Citation

BibTex format

@inproceedings{Goritzka:2014,
author = {Goritzka, M and Durant, LR and Pereira, C and Salek-Ardakani, S and Openshaw, P and Johansson, C},
pages = {6128--6136},
publisher = {Wiley},
title = {Interferon-a/b  receptor signalling is amplifying early proinflammatory cytokine production in the lung during Respiratory Syncytial Virus (RSV) infection},
url = {http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000327487700209&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202},
year = {2014}
}
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RIS format (EndNote, RefMan)

TY  - CPAPER
AB  - Type I interferons (IFNs) are produced early upon virus infection and signal through the alpha/beta interferon (IFN-/) receptor(IFNAR) to induce genes that encode proteins important for limiting viral replication and directing immune responses. Toinvestigate the extent to which type I IFNs play a role in the local regulation of inflammation in the airways, we examined theirimportance in early lung responses to infection with respiratory syncytial virus (RSV). IFNAR1-deficient (IFNAR1 / ) mice displayedincreased lung viral load and weight loss during RSV infection. As expected, expression of IFN-inducible genes was markedlyreduced in the lungs of IFNAR1 /  mice. Surprisingly, we found that the levels of proinflammatory cytokines and chemokinesin the lungs of RSV-infected mice were also greatly reduced in the absence of IFNAR signaling. Furthermore, low levels ofproinflammatory cytokines were also detected in the lungs of IFNAR1 /  mice challenged with noninfectious innate immunestimuli such as selected Toll-like receptor (TLR) agonists. Finally, recombinant IFN- was sufficient to potentiate the productionof inflammatory mediators in the lungs of wild-type mice challenged with innate immune stimuli. Thus, in addition to itswell-known role in antiviral resistance, type I IFN receptor signaling acts as a central driver of early proinflammatory responsesin the lung. Inhibiting the effects of type I IFNs may therefore be useful in dampening inflammation in lung diseases characterizedby enhanced inflammatory cytokine production.
AU  - Goritzka,M
AU  - Durant,LR
AU  - Pereira,C
AU  - Salek-Ardakani,S
AU  - Openshaw,P
AU  - Johansson,C
EP  - 6136
PB  - Wiley
PY  - 2014///
SN  - 0019-2805
SP  - 6128
TI  - Interferon-a/b  receptor signalling is amplifying early proinflammatory cytokine production in the lung during Respiratory Syncytial Virus (RSV) infection
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000327487700209&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
ER  -
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