{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T15:30:20Z","timestamp":1781019020010,"version":"3.54.1"},"reference-count":54,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2012,7]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>Inflammatory leukocyte accumulation drives atherosclerosis. Although monocytes\/macrophages and polymorphonuclear neutrophilic leukocytes (PMN) contribute to lesion formation, sequelae of myeloproliferative disease remain to be elucidated.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods and Results\u2014<\/jats:title>\n            <jats:p>\n              We used mice deficient in interferon regulatory factor 8 (IRF8\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              ) in hematopoietic cells that develop a chronic myelogenous leukemia-like phenotype. Apolipoprotein E-deficient mice reconstituted with IRF8\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              or IRF8\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              apolipoprotein E-deficient bone marrow displayed an exacerbated atherosclerotic lesion formation compared with controls. The chronic myelogenous leukemia-like phenotype in mice with IRF8\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              bone marrow, reflected by an expansion of PMN in the circulation, was associated with an increased lesional accumulation and apoptosis of PMN, and enlarged necrotic cores. IRF8\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              compared with IRF8\n              <jats:sup>+\/+<\/jats:sup>\n              PMN displayed unaffected reactive oxygen species formation and discharge of PMN granule components. In contrast, accumulating in equal numbers at sites of inflammation, IRF8\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              macrophages were defective in efferocytosis, lipid uptake, and interleukin-10 cytokine production. Importantly, depletion of PMN in low-density lipoprotein receptor or apolipoprotein E-deficient mice with IRF8\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              or IRF8\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              apolipoprotein E-deficient bone marrow abrogated increased lesion formation.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion\u2014<\/jats:title>\n            <jats:p>These findings indicate that a chronic myelogenous leukemia-like phenotype contributes to accelerated atherosclerosis in mice. Among proatherosclerotic effects of other cell types, this, in part, is linked to an expansion of functionally intact PMN.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.111.236539","type":"journal-article","created":{"date-parts":[[2012,5,4]],"date-time":"2012-05-04T05:52:27Z","timestamp":1336110747000},"page":"1613-1623","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":44,"title":["Hematopoietic Interferon Regulatory Factor 8-Deficiency Accelerates Atherosclerosis in Mice"],"prefix":"10.1161","volume":"32","author":[{"given":"Yvonne","family":"D\u00f6ring","sequence":"first","affiliation":[{"name":"From the Institute for Cardiovascular Prevention, Ludwig-Maximilians-University Munich, Munich (Y.D., O.S., M.D., H.H., M.H., R.R.K., C.W.); Institute for Biomedical Engineering, Department of Cell Biology, RWTH Aachen University (Y.D., T.H., M.Z.); Institute for Molecular Cardiovascular Research, University Hospital Aachen, Aachen (O.S., E.S., S.M., H.H., A.Z.); Rudolf-Virchow-Center\/DFG Research Center for Experimental Biomedicine, University of W\u00fcrzburg, W\u00fcrzburg, Germany (M.D., S.M.C., A.Z.);..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oliver","family":"Soehnlein","sequence":"additional","affiliation":[{"name":"From the Institute for Cardiovascular Prevention, Ludwig-Maximilians-University Munich, Munich (Y.D., O.S., M.D., H.H., M.H., R.R.K., C.W.); Institute for Biomedical Engineering, Department of Cell Biology, RWTH Aachen University (Y.D., T.H., M.Z.); Institute for Molecular Cardiovascular Research, University Hospital Aachen, Aachen (O.S., E.S., S.M., H.H., A.Z.); Rudolf-Virchow-Center\/DFG Research Center for Experimental Biomedicine, University of W\u00fcrzburg, W\u00fcrzburg, Germany (M.D., S.M.C., A.Z.);..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maik","family":"Drechsler","sequence":"additional","affiliation":[{"name":"From 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for Cardiovascular Prevention, Ludwig-Maximilians-University Munich, Munich (Y.D., O.S., M.D., H.H., M.H., R.R.K., C.W.); Institute for Biomedical Engineering, Department of Cell Biology, RWTH Aachen University (Y.D., T.H., M.Z.); Institute for Molecular Cardiovascular Research, University Hospital Aachen, Aachen (O.S., E.S., S.M., H.H., A.Z.); Rudolf-Virchow-Center\/DFG Research Center for Experimental Biomedicine, University of W\u00fcrzburg, W\u00fcrzburg, Germany (M.D., S.M.C., A.Z.);..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helene","family":"Hartwig","sequence":"additional","affiliation":[{"name":"From the Institute for Cardiovascular Prevention, Ludwig-Maximilians-University Munich, Munich (Y.D., O.S., M.D., H.H., M.H., R.R.K., C.W.); Institute for Biomedical Engineering, Department of Cell Biology, RWTH Aachen University (Y.D., T.H., M.Z.); Institute for Molecular Cardiovascular Research, University Hospital Aachen, Aachen (O.S., E.S., S.M., H.H., 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