IL-9 Inhibits Viral Replication in Coxsackievirus B3-Induced Myocarditis.
IL-9 Inhibits Viral Replication in Coxsackievirus B3-Induced Myocarditis.
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IL-9 抑制柯萨奇病毒 B3 诱发的心肌炎中的病毒复制
DOI:
10.3389/fimmu.2016.00409
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发表时间:
2016
影响因子:
7.3
通讯作者:
Cheng X
中科院分区:
文献类型:
--
作者:
Yu M;Long Q;Li HH;Liang W;Liao YH;Yuan J;Cheng X
Myocardial injuries in viral myocarditis (VMC) are caused by viral infection and related autoimmune disorders. Recent studies suggest that IL-9 mediated both antimicrobial immune and autoimmune responses in addition to allergic diseases. However, the role of IL-9 in viral infection and VMC remains controversial and uncertain. In this study, we infected Balb/c mice with Coxsackievirus B3 (CVB3), and found that IL-9 was enriched in the blood and hearts of VMC mice on days 5 and 7 after virus infection. Most of IL-9 was secreted by CD8+ T cells on day 5 and CD4+ T cells on day 7 in the myocardium. Further, IL-9 knockout exacerbated cardiac damage following CVB3 infection, along with a sharp increase in viral replication and IL-17a expression, as well as a decrease in TGF-β. In contrast, the repletion of IL-9 in Balb/c mice with CVB infection induced the opposite effect. Studies in vitro further revealed that IL-9 directly inhibited viral replication in cardiomyocytes by reducing coxsackie and adenovirus receptor expression, which might be associated with upregulation of TGF-β autocrine effect in these cells. However, IL-9 had no direct effect on apoptosis in cardiomyocytes. Our data indicated that IL-9 played a protective role in disease progression by inhibiting CVB3 replication in the early stages of VMC.
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影响因子:
4.8
作者:
Qing K;Weifeng W;Fan Y;Yuluan Y;Yu P;Yanlan H
通讯作者:
Yanlan H
影响因子:
37.8
作者:
Nishio, R;Matsumori, A;Sasayama, S
通讯作者:
Sasayama, S
影响因子:
3.5
作者:
Otsuka, Masak;Negishi, Yoichi;Aramaki, Yukihiko
通讯作者:
Aramaki, Yukihiko
影响因子:
5
作者:
Yu, Xian;Deng, Lingyan;Liao, Yuhua
通讯作者:
Liao, Yuhua
DOI:
10.1152/ajpheart.00154.2007
发表时间:
2007-07-01
影响因子:
4.8
作者:
Wang, Yi-Xin;Da Cunha, Valdeci;Croze, Ed
通讯作者:
Croze, Ed