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IL-4 treatment induces apoptosis of blood monocytes and proliferation of reparative macrophages to resolve liver injury.

GSE242411 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2026/02/20 Platform GPL24247
Summary
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.
Published in
IL-4 treatment induces apoptosis of blood monocytes and proliferation of recruited injury-associated macrophages to resolve liver injury
Lynch RW, Louwe PA, Martens L et al. · Cell reports 2026 · PMID 41865375 · doi:10.1016/j.celrep.2026.117136
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Also filed as BioProject PRJNA1013185 and SRA study SRP458740. Searching any of these in the dataset finder brings you back here.

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