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The mechanisms linking epigenetic regulation to metabolic reprogramming in monocyte-driven inflammation in psoriasis are poorly defined.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We examined the expression and activity of the histone demethylase KDM6B in classical monocytes in the imiquimod (IMQ)-induced psoriasis model. Epigenetic changes were assessed by measuring H3K27me3 levels at inflammatory and metabolic gene promoters. Pharmacological inhibition of KDM6-family H3K27 demethylase activity after disease onset was performed using GSK-J4, a cell-permeable prodrug that is intracellularly converted to the active inhibitor GSK-J1. In parallel, inflammatory and metabolic transcriptional programs, bioenergetic profiles, immune cell recruitment to inflamed skin, and single-cell transcriptomic changes in myeloid populations were analyzed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      KDM6B expression and KDM6A\/B demethylase activity were increased in classical monocytes during IMQ-induced psoriasis-like inflammation. This was associated with reduced levels of the repressive histone mark H3K27me3, an epigenetic modification linked to chromatin compaction and transcriptional silencing, at the\n                      <jats:italic>Il1b<\/jats:italic>\n                      ,\n                      <jats:italic>Tnf, Pgam1<\/jats:italic>\n                      ,\n                      <jats:italic>Pgk1<\/jats:italic>\n                      , and\n                      <jats:italic>Aldoa<\/jats:italic>\n                      promoters, together with an enhanced inflammatory and glycolytic gene signature. GSK-J4 treatment after disease onset restored H3K27me3 at inflammatory and metabolic loci, suppressed\n                      <jats:italic>Il1b<\/jats:italic>\n                      and\n                      <jats:italic>Tnf<\/jats:italic>\n                      transcription, normalized bioenergetic profiles, and reduced monocyte and neutrophil recruitment to inflamed skin. Single-cell transcriptomic profiling further revealed that GSK-J4 treatment was associated with reduced cytokine-mediated signaling, glycolysis, and chemotaxis pathways in monocytes, while enriching antigen presentation modules, consistent with a shift toward a homeostatic, antigen-presenting surveillance program in myeloid cells and a regulatory T cell (Treg)-supportive milieu.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Collectively, our data identify KDM6B-associated epigenetic-metabolic remodeling as a component of inflammatory monocyte activation in IMQ-induced psoriasis-like inflammation. GSK-J4 treatment attenuated ongoing inflammation when initiated after disease onset. These findings support further investigation of KDM6-family demethylases as therapeutic targets in psoriasis-like inflammation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12964-026-03220-4","type":"journal-article","created":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T13:03:28Z","timestamp":1789131808000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["KDM6B inhibition modulates monocyte activation and alleviates IMQ-induced psoriasis-like skin inflammation"],"prefix":"10.1186","volume":"24","author":[{"given":"Aman","family":"Damara","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Najla","family":"Abassi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Delia","family":"Mihoc","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mahsa","family":"Nastaranpour","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pauline","family":"Kraft","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tina","family":"Sarkar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tanja","family":"K\u00fcbelbeck","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniela","family":"Kramer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carsten","family":"Deppermann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes U.","family":"Mayer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephan","family":"Grabbe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Delacher","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Federico","family":"Marini","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1837-8848","authenticated-orcid":false,"given":"Fatemeh","family":"Shahneh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,9,11]]},"reference":[{"key":"3220_CR1","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2018.01549","author":"C Albanesi","year":"2018","unstructured":"Albanesi C, Madonna S, Gisondi P, Girolomoni G. 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