Cardiac Autoimmunity: Myocarditis.
Cardiac Autoimmunity: Myocarditis.
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DOI：
10.1007/978-3-319-57613-8_10
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发表时间：
2017
影响因子：
--
通讯作者：
Čiháková D
中科院分区：
文献类型：
--
作者：
Bracamonte-Baran W;Čiháková D
心肌炎是心脏肌肉组织（心肌）的炎症。在病理性心脏特异性炎症过程后，可能进展为慢性损伤和扩张型心肌病。后者的特征是收缩功能障碍，其临床相关性是心力衰竭。然而，由于组织损伤和电生理紊乱，可能会出现其他急性并发症。不同的病因涉及触发心肌炎。在某些情况下，如巨细胞心肌炎或嗜酸性坏死性心肌炎，这是一个自身免疫过程。有几个因素易导致自身免疫性心肌炎的发生，如全身/局部原发性自身免疫、病毒感染、HLA和性别偏倚、隐藏抗原暴露、拟态和胸腺训练/Treg诱导缺陷。一旦抗心肌自身免疫过程被触发，免疫应答的几个组成部分就以特定的时机和免疫病理学特征协调对心肌组织的持续攻击。由单核细胞/巨噬细胞、中性粒细胞和嗜酸性粒细胞介导的先天性反应与适应性反应平行，发挥最终效应器作用，而不仅仅是启动功能。基质细胞如成纤维细胞也通过特定的细胞因子参与该过程。此外，适应性T细胞应答具有反范式特征，因为Th 17应答对于急性心肌炎是无效的，但却是导致扩张型心肌病的过程的主要驱动力。体液反应被认为是旁观者，在晚期血流动力学并发症的出现中很重要。这一过程的复杂性，以及非特异性和多变的临床表现，给诊断和治疗带来了困难，目前仍不理想。在本章中，我们将从基础科学和临床角度讨论最相关的免疫病理学发现。
Myocarditis is the inflammation of the muscle tissues of the heart (myocardium). After a pathologic cardiac-specific inflammatory process, it may progress to chronic damage and dilated cardiomyopathy. The latter is characterized by systolic dysfunction, whose clinical correlate is heart failure. Nevertheless, other acute complications may arise as consequence of tissue damage and electrophysiologic disturbances. Different etiologies are involved in triggering myocarditis. In some cases, such as giant cell myocarditis or eosinophilic necrotizing myocarditis, it is an autoimmune process. Several factors predispose the development of autoimmune myocarditis such as systemic/local primary autoimmunity, viral infection, HLA and gender bias, exposure of cryptic antigens, mimicry, and deficient thymic training/Treg induction. Once the anti-myocardium autoimmune process is triggered, several components of the immune response orchestrate a sustained attack toward myocardial tissues with particular timing and immunopathogenic features. Innate response mediated by monocytes/macrophages, neutrophils, and eosinophils parallels the adaptive response, playing a final effector role and not only a priming function. Stromal cells like fibroblast are also involved in the process through specific cytokines. Furthermore, adaptive T cell responses have anti-paradigmatic features, as Th17 response is dispensable for acute myocarditis but is the main driver of the process leading to dilated cardiomyopathy. Humoral response, thought to be a bystander, is important in the appearance of late-stage hemodynamic complications. The complexity of that process, as well as the unspecific and variable clinical presentation, had generated difficulties for diagnosis and treatment, which remain suboptimal. In this chapter, we will discuss the most relevant immunopathogenic findings from a basic science and clinical perspective.
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影响因子：
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通讯作者：
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