Type I interferon protects neurons from prions in in vivo models

Ishibashi, Daisuke; Homma, Takujiro; Nakagaki, Takehiro; Fuse, Takayuki; Sano, Kazunori; Satoh, Katsuya; Mori, Tsuyoshi; Atarashi, Ryuichiro; Nishida, Noriyuki

In conclusion, the I-IFN pathway contributes to host defence mechanism against prion infection. Although we do not yet know exactly how host cells can recognize the prion pathogen, which lacks its own genetic material, the IFR3-IFN pathway serves as an important line of defence. Interference with this pathway permits persistent prion infection. The reciprocal interaction between innate host immunity and invading prions may explain the long latency of prion diseases. I-IFN and TLR signalling have diverse functions, including activation of autophagic systems that promote degradation of -synuclein-derived aggregations (Ejlerskov et al., 2015; Kim et al., 2015) and contribute to neuronal homeostasis (Taniguchi and Takaoka, 2001) . Therefore, effects of I-IFN should be considered in further investigations. Elucidating the role of host immunity in prion diseases could facilitate development of novel therapeutics for this deadly disease.