{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Deochand DK"],"funding":["NIDDK NIH HHS","NIAID NIH HHS","NHLBI NIH HHS","U.S. Department of Health &amp; Human Services | National Institutes of Health (NIH)","The Hospital for Special Surgery David Rosensweig Genomics Center","U.S. Department of Health &amp; Human Services | National Institutes of Health"],"pagination":["9000"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11489752"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["Macrophages adopt distinct phenotypes in response to environmental cues, with type-2 cytokine interleukin-4 promoting a tissue-repair homeostatic state (M2<sub>IL4</sub>). Glucocorticoids (GC), widely used anti-inflammatory therapeutics, reportedly impart a similar phenotype (M2<sub>GC</sub>), but how such disparate pathways may functionally converge is unknown. We show using integrative functional genomics that M2<sub>IL4</sub> and M2<sub>GC</sub> transcriptomes share a striking overlap mirrored by a shift in chromatin landscape in both common and signal-specific gene subsets. This core homeostatic program is enacted by transcriptional effectors KLF4 and the glucocorticoid receptor, whose genome-wide occupancy and actions are integrated in a stimulus-specific manner by the nuclear recepto"],"journal":["Nature communications"],"pubmed_title":["Mechanisms of epigenomic and functional convergence between glucocorticoid- and IL4-driven macrophage programming."],"pmcid":["PMC11489752"],"funding_grant_id":["NIH R01AI148416","F31 HL152706","F31 HL152706-01A1","R01 AI148129","R01 AI148416","NIH R01AI148129","NIH R01DK099087","R01 DK099087"],"pubmed_authors":["Deochand DK","Oliver D","Bale MJ","Chinenov Y","Chaudhary V","Rogatsky I","Josefowicz SZ","Dacic M","Daman AW"],"additional_accession":[]},"is_claimable":false,"name":"Mechanisms of epigenomic and functional convergence between glucocorticoid- and IL4-driven macrophage programming.","description":"Macrophages adopt distinct phenotypes in response to environmental cues, with type-2 cytokine interleukin-4 promoting a tissue-repair homeostatic state (M2<sub>IL4</sub>). Glucocorticoids (GC), widely used anti-inflammatory therapeutics, reportedly impart a similar phenotype (M2<sub>GC</sub>), but how such disparate pathways may functionally converge is unknown. We show using integrative functional genomics that M2<sub>IL4</sub> and M2<sub>GC</sub> transcriptomes share a striking overlap mirrored by a shift in chromatin landscape in both common and signal-specific gene subsets. This core homeostatic program is enacted by transcriptional effectors KLF4 and the glucocorticoid receptor, whose genome-wide occupancy and actions are integrated in a stimulus-specific manner by the nuclear recepto","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Oct","modification":"2026-07-15T04:58:36.812Z","creation":"2025-04-04T01:46:45.888Z"},"accession":"S-EPMC11489752","cross_references":{"pubmed":["39424780"],"doi":["10.1038/s41467-024-52942-x"]}}