Display Settings:   Send to:  Choose Destination Proc Natl Acad
Sci U S A. 2008 Dec 23;105(51):20446-51. doi:
10.1073/pnas.0810372105. Epub 2008 Dec 11.   Author information
A conundrum of innate antiviral immunity is how nucleic acid-
sensing Toll-like receptors (TLRs) and RIG-I/MDA5 receptors
cooperate during virus infection. The conventional wisdom has
been that the activation of these receptor pathways evokes type
I IFN (IFN) responses. Here, we provide evidence for a critical
role of a Toll-like receptor 3 (TLR3)-dependent type II IFN
signaling pathway in antiviral innate immune response against
Coxsackievirus group B serotype 3 (CVB3), a member of the
positive-stranded RNA virus family picornaviridae and most
prevalent virus associated with chronic dilated cardiomyopathy.
TLR3-deficient mice show a vulnerability to CVB3, accompanied by
acute myocarditis, whereas transgenic expression of TLR3 endows
even type I IFN signal-deficient mice resistance to CVB3 and
other types of viruses, provided that type