Hepatocyte-macrophage crosstalk via the PGRN-EGFR axis modulates ADAR1-mediated immunity in the liver -bulk RNA-seq
ADAR1 is thought to be an immune suppressor maintaining self-tolerance to endogenous nucleic acids. Lack of ADAR1 results in MDA5 (Ifih1) activation and MDA5 deletion rescues ADAR1 null embryonic lethality. We generated liver specific ADAR1; MDA5 double KO mice and performed high throughput sequencing to investigate hepatic inflammation in these mice. Bulk RNA was sequenced on the HiSeq X platform. Over 100 million pairs of mappable reads for each sample were obtained. Overall design: Transcriptomes of Ifih1-/- Adar1wt/wt Alb-Cre+ (n=3), Ifih1-/- Adar1wt/flox Alb-Cre+ (n=2), and Ifih1-/- Adar1flox/flox Alb-Cre+ (n=2) mice livers were compared to examine the effects of Adar1 depletion against Ifih1 null background.