Back

PKR and the Integrated Stress Response drive immunopathology caused by ADAR1 mutation

Maurano, M.; Snyder, J. M.; Connelly, C.; Henao-Mejia, J.; Sidrauski, C.; Stetson, D. B.

2020-12-01 immunology
10.1101/2020.11.30.405498 bioRxiv
Show abstract

Mutations in ADAR, the gene that encodes the ADAR1 RNA deaminase, cause numerous human diseases, including Aicardi-Goutieres Syndrome (AGS). ADAR1 is an essential negative regulator of the RNA sensor MDA5, and loss of ADAR1 function triggers inappropriate activation of MDA5 by self-RNAs. However, the mechanisms of MDA5-dependent disease pathogenesis in vivo remain unknown. Here, we introduce a knockin mouse that models the most common ADAR AGS mutation in humans. These Adar-mutant mice develop lethal disease that requires MDA5, the RIG-I-like receptor LGP2, type I interferons, and the eIF2 kinase PKR. We show that a small molecule inhibitor of the integrated stress response (ISR) that acts downstream of eIF2 phosphorylation prevents immunopathology and rescues the mice from mortality. These findings place PKR and the ISR as central components of immunopathology in vivo and identify new therapeutic targets for treatment of human diseases associated with the ADAR1-MDA5 axis.

Matching journals

The top 2 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.