{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T20:25:52Z","timestamp":1793219152315,"version":"4.5.0"},"reference-count":49,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2016,8,28]],"date-time":"2016-08-28T00:00:00Z","timestamp":1472342400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2016,11]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:p>\n                    Interleukin\u20101\n                    <jats:italic>\u03b2<\/jats:italic>\n                    (\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20101\n                    <jats:italic>\u03b2<\/jats:italic>\n                    ), a potent pro\u2010inflammatory cytokine, has been implicated in many diseases, including atherosclerosis. Activation of\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20101\n                    <jats:italic>\u03b2<\/jats:italic>\n                    is controlled by a multi\u2010protein complex, the inflammasome. The exact initiating event in atherosclerosis is unknown, but recent work has demonstrated that cholesterol crystals (\n                    <jats:styled-content style=\"fixed-case\">CC<\/jats:styled-content>\n                    ) may promote atherosclerosis development by activation of the inflammasome. High\u2010density lipoprotein (\n                    <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\n                    ) has consistently been shown to be anti\u2010atherogenic and to have anti\u2010inflammatory effects, but its mechanism of action is unclear. We demonstrate here that\n                    <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\n                    is able to suppress\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20101\n                    <jats:italic>\u03b2<\/jats:italic>\n                    secretion in response to cholesterol crystals in\n                    <jats:styled-content style=\"fixed-case\">THP<\/jats:styled-content>\n                    \u20101 cells and in human\u2010monocyte\u2010derived macrophages.\n                    <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\n                    is able to blunt inflammatory monocyte cell recruitment\n                    <jats:italic>in vivo<\/jats:italic>\n                    following intraperitoneal\n                    <jats:styled-content style=\"fixed-case\">CC<\/jats:styled-content>\n                    injection in mice.\n                    <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\n                    appears to modulate inflammasome activation in several ways. It reduces the loss of lysosomal membrane integrity following the phagocytosis of\n                    <jats:styled-content style=\"fixed-case\">CC<\/jats:styled-content>\n                    , but the major mechanism for the suppression of inflammasome activation by\n                    <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\n                    is decreased expression of pro\u2010\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20101\n                    <jats:italic>\u03b2<\/jats:italic>\n                    and\n                    <jats:styled-content style=\"fixed-case\">NLRP<\/jats:styled-content>\n                    3, and reducing caspase\u20101 activation. In summary, we have described a novel anti\u2010inflammatory effect of\n                    <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\n                    , namely its ability to suppress inflammasome activation by\n                    <jats:styled-content style=\"fixed-case\">CC<\/jats:styled-content>\n                    by modulating the expression of several key components of the inflammasome.\n                  <\/jats:p>","DOI":"10.1111\/imm.12638","type":"journal-article","created":{"date-parts":[[2016,6,22]],"date-time":"2016-06-22T18:05:09Z","timestamp":1466618709000},"page":"306-319","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":121,"title":["High\u2010density lipoprotein reduces inflammation from cholesterol crystals by inhibiting inflammasome activation"],"prefix":"10.1111","volume":"149","author":[{"given":"Seth G.","family":"Thacker","sequence":"first","affiliation":[{"name":"Lipoprotein Metabolism Section Cardiovascular\u2010Pulmonary Branch National Heart, Lung, and Blood Institute National Institutes of Health Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abdalrahman","family":"Zarzour","sequence":"additional","affiliation":[{"name":"Lipoprotein Metabolism Section Cardiovascular\u2010Pulmonary Branch National Heart, Lung, and Blood Institute National Institutes of Health Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ye","family":"Chen","sequence":"additional","affiliation":[{"name":"Systems Biology Center National Heart, Lung, and Blood Institute National Institutes of Health Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mustafa S.","family":"Alcicek","sequence":"additional","affiliation":[{"name":"Lipoprotein Metabolism Section Cardiovascular\u2010Pulmonary Branch National Heart, Lung, and Blood Institute National Institutes of Health Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lita A.","family":"Freeman","sequence":"additional","affiliation":[{"name":"Lipoprotein Metabolism Section Cardiovascular\u2010Pulmonary Branch National Heart, Lung, and Blood Institute National Institutes of Health Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dennis O.","family":"Sviridov","sequence":"additional","affiliation":[{"name":"Lipoprotein Metabolism Section Cardiovascular\u2010Pulmonary Branch National Heart, Lung, and Blood Institute National Institutes of Health Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr.","given":"Stephen J.","family":"Demosky","sequence":"additional","affiliation":[{"name":"Lipoprotein Metabolism Section Cardiovascular\u2010Pulmonary Branch National Heart, Lung, and Blood Institute National Institutes of Health Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alan T.","family":"Remaley","sequence":"additional","affiliation":[{"name":"Lipoprotein Metabolism Section Cardiovascular\u2010Pulmonary Branch National Heart, Lung, and Blood Institute National Institutes of Health Bethesda MD 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