{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T16:01:43Z","timestamp":1791475303792,"version":"4.3.4"},"reference-count":88,"publisher":"National Academy of Sciences","issue":"41","license":[{"start":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T00:00:00Z","timestamp":1791417600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["HL106173"],"award-info":[{"award-number":["HL106173"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["DK124782"],"award-info":[{"award-number":["DK124782"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2026,10,13]]},"abstract":"<jats:p>\n                    Resolution of inflammation is mediated in part by agonists that engage immune cells to dampen inflammatory signaling, promote phagocytic functions, and facilitate tissue repair. G protein\u2013coupled receptor 18 (GPR18) has emerged as an important proresolving receptor that is activated by endogenous mediators including Resolvin D2. However, very little is known about how GPR18 expression is controlled in immune cells, and its cell-autonomous roles during resolution of inflammation remain of interest. Here, we elucidated transcriptional and epigenetic regulation of\n                    <jats:italic toggle=\"yes\">Gpr18<\/jats:italic>\n                    in macrophages (MFs). We identified binding of monocyte\/macrophage lineage-determining transcription factors (LDTFs) including PU.1, IRF8, and RUNX1 at the\n                    <jats:italic toggle=\"yes\">Gpr18<\/jats:italic>\n                    locus in the basal state in murine bone marrow\u2013derived macrophages (BMDM). We found that\n                    <jats:italic toggle=\"yes\">Gpr18<\/jats:italic>\n                    is highly induced in BMDM by inflammatory stimuli including interferon gamma (IFN\u03b3) and ligands for multiple toll-like receptors. Motif analysis predicted enrichment for LDTFs and signal-dependent TFs including nuclear factor \u03baB (NF\u03baB) and interferon regulatory factors (IRF) at the\n                    <jats:italic toggle=\"yes\">Gpr18<\/jats:italic>\n                    locus. Stimulation of BMDM with lipopolysaccharide (LPS) or IFN\u03b3 increased the binding of NF\u03baB p65 and IRF1 at the\n                    <jats:italic toggle=\"yes\">Gpr18<\/jats:italic>\n                    locus, which played a causal role in the induction of\n                    <jats:italic toggle=\"yes\">Gpr18<\/jats:italic>\n                    by LPS or IFN\u03b3, respectively. Mice with myeloid deficiency of\n                    <jats:italic toggle=\"yes\">Gpr18<\/jats:italic>\n                    had increased tissue swelling and accumulation of \u201cinflammatory\u201d Ly6C\n                    <jats:sup>hi<\/jats:sup>\n                    monocytes\/MFs during contact hypersensitivity, which was recapitulated during acute peritonitis and led to altered transcriptomes of resolution-phase MFs. These results demonstrate that inflammatory signaling primes MFs for resolution in part by inducing\n                    <jats:italic toggle=\"yes\">Gpr18<\/jats:italic>\n                    , which plays a cell-autonomous role to regulate MF phenotypic transitions.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2612173123","type":"journal-article","created":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T15:42:01Z","timestamp":1791474121000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":0,"title":["Transcriptional regulation and function of GPR18 in macrophage subtype specification"],"prefix":"10.1073","volume":"123","author":[{"given":"Hebe Agustina","family":"Mena","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04b6nzv94","id-type":"ROR","asserted-by":"publisher"}],"name":"Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Brigham and Women\u2019s Hospital, Harvard Medical School","place":["Boston"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9022-4985","authenticated-orcid":false,"given":"Andreas","family":"Patsalos","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00za53h95","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, Johns Hopkins University School of Medicine","place":["Baltimore"]},{"id":[{"id":"https:\/\/ror.org\/013x5cp73","id-type":"ROR","asserted-by":"publisher"}],"name":"Institute for Fundamental Biomedical Research, Johns Hopkins All Children\u2018s