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Macrophages adopt distinct phenotypes in response to environmental cues, with type-2 cytokine interleukin-4 promoting a tissue-repair homeostatic state (M2). Glucocorticoids (GC), widely used anti-inflammatory therapeutics, reportedly impart a similar phenotype (M2), but how such disparate pathways may functionally converge is unknown. We show using integrative functional genomics that M2 and M2 transcriptomes share a striking overlap mirrored by a shift in chromatin landscape in both common and signal-specific gene subsets.

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