Hepatocyte-macrophage crosstalk via the PGRN-EGFR axis modulates ADAR1-mediated immunity in the liver -scRNAseq
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. Single cell RNA sequencing was performed on cells isolated from mice livers. Constructed libraries were sequenced on the HiSeq X platform. Over 100 million pairs of mappable reads for each sample were obtained. Overall design: Transcriptomes of single cells isolated from Ifih1-/- Adar1wt/wt Alb-Cre+, Ifih1-/- Adar1wt/flox Alb-Cre+, and Ifih1-/- Adar1flox/flox Alb-Cre+ mice livers were compared to examine the effects of Adar1 depletion against Ifih1 null background.