GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE242nnn/GSE242411/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE242411GEOGSEfalseIL-4 treatment induces apoptosis of blood monocytes and proliferation of reparative macrophages to resolve liver injury.IL-4 can have significant therapeutic benefit in many injury settings, but its mechanism of action is unclear. Here, we show that, in a model ofCCl4-mediatedacuteliver injury, exogenous IL-4 caused adramatic shift from recruited Ly6Chimonocytes to an abundance of monocyte-derived macrophages. This shift in macrophage dynamics was associated with accelerated clearance of necrotic tissue and enhanced hepatocyte regeneration that required IL-4 receptor-signalling to leukocytes. IL-4 did not alter monocyte recruitment or differentiation but instead stimulated monocyte apoptosis and acted on previously-recruited macrophages to drive proliferation and pro-repair characteristics, including expression of key genes involved in dismantling necrotic tissue. Further scRNA-seq analysis of the impact of IL-4 on all hepatic myeloid lineages revealed injury and cell-type specific responses. Together, our data reveal a novel pathway by which IL-4 alters the composition and functional specification of injury-associated myeloid cells and resolves injury in the liver.2026/02/20GSE242411GSM7763229GSM7763228GSM7763227GSM776322624247242411Mus musculus