Key Laboratory of Viral Heart Diseases, Ministry of Public Health, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Virology. 2011 Dec 5;421(1):78-84. doi: 10.1016/j.virol.2011.09.006. Epub 2011 Oct 11.
IL-17-producing (Th17) and regulatory T (Treg) cells have been well established in the pathogenesis of many inflammatory diseases. To assess whether Th17 and Treg were altered in acute virus-induced myocarditis (AVMC) mice, we assessed Th17/Treg functions on different levels in AVMC. It was shown that the expression of splenic Th17 cells and Th17-related cytokines (IL-17A, IL-21) markedly increased. Interestingly, the expression of splenic Treg cells and Treg-related cytokines (TGF-β, IL-10) also significantly increased. Using neutralization of IL-17 in the AVMC, we found that Treg cells roughly decreased compared with isotype control mice. However, T cells and perforin dramatically increased, followed by a marked reduction in CVB3 replication. The results suggested that Th17 cells possibly contributed to viral replication through the action of Treg cells in mediating T cells and perforin response in AVMC.
IL-17 产生细胞 (Th17) 和调节性 T (Treg) 细胞已被充分证实参与了许多炎症性疾病的发病机制。为了评估 Th17 和 Treg 是否在急性病毒诱导的心肌炎 (AVMC) 小鼠中发生改变，我们在不同水平上评估了 AVMC 中 Th17/Treg 的功能。结果表明，脾 Th17 细胞和 Th17 相关细胞因子 (IL-17A、IL-21) 的表达显著增加。有趣的是，脾 Treg 细胞和 Treg 相关细胞因子 (TGF-β、IL-10) 的表达也明显增加。在 AVMC 中使用 IL-17 的中和抗体，我们发现与同型对照小鼠相比，Treg 细胞大致减少。然而，T 细胞和穿孔素显著增加，随后 CVB3 复制明显减少。结果表明，Th17 细胞可能通过 Treg 细胞介导 T 细胞和穿孔素反应在 AVMC 中促进病毒复制。
