Modern aspects of immunopathogenesis of autoimmune myocarditis.

Filipp N Paleev, Alevtina A Kotova, Sergey V Suchkov, Nikolay R Paleev
{"title":"Modern aspects of immunopathogenesis of autoimmune myocarditis.","authors":"Filipp N Paleev,&nbsp;Alevtina A Kotova,&nbsp;Sergey V Suchkov,&nbsp;Nikolay R Paleev","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Myocarditis (MC) is an inflammation of the cardiac muscle. Viral infections appear to be the most frequent cause for induction of MC. According to the I. Roitt's classification, autoimmune (AI) MC is an organ-specific form of AI pathology. Thus, autoreactive antibodies (auto-Abs) against myocardial antigens and autoreactive T cells are major pathogenic mechanisms, and they are a common cause of cardiac muscle disorder progression. The autoantigens from myocardial tissue (like cardiomyosin and etc.) and/or the phenomena of virus mimicry stimulate auto-Ab production and their cross-reactivity with myocardial antigens. Some auto-Abs in patients with AI diseases demonstrate DNA-hydrolytic or proteolytic abilities against autoantigen. We found both DNA-abzymes and protabzymes in some MC patients. They showed catalytic activity not only against non-specific polypeptide, but also specific activity against cardiomyosine. Proteolytic activities of protabzymes differ depending on the clinical form and activity of MC. This suggests a role of protabzymes in the pathogenesis of AI-MC. According to some authors, auto-Abs (including auto-Abs with catalytic ability) in patients with AI diseases can be additional regulatory factors of apoptosis.</p>","PeriodicalId":21507,"journal":{"name":"Russian journal of immunology : RJI : official journal of Russian Society of Immunology","volume":"7 4","pages":"323-7"},"PeriodicalIF":0.0000,"publicationDate":"2002-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Russian journal of immunology : RJI : official journal of Russian Society of Immunology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Myocarditis (MC) is an inflammation of the cardiac muscle. Viral infections appear to be the most frequent cause for induction of MC. According to the I. Roitt's classification, autoimmune (AI) MC is an organ-specific form of AI pathology. Thus, autoreactive antibodies (auto-Abs) against myocardial antigens and autoreactive T cells are major pathogenic mechanisms, and they are a common cause of cardiac muscle disorder progression. The autoantigens from myocardial tissue (like cardiomyosin and etc.) and/or the phenomena of virus mimicry stimulate auto-Ab production and their cross-reactivity with myocardial antigens. Some auto-Abs in patients with AI diseases demonstrate DNA-hydrolytic or proteolytic abilities against autoantigen. We found both DNA-abzymes and protabzymes in some MC patients. They showed catalytic activity not only against non-specific polypeptide, but also specific activity against cardiomyosine. Proteolytic activities of protabzymes differ depending on the clinical form and activity of MC. This suggests a role of protabzymes in the pathogenesis of AI-MC. According to some authors, auto-Abs (including auto-Abs with catalytic ability) in patients with AI diseases can be additional regulatory factors of apoptosis.

自身免疫性心肌炎免疫发病机制的现代观点。
心肌炎(MC)是一种心肌炎症。病毒感染似乎是诱导MC的最常见原因。根据I. Roitt的分类,自身免疫性(AI) MC是AI病理的一种器官特异性形式。因此,针对心肌抗原和自身反应性T细胞的自身反应性抗体(auto-Abs)是主要的致病机制,也是心肌疾病进展的常见原因。心肌组织的自身抗原(如心肌凝蛋白等)和/或病毒模仿现象刺激自身抗体的产生及其与心肌抗原的交叉反应性。AI患者的一些自身抗体表现出对自身抗原的dna水解或蛋白水解能力。我们在一些MC患者中发现了dna酶和原酶。它们不仅对非特异性多肽具有催化活性,而且对心肌苷具有特异性活性。原酶的蛋白水解活性取决于MC的临床形式和活性,这表明原酶在AI-MC的发病机制中起作用。一些作者认为,AI患者的自身抗体(包括具有催化能力的自身抗体)可能是细胞凋亡的额外调节因子。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信