心肌炎发病机制的免疫病理方面

F. Hladkykh
{"title":"心肌炎发病机制的免疫病理方面","authors":"F. Hladkykh","doi":"10.31928/2664-4479-2024.1.103112","DOIUrl":null,"url":null,"abstract":"Myocarditis is a group of inflammatory diseases of the heart muscle against the background of the absence of acute or chronic ischemic heart disease, which are diagnosed according to established histological, immunological and immunohistochemical criteria.Objective. Summarize current information on the immunopathogenesis of myocarditis based on data from open sources of information.Methods. Publications were selected based on PubMed, Clinical Key Elsevier, Cochrane Library, eBook Business Collection and Google Scholar databases, which covered information on the immunopathogenesis of myocarditis.Results. Viral infections are the most common cause of myocarditis, along with some bacteria and protozoa. Chronic immune stimulation or autoimmunity in chronic viral myocarditis results from incomplete resolution of the viral infection or response to a previous virus or immune-mediated chronic tissue injury. An active autoimmune response in human myocarditis, both at the cellular and humoral levels, is the immunological basis for the development of this pathology. Myocarditis caused by COVID-19 is a new entity. At the moment, four main manifestations of myocarditis in the context of SARS-CoV-2 have been identified: myocarditis associated with an acute infection of COVID-19, post-acute syndrome of COVID-19 (or prolonged syndrome of COVID-19), multisystem inflammatory syndrome, and myocarditis due to related to vaccination. Autoimmune reactions probably contribute to molecular mimicry – they activate virus-specific T-cells that attack the myocardium. During this phase, high concentrations of cytokines (eg, tumor necrosis factor, interleukins 1a, 1b, 2, and interferon-γ) are produced. These cytokines, together with antibodies against viral and cardiac proteins, further exacerbate cardiac damage and systolic dysfunction due to contractile dysfunction and matrix proteins.Conclusions. CD4+T-cells are defined as the main driving forces of heart-specific autoimmunity in myocarditis. Dysregulated CD4+ T-cell populations and their associated cytokines are critical for the development and progression of myocarditis and may serve as therapeutic targets and the development of new treatment approaches.","PeriodicalId":23419,"journal":{"name":"Ukrainian Journal of Cardiology","volume":"117 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Імунопатологічні аспекти етіопатогенезу міокардиту\",\"authors\":\"F. Hladkykh\",\"doi\":\"10.31928/2664-4479-2024.1.103112\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Myocarditis is a group of inflammatory diseases of the heart muscle against the background of the absence of acute or chronic ischemic heart disease, which are diagnosed according to established histological, immunological and immunohistochemical criteria.Objective. Summarize current information on the immunopathogenesis of myocarditis based on data from open sources of information.Methods. Publications were selected based on PubMed, Clinical Key Elsevier, Cochrane Library, eBook Business Collection and Google Scholar databases, which covered information on the immunopathogenesis of myocarditis.Results. Viral infections are the most common cause of myocarditis, along with some bacteria and protozoa. Chronic immune stimulation or autoimmunity in chronic viral myocarditis results from incomplete resolution of the viral infection or response to a previous virus or immune-mediated chronic tissue injury. An active autoimmune response in human myocarditis, both at the cellular and humoral levels, is the immunological basis for the development of this pathology. Myocarditis caused by COVID-19 is a new entity. At the moment, four main manifestations of myocarditis in the context of SARS-CoV-2 have been identified: myocarditis associated with an acute infection of COVID-19, post-acute syndrome of COVID-19 (or prolonged syndrome of COVID-19), multisystem inflammatory syndrome, and myocarditis due to related to vaccination. Autoimmune reactions probably contribute to molecular mimicry – they activate virus-specific T-cells that attack the myocardium. During this phase, high concentrations of cytokines (eg, tumor necrosis factor, interleukins 1a, 1b, 2, and interferon-γ) are produced. These cytokines, together with antibodies against viral and cardiac proteins, further exacerbate cardiac damage and systolic dysfunction due to contractile dysfunction and matrix proteins.Conclusions. CD4+T-cells are defined as the main driving forces of heart-specific autoimmunity in myocarditis. Dysregulated CD4+ T-cell populations and their associated cytokines are critical for the development and progression of myocarditis and may serve as therapeutic targets and the development of new treatment approaches.