{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T18:46:42Z","timestamp":1792003602550,"version":"4.4.0"},"reference-count":96,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"19","license":[{"start":{"date-parts":[[2025,5,13]],"date-time":"2025-05-13T00:00:00Z","timestamp":1747094400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2025,5,13]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>The activation and polarization of T cells play a crucial role in atherosclerosis and dictate athero-inflammation. The epigenetic enzyme EZH2 (enhancer of zeste homolog 2) mediates the H3K27me3 (trimethylation of histone H3 lysine 27) and is pivotal in controlling T cell responses.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>\n              To detail the role of T cell EZH2 in atherosclerosis, we used human carotid endarterectomy specimens to reveal plaque expression and geography of EZH2. Atherosclerosis-prone\n              <jats:italic toggle=\"yes\">Apoe<\/jats:italic>\n              (apolipoprotein E)\u2013deficient mice with CD (cluster of differentiation) 4\n              <jats:sup>+<\/jats:sup>\n              or CD8\n              <jats:sup>+<\/jats:sup>\n              T cell\u2013specific\n              <jats:italic toggle=\"yes\">Ezh2<\/jats:italic>\n              deletion (Ezh2\n              <jats:sup>cd4<\/jats:sup>\n              -knockout [KO], Ezh2\n              <jats:sup>cd8<\/jats:sup>\n              -KO) were analyzed to unravel the role of T cell Ezh2 in atherosclerosis and T cell\u2013associated immune status.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              <jats:italic toggle=\"yes\">EZH2<\/jats:italic>\n              expression is elevated in advanced human atherosclerotic plaques and primarily expressed in the T cell nucleus, suggesting the importance of canonical EZH2 function in atherosclerosis. Ezh2\n              <jats:sup>cd4<\/jats:sup>\n              -KO, but not Ezh2\n              <jats:sup>cd8<\/jats:sup>\n              -KO, mice showed reduced atherosclerosis with fewer advanced plaques, which contained less collagen and macrophages, indicating that Ezh2 in CD4\n              <jats:sup>+<\/jats:sup>\n              T cells drives atherosclerosis. In-depth analysis of CD4\n              <jats:sup>+<\/jats:sup>\n              T cells of Ezh2\n              <jats:sup>cd4<\/jats:sup>\n              -KO mice revealed that absence of Ezh2 results in a type 2 immune response with increased Il-4 (interleukin 4) gene and protein expression in the aorta and lymphoid organs. In vitro,\n              <jats:italic toggle=\"yes\">Ezh2<\/jats:italic>\n              -deficient T cells polarized macrophages toward an anti-inflammatory phenotype. Single-cell RNA-sequencing of splenic T cells revealed that\n              <jats:italic toggle=\"yes\">Ezh2<\/jats:italic>\n              deficiency reduced naive, Ccl5\n              <jats:sup>+<\/jats:sup>\n              (C-C motif chemokine ligand 5) and regulatory T cell populations and increased the frequencies of memory T cells and invariant natural killer T (iNKT) cells. Flow cytometric analysis identified a shift toward Th2 (type 2 T helper) effector CD4\n              <jats:sup>+<\/jats:sup>\n              T cells in Ezh2\n              <jats:sup>cd4<\/jats:sup>\n              -KO mice and confirmed a profound increase in splenic iNKT cells with increased expression of Plzf (promyelocytic leukemia zinc finger), which is the characteristic marker of the iNKT2 subset. Likewise,\n              <jats:italic toggle=\"yes\">Zbtb16<\/jats:italic>\n              ([zinc finger and BTB domain containing 16], the Plzf-encoding gene) transcripts were elevated in the aorta of Ezh2\n              <jats:sup>cd4<\/jats:sup>\n              -KO mice, suggesting an accumulation of iNKT2 cells in the plaque. H3K27me3\u2013chromatin immunoprecipitation followed by quantitative polymerase chain reaction showed that T cell\u2013Ezh2 regulates the transcription of the\n              <jats:italic toggle=\"yes\">Il-4<\/jats:italic>\n              and\n              <jats:italic toggle=\"yes\">Zbtb16<\/jats:italic>\n              genes.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>\n              Our study uncovers the importance of T cell EZH2 in human and mouse atherosclerosis. Inhibition of Ezh2 in CD4\n              <jats:sup>+<\/jats:sup>\n              T cells drives type 2 immune responses, resulting in an accumulation of iNKT2 and Th2 cells, memory T cells and anti-inflammatory macrophages that limit the progression of atherosclerosis.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circulationaha.124.072384","type":"journal-article","created":{"date-parts":[[2025,2,7]],"date-time":"2025-02-07T10:00:14Z","timestamp":1738922414000},"page":"1391-1408","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":32,"title":["Ezh2 Shapes T Cell Plasticity to Drive Atherosclerosis"],"prefix":"10.1161","volume":"151","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7422-0503","authenticated-orcid":true,"given":"Cecilia Assunta","family":"Bonfiglio","sequence":"first","affiliation":[{"name":"Institute for Cardiovascular Prevention (C.A.B., M.L., V.T., F.M.F., K.N., Y.W., V.B., I.A-K., Y.F.S.M., M.K., K.R., C.W., D.S., E.L., D.A.), Ludwig Maximilians Universit\u00e4t, Munich, Germany."},{"name":"DZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance, Germany (C.A.B., F.M.F., V.B., I.A-K., M.K., L.M., C.W., D.S., E.L., D.A.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Lacy","sequence":"additional","affiliation":[{"name":"Institute for Cardiovascular Prevention (C.A.B., M.L., V.T., F.M.F., K.N., Y.W., V.B., I.A-K., Y.F.S.M., M.K., K.R., C.W., D.S., E.L., D.A.), Ludwig Maximilians Universit\u00e4t, Munich, Germany."},{"name":"Department of Medical Laboratory Sciences, Virginia Commonwealth University, Richmond (M.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vasiliki","family":"Triantafyllidou","sequence":"additional","affiliation":[{"name":"Institute for Cardiovascular Prevention (C.A.B., M.L., V.T., F.M.F., K.N., Y.W., V.B., I.A-K., Y.F.S.M., M.K., K.R., C.W., D.S., E.L., D.A.), Ludwig Maximilians Universit\u00e4t, Munich, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5105-5672","authenticated-orcid":true,"given":"Floriana Maria","family":"Farina","sequence":"additional","affiliation":[{"name":"Institute for Cardiovascular Prevention (C.A.B., M.L., V.T., F.M.F., K.N., Y.W., V.B., I.A-K., Y.F.S.M., M.K., K.R., C.W., D.S., E.L., D.A.), Ludwig Maximilians Universit\u00e4t, Munich, Germany."},{"name":"DZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance, Germany (C.A.B., F.M.F., V.B., I.A-K., M.K., L.M., C.W., D.S., E.L., D.A.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7180-5381","authenticated-orcid":true,"given":"Aleksandar","family":"Janjic","sequence":"additional","affiliation":[{"name":"Anthropology and Human Genetics, Faculty of Biology (A.J., W.E.), Ludwig Maximilians Universit\u00e4t, Munich, 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