Paul C. Dimayuga PhD , Kuang-Yuh Chyu MD, PhD , Xiaoning Zhao PhD , Jianchang Zhou PhD , Nicole Wai Man Lio BS , Fernando Chernomordik MD , Daniel Berman MD , Prediman K. Shah MD , Bojan Cercek MD, PhD
{"title":"由 LL-37 免疫球蛋白 G 自身抗体免疫复合物介导的 ACS 中血小板活化的新途径","authors":"Paul C. Dimayuga PhD , Kuang-Yuh Chyu MD, PhD , Xiaoning Zhao PhD , Jianchang Zhou PhD , Nicole Wai Man Lio BS , Fernando Chernomordik MD , Daniel Berman MD , Prediman K. Shah MD , Bojan Cercek MD, PhD","doi":"10.1016/j.jacbts.2024.04.012","DOIUrl":null,"url":null,"abstract":"<div><p>The cathelicidin antimicrobial peptide LL-37 is a self-antigen in neutrophil extracellular traps that provokes autoantibody responses in autoimmune/autoinflammatory conditions. LL-37 immunoglobulin (Ig) G autoantibody levels were measured in subjects with and without atherosclerotic cardiovascular disease assessed using the coronary artery calcium score, in patients who had a future myocardial infarction and in a cohort of acute coronary syndrome (ACS) patients. LL-37 IgG levels were not associated with coronary artery calcium score, but future myocardial infarction patients had significantly higher LL-37 IgG at baseline. Reduced LL-37 IgG in ACS was associated with increased LL-37 IgG–immune complex. ACS plasma increased activated CD62P+ platelets from healthy donors mediated in part by LL-37 IgG–immune complexes and platelet Fc gamma receptor 2a.</p></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"9 7","pages":"Pages 877-887"},"PeriodicalIF":8.4000,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24001852/pdfft?md5=a6e5c6a86e9151e8b8e985941cfea515&pid=1-s2.0-S2452302X24001852-main.pdf","citationCount":"0","resultStr":"{\"title\":\"A Novel Pathway of Platelet Activation in ACS Mediated by LL-37 Immunoglobulin G Autoantibody Immune Complexes\",\"authors\":\"Paul C. Dimayuga PhD , Kuang-Yuh Chyu MD, PhD , Xiaoning Zhao PhD , Jianchang Zhou PhD , Nicole Wai Man Lio BS , Fernando Chernomordik MD , Daniel Berman MD , Prediman K. Shah MD , Bojan Cercek MD, PhD\",\"doi\":\"10.1016/j.jacbts.2024.04.012\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>The cathelicidin antimicrobial peptide LL-37 is a self-antigen in neutrophil extracellular traps that provokes autoantibody responses in autoimmune/autoinflammatory conditions. LL-37 immunoglobulin (Ig) G autoantibody levels were measured in subjects with and without atherosclerotic cardiovascular disease assessed using the coronary artery calcium score, in patients who had a future myocardial infarction and in a cohort of acute coronary syndrome (ACS) patients. LL-37 IgG levels were not associated with coronary artery calcium score, but future myocardial infarction patients had significantly higher LL-37 IgG at baseline. Reduced LL-37 IgG in ACS was associated with increased LL-37 IgG–immune complex. ACS plasma increased activated CD62P+ platelets from healthy donors mediated in part by LL-37 IgG–immune complexes and platelet Fc gamma receptor 2a.</p></div>\",\"PeriodicalId\":14831,\"journal\":{\"name\":\"JACC: Basic to Translational Science\",\"volume\":\"9 7\",\"pages\":\"Pages 877-887\"},\"PeriodicalIF\":8.4000,\"publicationDate\":\"2024-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.sciencedirect.com/science/article/pii/S2452302X24001852/pdfft?md5=a6e5c6a86e9151e8b8e985941cfea515&pid=1-s2.0-S2452302X24001852-main.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"JACC: Basic to Translational Science\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2452302X24001852\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"JACC: Basic to Translational Science","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2452302X24001852","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
A Novel Pathway of Platelet Activation in ACS Mediated by LL-37 Immunoglobulin G Autoantibody Immune Complexes
The cathelicidin antimicrobial peptide LL-37 is a self-antigen in neutrophil extracellular traps that provokes autoantibody responses in autoimmune/autoinflammatory conditions. LL-37 immunoglobulin (Ig) G autoantibody levels were measured in subjects with and without atherosclerotic cardiovascular disease assessed using the coronary artery calcium score, in patients who had a future myocardial infarction and in a cohort of acute coronary syndrome (ACS) patients. LL-37 IgG levels were not associated with coronary artery calcium score, but future myocardial infarction patients had significantly higher LL-37 IgG at baseline. Reduced LL-37 IgG in ACS was associated with increased LL-37 IgG–immune complex. ACS plasma increased activated CD62P+ platelets from healthy donors mediated in part by LL-37 IgG–immune complexes and platelet Fc gamma receptor 2a.
期刊介绍：
JACC: Basic to Translational Science is an open access journal that is part of the renowned Journal of the American College of Cardiology (JACC). It focuses on advancing the field of Translational Cardiovascular Medicine and aims to accelerate the translation of new scientific discoveries into therapies that improve outcomes for patients with or at risk for Cardiovascular Disease. The journal covers thematic areas such as pre-clinical research, clinical trials, personalized medicine, novel drugs, devices, and biologics, proteomics, genomics, and metabolomics, as well as early phase clinical trial methodology.
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