\",\"PeriodicalId\":23419,\"journal\":{\"name\":\"Ukrainian Journal of Cardiology\",\"volume\":\"117 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-02-28\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Ukrainian Journal of Cardiology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.31928/2664-4479-2024.1.103112\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Ukrainian Journal of Cardiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.31928/2664-4479-2024.1.103112","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

心肌炎是在没有急性或慢性缺血性心脏病的背景下发生的一组心肌炎性疾病,根据既定的组织学、免疫学和免疫组化标准进行诊断。根据公开信息来源的数据,总结当前有关心肌炎免疫发病机制的信息。根据PubMed、Clinical Key Elsevier、Cochrane Library、eBook Business Collection和Google Scholar数据库中涉及心肌炎免疫发病机制信息的文献进行筛选。病毒感染是心肌炎最常见的病因,此外还有一些细菌和原生动物。慢性病毒性心肌炎中的慢性免疫刺激或自身免疫是由于病毒感染未完全清除或对先前病毒的反应或免疫介导的慢性组织损伤所致。人类心肌炎在细胞和体液水平上的活跃自身免疫反应是这种病变发生的免疫学基础。由 COVID-19 引起的心肌炎是一种新的疾病。目前,SARS-CoV-2 导致的心肌炎主要有四种表现形式:与 COVID-19 急性感染相关的心肌炎、COVID-19 急性后综合征(或 COVID-19 延长综合征)、多系统炎症综合征以及与疫苗接种相关的心肌炎。自身免疫反应可能有助于分子模拟--它们激活了攻击心肌的病毒特异性 T 细胞。在这一阶段,会产生高浓度的细胞因子(如肿瘤坏死因子、白细胞介素 1a、1b、2 和干扰素-γ)。这些细胞因子与针对病毒和心脏蛋白的抗体一起,进一步加剧了由于收缩功能障碍和基质蛋白导致的心脏损伤和收缩功能障碍。CD4+T细胞被定义为心肌炎中心脏特异性自身免疫的主要驱动力。失调的 CD4+ T 细胞群及其相关细胞因子对心肌炎的发生和发展至关重要,可作为治疗靶点并开发新的治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Імунопатологічні аспекти етіопатогенезу міокардиту
Myocarditis is a group of inflammatory diseases of the heart muscle against the background of the absence of acute or chronic ischemic heart disease, which are diagnosed according to established histological, immunological and immunohistochemical criteria.Objective. Summarize current information on the immunopathogenesis of myocarditis based on data from open sources of information.Methods. Publications were selected based on PubMed, Clinical Key Elsevier, Cochrane Library, eBook Business Collection and Google Scholar databases, which covered information on the immunopathogenesis of myocarditis.Results. Viral infections are the most common cause of myocarditis, along with some bacteria and protozoa. Chronic immune stimulation or autoimmunity in chronic viral myocarditis results from incomplete resolution of the viral infection or response to a previous virus or immune-mediated chronic tissue injury. An active autoimmune response in human myocarditis, both at the cellular and humoral levels, is the immunological basis for the development of this pathology. Myocarditis caused by COVID-19 is a new entity. At the moment, four main manifestations of myocarditis in the context of SARS-CoV-2 have been identified: myocarditis associated with an acute infection of COVID-19, post-acute syndrome of COVID-19 (or prolonged syndrome of COVID-19), multisystem inflammatory syndrome, and myocarditis due to related to vaccination. Autoimmune reactions probably contribute to molecular mimicry – they activate virus-specific T-cells that attack the myocardium. During this phase, high concentrations of cytokines (eg, tumor necrosis factor, interleukins 1a, 1b, 2, and interferon-γ) are produced. These cytokines, together with antibodies against viral and cardiac proteins, further exacerbate cardiac damage and systolic dysfunction due to contractile dysfunction and matrix proteins.Conclusions. CD4+T-cells are defined as the main driving forces of heart-specific autoimmunity in myocarditis. Dysregulated CD4+ T-cell populations and their associated cytokines are critical for the development and progression of myocarditis and may serve as therapeutic targets and the development of new treatment approaches.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
CiteScore
0.10
自引率
0.00%
发文量
0
期刊最新文献
Risk factors for adverse outcome among patients with non-high risk pulmonary embolism Статеві та клініко-інструментальні паралелі рівнів ліпопротеїн(а) в пацієнтів з дуже високим серцево-судинним ризиком Вибір блокатора ренін-ангіотензин-альдостеронової системи для лікування серцевої недостатності при гострому міокардиті Характеристика пацієнтів з ішемічною хворобою серця та стабільною стенокардією в Україні, оцінка підходів до їх лікування за даними багатоцентрового дослідження GO-OD Порівняльний аналіз субклінічного тривожно-депресивного синдрому в пацієнтів із гострим інфарктом міокарда з елевацією сегмента ST до та під час активних бойових дій у Харківській області
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1