Role of T Cells in Viral and Immune-mediated Myocarditis

Chunyan Cheng, A. Baritussio, A. Giordani, R. Marcolongo, A. Caforio, S. Iliceto
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引用次数: 0

Abstract

Myocarditis is characterized by inflammatory cell infiltration into the myocardium and a high risk of deteriorating cardiac function with a heterogeneous etiology. Both viral- and myosin-induced myocarditis experimental models are used to mimic myocarditis in humans. Here, coxsackie virus B3 (CVB3)-induced and non-virus-induced myocarditis models and data obtained in clinical studies were reviewed. Experimental murine myocarditis following immunization with α-myosin together with complete Freund adjuvant represents the classical immune-mediated model. T helper 1 (Th1) and Th2 pathways and important cytokines are involved in the autoimmunity of myocarditis, and the dynamic balance between Th17 and regulatory T cell (Treg) seems to have an important role in the process of myocarditis. The purpose of this review is to summarize the existing understanding of the immunological mechanisms underlying myocarditis and exploring gaps in knowledge in both animal and human studies, since these mechanistic insights are a critical requirement for the development of novel therapeutic and vaccination strategies.
T 细胞在病毒和免疫介导的心肌炎中的作用
心肌炎的特点是心肌中的炎性细胞浸润和心功能恶化的高风险,其病因多种多样。病毒和肌球蛋白诱导的心肌炎实验模型都被用来模拟人类心肌炎。本文回顾了柯萨奇病毒 B3(CVB3)诱导和非病毒诱导的心肌炎模型以及临床研究获得的数据。用α-肌球蛋白和完全弗罗因德佐剂进行免疫后的实验性小鼠心肌炎是经典的免疫介导模型。T辅助细胞1(Th1)和Th2通路及重要的细胞因子参与了心肌炎的自身免疫,而Th17和调节性T细胞(Treg)之间的动态平衡似乎在心肌炎的过程中起着重要作用。本综述的目的是总结对心肌炎免疫学机制的现有认识,并探讨动物和人体研究中存在的知识空白,因为这些机理认识是开发新型治疗和疫苗策略的关键要求。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
0.90
自引率
0.00%
发文量
31
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