@article{oai:nagasaki-u.repo.nii.ac.jp:00008359,
 author = {Ishibashi, Daisuke and Atarashi, Ryuichiro and Nishida, Noriyuki},
 issue = {5},
 journal = {Prion},
 month = {Nov},
 note = {Despite recent progress in the understanding of prion diseases, little is known about the host-defense mechanisms against prion. Although it has long been thought that type I interferon (IFN-I) has no protective effect on prion infection, certain key molecules in innate immunity such as toll-like receptor (TLR) 4 seemed to be involved in the host response. For this reason we decided to focus on TLRs and investigate the role of a transcription factor, interferon regulatory factor 3 (IRF3), because the absence of MyD88, a major adaptor signaling molecule of TLRs, has no effect on the survival of prion infected mice. Intriguingly, survival periods of prion inoculated IRF3-knockout mice became significantly shorter than those of wildtype mice. In addition, IRF3 stimulation inhibited PrPSc replication in prion persistently- infected cells, and a de novo prion infection assay revealed that IRF3-overexpression could make host cells resistant to prion infection. Our work suggests that IRF3 may play a key role in innate immune responses against invasion of prion pathogens. Activated IRF3 could upregulate several anti-pathogen factors, including IFN-I, and induce sequential responses. Although the mechanism for the anti-prion effects mediated by IRF3 has yet to be clarified, certain interferon responsive genes might be involved in the anti-prion host-defense mechanism., Prion, 6(5), pp.443-446; 2012},
 pages = {443--446},
 title = {Protective role of MyD88-independent innate immune responses against prion infection},
 volume = {6},
 year = {2012}
}