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自身免疫性心肌炎、心瓣炎和心肌病。

Autoimmune myocarditis, valvulitis, and cardiomyopathy.

作者信息

Myers Jennifer M, Fairweather DeLisa, Huber Sally A, Cunningham Madeleine W

机构信息

University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.

出版信息

Curr Protoc Immunol. 2013;Chapter 15:Unit 15.14.1-51. doi: 10.1002/0471142735.im1514s101.

DOI:10.1002/0471142735.im1514s101
PMID:23564686
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3672855/
Abstract

Myocarditis and valvulitis are inflammatory diseases affecting myocardium and valve. Myocarditis, a viral-induced disease of myocardium, may lead to dilated cardiomyopathy and loss of heart function. Valvulitis leads to deformed heart valves and altered blood flow in rheumatic heart disease. Animal models recapitulating these diseases are important in understanding the human condition. Cardiac myosin is a major autoantigen in heart, and antibodies and T cells to cardiac myosin are evident in inflammatory heart diseases. This unit is a practical guide to induction and evaluation of experimental autoimmune myocarditis (EAM) in several mouse strains and the Lewis rat. Purification protocols for cardiac myosin and protocols for induction of EAM by cardiac myosin and its myocarditis-producing peptides, and coxsackievirus CVB3, are defined. Protocols for assessment of myocarditis and valvulitis in humans and animal models provide methods to define functional autoantibodies targeting cardiac myosin, β-adrenergic, and muscarinic receptors, and their deposition in tissues.

摘要

心肌炎和心瓣膜炎是影响心肌和瓣膜的炎症性疾病。心肌炎是一种由病毒引起的心肌疾病,可能导致扩张型心肌病和心功能丧失。心瓣膜炎会导致风湿性心脏病中的心瓣膜变形和血流改变。能够重现这些疾病的动物模型对于理解人类病情很重要。心肌肌球蛋白是心脏中的主要自身抗原,在炎症性心脏病中可明显检测到针对心肌肌球蛋白的抗体和T细胞。本单元是在几种小鼠品系和刘易斯大鼠中诱导和评估实验性自身免疫性心肌炎(EAM)的实用指南。定义了心肌肌球蛋白的纯化方案以及通过心肌肌球蛋白及其产生心肌炎的肽和柯萨奇病毒CVB3诱导EAM的方案。评估人类和动物模型中心肌炎和心瓣膜炎的方案提供了定义靶向心肌肌球蛋白、β-肾上腺素能和毒蕈碱受体的功能性自身抗体及其在组织中沉积的方法。

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本文引用的文献

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IL-33 independently induces eosinophilic pericarditis and cardiac dilation: ST2 improves cardiac function.IL-33 可独立诱导嗜酸性心包炎和心脏扩张:ST2 可改善心功能。
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Th2 regulation of viral myocarditis in mice: different roles for TLR3 versus TRIF in progression to chronic disease.小鼠病毒性心肌炎中Th2的调节作用:Toll样受体3(TLR3)与TIR结构域衔接蛋白(TRIF)在疾病进展为慢性病过程中的不同作用
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PD-1 deficiency results in the development of fatal myocarditis in MRL mice.PD-1 缺乏导致 MRL 小鼠发生致命性心肌炎。
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