Hospital","place":["St. Petersburg"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-4332-5242","authenticated-orcid":false,"given":"Jake","family":"Altomare","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04b6nzv94","id-type":"ROR","asserted-by":"publisher"}],"name":"Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Brigham and Women\u2019s Hospital, Harvard Medical School","place":["Boston"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Filippa","family":"Davidsson","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04b6nzv94","id-type":"ROR","asserted-by":"publisher"}],"name":"Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Brigham and Women\u2019s Hospital, Harvard Medical School","place":["Boston"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gergely","family":"Nagy","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02xf66n48","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen","place":["Debrecen, Hungary"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0727-7064","authenticated-orcid":false,"given":"Wilhelm K.","family":"Berger","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00za53h95","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, Johns Hopkins University School of Medicine","place":["Baltimore"]},{"id":[{"id":"https:\/\/ror.org\/013x5cp73","id-type":"ROR","asserted-by":"publisher"}],"name":"Institute for Fundamental Biomedical Research, Johns Hopkins All Children\u2018s Hospital","place":["St. Petersburg"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Blenda","family":"Wong","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04b6nzv94","id-type":"ROR","asserted-by":"publisher"}],"name":"Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Brigham and Women\u2019s Hospital, Harvard Medical School","place":["Boston"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allison","family":"Rahtes","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03g66yt05","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Molecular and Cellular Immunology, Albany Medical College","place":["Albany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabrielle","family":"Fredman","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/03g66yt05","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Molecular and Cellular Immunology, Albany Medical College","place":["Albany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6653-2155","authenticated-orcid":false,"given":"Laszlo","family":"Nagy","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00za53h95","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, Johns Hopkins University School of Medicine","place":["Baltimore"]},{"id":[{"id":"https:\/\/ror.org\/013x5cp73","id-type":"ROR","asserted-by":"publisher"}],"name":"Institute for Fundamental Biomedical Research, Johns Hopkins All Children\u2018s Hospital","place":["St. Petersburg"]},{"id":[{"id":"https:\/\/ror.org\/02xf66n48","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen","place":["Debrecen, Hungary"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8868-3648","authenticated-orcid":false,"given":"Matthew","family":"Spite","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04b6nzv94","id-type":"ROR","asserted-by":"publisher"}],"name":"Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Brigham and Women\u2019s Hospital, Harvard Medical 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A. Mena M. Spite A. Patsalos K. W. Berger L. Nagy Transcriptional regulation and function of GPR18 in macrophage subtype specification. Gene Expression Omnibus. https:\/\/www.ncbi.nlm.nih.gov\/geo\/query\/acc.cgi?acc=GSE319753. Deposited 17 February 2026."},{"key":"e_1_3_4_68_2","unstructured":"Immunological Genome Project Consortium Immunological Genome Project Data Browsers. https:\/\/www.immgen.org\/Databrowser19\/DatabrowserPage.html. Accessed 7 April 2025."},{"key":"e_1_3_4_69_2","unstructured":"C. K. Glass Tissue damage signals repurpose NF-\u03baB AP-1 and Smad3 to direct a Rev-erb sensitive wound healing program in macrophages. NCBI Gene Expression Omnibus. https:\/\/ncbi.nlm.nih.gov\/geo\/query\/acc.cgi?acc=GSE72964. Deposited 11 September 2015."},{"key":"e_1_3_4_70_2","unstructured":"M. H. Sieweke E. Soucie A. Sidow Lineage-specific enhancers activate self-renewal genes in macrophages and embryonic stem cells. NCBI Gene Expression Omnibus. https:\/\/www.ncbi.nlm.nih.gov\/geo\/query\/acc.cgi?acc=GSE75722. Deposited 4 December 2015."