJ-4-1
Article History:Received Date: 1/10/2009
Revision Received Date: 17/2/2010
Acceptance Date: 30/3/2010
Electronic publication date: 4/4/2010
Collection year: 2010
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Viral infection is detected by the innate immune system which mounts a rapid semi-selective defence involving inflammation and production of type 1 interferons. Several sensors, both cell surface and intracellular, exist to detect different types of viral motifs. Double-stranded RNA viruses and dsRNA replication intermediates are detected by tolllike receptor 3 (TLR3) as well as by retinoid-inducible gene 1 (RIG-I) like receptors. Binding of dsRNA or its synthetic analogue poly I:C to TLR3 recruits the adaptor protein TRIF and stimulates distinct pathways leading to activation of interferon regulatory factor (IRF) and NF-κB. Here, we review the signalling cascades initiated by TLR3 and the modulation of these pathways.