{"title":"中性粒细胞胞外捕获物引发中风和心肌梗死后的 IgA 损失","authors":"","doi":"10.1038/s44161-024-00465-5","DOIUrl":null,"url":null,"abstract":"The mechanisms by which stroke and myocardial infarction trigger lymphocyte loss remain poorly defined. This study shows that the release of neutrophil extracellular traps (NETs) after stroke and myocardial infarction triggers B cell apoptosis and reduces the number of IgA-producing plasma cells. Therapeutic targeting of NETs is immunoprotective in mice and humans.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"3 5","pages":"496-497"},"PeriodicalIF":9.4000,"publicationDate":"2024-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Neutrophil extracellular traps trigger IgA loss after stroke and myocardial infarction\",\"authors\":\"\",\"doi\":\"10.1038/s44161-024-00465-5\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The mechanisms by which stroke and myocardial infarction trigger lymphocyte loss remain poorly defined. This study shows that the release of neutrophil extracellular traps (NETs) after stroke and myocardial infarction triggers B cell apoptosis and reduces the number of IgA-producing plasma cells. Therapeutic targeting of NETs is immunoprotective in mice and humans.\",\"PeriodicalId\":74245,\"journal\":{\"name\":\"Nature cardiovascular research\",\"volume\":\"3 5\",\"pages\":\"496-497\"},\"PeriodicalIF\":9.4000,\"publicationDate\":\"2024-04-24\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nature cardiovascular research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.nature.com/articles/s44161-024-00465-5\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature cardiovascular research","FirstCategoryId":"1085","ListUrlMain":"https://www.nature.com/articles/s44161-024-00465-5","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0
摘要
中风和心肌梗死引发淋巴细胞丢失的机制仍不十分明确。这项研究表明,中风和心肌梗死后中性粒细胞胞外捕获物(NET)的释放会引发 B 细胞凋亡,并减少产生 IgA 的浆细胞数量。针对中性粒细胞胞外捕获物的治疗对小鼠和人类都有免疫保护作用。
Neutrophil extracellular traps trigger IgA loss after stroke and myocardial infarction
The mechanisms by which stroke and myocardial infarction trigger lymphocyte loss remain poorly defined. This study shows that the release of neutrophil extracellular traps (NETs) after stroke and myocardial infarction triggers B cell apoptosis and reduces the number of IgA-producing plasma cells. Therapeutic targeting of NETs is immunoprotective in mice and humans.