},{"key":"e_1_3_4_71_2","unstructured":"University of Debrecen Transcriptional memory and augmented signaling is conferred by STAT6-mediated RXR cistrome expansion in polarized macrophages: PU.1 ChIP-Seq analysis of Wt mouse BMDM cells differentiated in the presence of MCSF. NCBI Sequence Read Archive. https:\/\/www.ncbi.nlm.nih.gov\/sra\/SRX1716773. Deposited 1 November 2016."},{"key":"e_1_3_4_72_2","unstructured":"University of Debrecen Transcriptional memory and augmented signaling is conferred by STAT6-mediated RXR cistrome expansion in polarized macrophages: RXR ChIP-seq of Wt murine BMDM cells. NCBI Sequence Read Archive. https:\/\/www.ncbi.nlm.nih.gov\/sra\/SRX21643159. Deposited 6 September 2023."},{"key":"e_1_3_4_73_2","unstructured":"University of Debrecen Transcriptional memory and augmented signaling is conferred by STAT6-mediated RXR cistrome expansion in polarized macrophages: IRF8 ChIP-Seq analysis of Wt mouse BMDM cells differentiated in the presence of MCSF. NCBI Sequence Read Archive. https:\/\/www.ncbi.nlm.nih.gov\/sra\/SRX2196774. Deposited 1 December 2016."},{"key":"e_1_3_4_74_2","unstructured":"University of Debrecen Transcriptional memory and augmented signaling is conferred by STAT6-mediated RXR cistrome expansion in polarized macrophages: RUNX1 ChIP-Seq analysis of Wt mouse BMDM cells differentiated in the presence of MCSF. NCBI Sequence Read Archive. https:\/\/www.ncbi.nlm.nih.gov\/sra\/SRX2196776. Deposited 1 December 2016."},{"key":"e_1_3_4_75_2","doi-asserted-by":"crossref","unstructured":"D. Langlais L. B. Barreiro P. Gros The macrophage IRF8-IRF1 regulome is required for protection against infections and is associated with chronic inflammation. NCBI Gene Expression Omnibus. https:\/\/www.ncbi.nlm.nih.gov\/geo\/query\/acc.cgi?acc=GSE77886. Deposited 12 February 2016.","DOI":"10.1084\/jem.20151764"},{"key":"e_1_3_4_76_2","unstructured":"L. Halasz Z. Czimmerer L. Nagy Prior IL-4 exposure induces epigenetic reprogramming enabling activated NF-\u03baB p65 cistrome expansion extreme synergistic gene activation and unique immune response in macrophages. NCBI Gene Expression Omnibus. https:\/\/www.ncbi.nlm.nih.gov\/geo\/query\/acc.cgi?acc=GSE181223. Deposited 30 July 2021."},{"key":"e_1_3_4_77_2","unstructured":"V. M. Link C. K. Glass Analysis of genetically diverse macrophages reveals local and domain-wide mechanisms that control transcription factor binding and function. NCBI Gene Expression Omnibus. https:\/\/www.ncbi.nlm.nih.gov\/geo\/query\/acc.cgi?acc=GSE109965. Deposited 31 January 2018."},{"key":"e_1_3_4_78_2","unstructured":"G. Nagy L. Nagy The IL-4\/STAT6\/PPAR\u03b3 signaling axis is driving the expansion of the RXR heterodimer cistrome providing complex ligand responsiveness in macrophages I. NCBI Gene Expression Omnibus. https:\/\/www.ncbi.nlm.nih.gov\/geo\/query\/acc.cgi?acc=GSE107455. Deposited 28 November 2017."},{"key":"e_1_3_4_79_2","unstructured":"B. Daniel L. Nagy Ligand-insensitive PPAR\u03b3 controls progressive or reinforcing macrophage polarization as an epigenomic ratchet of transcriptional memory [ChIP-seq]. NCBI Gene Expression Omnibus. https:\/\/www.ncbi.nlm.nih.gov\/geo\/query\/acc.cgi?acc=GSE115083. Deposited 30 May 2018."},{"key":"e_1_3_4_80_2","unstructured":"X. Liu S. T. Smale ChIP-seq of transcription factors regulating the TLR-induced transcriptional cascades in macrophages. NCBI Gene Expression Omnibus. https:\/\/www.ncbi.nlm.nih.gov\/geo\/query\/acc.cgi?acc=GSE99895. Deposited 10 June 2017."},{"key":"e_1_3_4_81_2","unstructured":"A. Curina S. Ghisletti A. Termanini E. Prosperini G. Natoli High activity of a broad panel of housekeeping and tissue-specific cis-regulatory elements depends on a subset of ETS proteins. NCBI Gene Expression Omnibus. https:\/\/www.ncbi.nlm.nih.gov\/geo\/query\/acc.cgi?acc=GSE88699. Deposited 13 October 2016."},{"key":"e_1_3_4_82_2","unstructured":"A. Horvath G. Nagy Characterization of transcriptional and epigenetic changes during mouse alternative macrophage polarization. NCBI Gene Expression Omnibus. https:\/\/www.ncbi.nlm.nih.gov\/geo\/query\/acc.cgi?acc=GSE106706. Deposited 8 November 2017."},{"key":"e_1_3_4_83_2","unstructured":"University of Debrecen Characterization of transcriptional and epigenetic changes during mouse alternative macrophage activation: H3K4me1 ChIP-Seq analysis of Wt mouse BMDM cells differentiated in the presence of MCSF (ctrl). 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