{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,19]],"date-time":"2026-06-19T13:51:14Z","timestamp":1781877074155,"version":"3.54.5"},"reference-count":37,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T00:00:00Z","timestamp":1773619200000},"content-version":"vor","delay-in-days":15,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,3,1]],"date-time":"2026-03-01T00:00:00Z","timestamp":1772323200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HL125941"],"award-info":[{"award-number":["HL125941"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100002129","name":"Heart Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100002129","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clin &amp; Trans Imm"],"published-print":{"date-parts":[[2026,3]]},"abstract":"Abstract<\/jats:title>\n \n \n Atherosclerosis is the common underlying pathology in atherosclerotic cardiovascular disease (ASCVD) phenotypes of myocardial infarction (MI), stroke or peripheral artery disease (PAD). Single immune cell profiling of atherosclerotic plaques demonstrates a site\u2010specific immune profile associated with the ASCVD phenotype, and LL\u201037 is a reported autoantigen in atherosclerosis.<\/jats:p>\n <\/jats:sec>\n \n Objective<\/jats:title>\n To investigate whether the immune response to LL\u201037 would be common among different ASCVD phenotypes.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n Peripheral blood mononuclear cells (PBMCs) and plasma were collected from stable ASCVD patients enrolled within 12\u2009months after MI or stroke or diagnosed with PAD. A subgroup of post\u2010acute patients provided PBMCs at follow\u2010up (14.7\u2009\u00b1\u20093.6\u2009months). T\u2010cell response to LL\u201037 was profiled using activation\u2010induced markers. LL\u201037 IgG, immune complex (IC) levels and subclass were evaluated with ELISA. LDL is a reported binding partner of LL\u201037 in plasma. Therefore, cross\u2010reactivity of LL\u201037 IgG\u2010ICs with native LL\u201037 or LL\u201037 complexed\u00a0with LDL (LL\u201037_LDL) was assessed using immune depletion.<\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n LL\u201037 provokes increased CD4\n +<\/jats:sup>\n CD25\n +<\/jats:sup>\n CD134\n +<\/jats:sup>\n T\u2010cell response in stable post\u2010MI patients whereas CD8\n +<\/jats:sup>\n CD25\n +<\/jats:sup>\n CD69\n +<\/jats:sup>\n T\u00a0cells were reduced in PAD. CD4\n +<\/jats:sup>\n T\u2010cell response to LL\u201037 in post\u2010MI patients persisted at follow\u2010up with increased CD4\n +<\/jats:sup>\n CD25\n +<\/jats:sup>\n CD69\n +<\/jats:sup>\n FoxP3\n +<\/jats:sup>\n T regulatory cells while post\u2010stroke patients had increased CD8\n +<\/jats:sup>\n CD134\n +<\/jats:sup>\n T\u00a0cells. LL\u201037 IgG\u2010ICs were significantly increased in ASCVD patients with IgG3 subclass reduced in post\u2010MI compared to post\u2010stroke. Immune\u2010depletion showed cross\u2010reactivity of LL\u201037 IgG\u2010ICs with both native LDL and LL\u201037_LDL only in post\u2010MI plasma.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusion<\/jats:title>\n LL\u201037 antigen specific profiling of immune response may differentiate various ASCVD phenotypes and provide mechanistic insight in pathophysiology.<\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/cti2.70083","type":"journal-article","created":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T14:10:25Z","timestamp":1773756625000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Adaptive immune response to the autoantigen\n LL<\/scp>\n \u201037 differentiates atherosclerotic cardiovascular disease phenotypes"],"prefix":"10.1002","volume":"15","author":[{"given":"Paul C.","family":"Dimayuga","sequence":"first","affiliation":[{"name":"Oppenheimer Atherosclerosis Research Center, Department of Cardiology Smidt Heart Institute, Cedars\u2010Sinai Medical Center Los Angeles CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kuang\u2010Yuh","family":"Chyu","sequence":"additional","affiliation":[{"name":"Oppenheimer Atherosclerosis Research Center, Department of Cardiology Smidt Heart Institute, Cedars\u2010Sinai Medical Center Los Angeles CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianchang","family":"Zhou","sequence":"additional","affiliation":[{"name":"Oppenheimer Atherosclerosis Research Center, Department of Cardiology Smidt Heart Institute, Cedars\u2010Sinai Medical Center Los Angeles CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoning","family":"Zhao","sequence":"additional","affiliation":[{"name":"Oppenheimer Atherosclerosis Research Center, Department of Cardiology Smidt Heart Institute, Cedars\u2010Sinai Medical Center Los Angeles CA 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