Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA.
Curr Opin Rheumatol. 2012 Jul;24(4):401-7. doi: 10.1097/BOR.0b013e328353372d.
To present recent findings on the pathogenesis of coxsackievirus B3 (CVB3) myocarditis based on animal models, with a focus on the role of T helper (Th) immune responses in disease progression.
Acute CVB3 myocarditis is known to be increased by Th1 immune responses, but recent findings indicate that Th1-type immunity protects against acute myocarditis by reducing viral replication and prevents the progression to chronic myocarditis and dilated cardiomyopathy (DCM) by inhibiting Th2 responses. Th2 responses reduce acute myocarditis by inhibiting Th1 responses via regulatory T cells and anti-inflammatory cytokines, but can be deleterious when they induce acute cardiac remodeling leading to chronic myocarditis/DCM. Th2-skewed immune responses allow resistant strains of mice to progress from myocarditis to DCM. In contrast, Th17 responses are elevated during acute and chronic myocarditis and have been found to contribute to cardiac remodeling and DCM.
Recent data indicate that elevated Th2 and Th17 responses during acute CVB3 myocarditis are critical for the progression from myocarditis to DCM and heart failure because of their ability to induce cardiac remodeling. Th1 responses protect against CVB3 myocarditis by inhibiting Th2 responses and viral replication, but increase acute inflammation.
基于动物模型，介绍柯萨奇病毒 B3（CVB3）心肌炎发病机制的最新研究发现，重点关注辅助性 T 细胞（Th）免疫应答在疾病进展中的作用。
急性 CVB3 心肌炎已知与 Th1 免疫应答增加有关，但最近的研究结果表明，Th1 型免疫通过减少病毒复制来保护机体免受急性心肌炎的侵害，并通过抑制 Th2 应答来防止其进展为慢性心肌炎和扩张型心肌病（DCM）。Th2 应答通过调节性 T 细胞和抗炎细胞因子抑制 Th1 应答来减轻急性心肌炎，但当它们诱导急性心脏重构导致慢性心肌炎/DCM 时，可能会产生有害作用。Th2 偏向的免疫应答使具有抗性的小鼠能够从心肌炎进展为 DCM。相反，Th17 应答在急性和慢性心肌炎期间升高，并且已被发现有助于心脏重构和 DCM。
最近的数据表明，急性 CVB3 心肌炎期间升高的 Th2 和 Th17 应答是从心肌炎进展为 DCM 和心力衰竭的关键，因为它们具有诱导心脏重构的能力。Th1 应答通过抑制 Th2 应答和病毒复制来保护机体免受 CVB3 心肌炎的侵害，但会增加急性炎症。
