RESEARCH ARTICLE
TLR3 Sensing of Viral Infection
F. Dunlevy, N. G. McElvaney, C. M. Greene*
Respiratory Research Division, Department of Medicine, Royal College of Surgeons in Ireland, Education and Research Centre, Beaumont Hospital, Dublin 9, Ireland.
Article Information
Identifiers and Pagination:
Year: 2010Volume: 4
First Page: 1
Last Page: 10
Publisher Id: TOIDJ-4-1
DOI: 10.2174/1874279301004010001
Article History:
Received Date: 1/10/2009Revision Received Date: 17/2/2010
Acceptance Date: 30/3/2010
Electronic publication date: 4/4/2010
Collection year: 2010
© 2010 Dunlevy et al.
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.
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.
Abstract
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.
Keywords: TLR3, virus, dsRNA, signalling, type 1 interferons, NF-kB..
