Distinct different expression of Th17 and Th9 cells in coxsackie virus B3-induced mice viral myocarditis.

Distinct different expression of Th17 and Th9 cells in coxsackie virus B3-induced mice viral myocarditis.
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柯萨奇病毒B3诱导的小鼠病毒性心肌炎中Th17和Th9细胞的明显差异表达

DOI:
10.1186/1743-422x-8-267
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发表时间:
2011-06-02
期刊:
影响因子:
4.8
通讯作者:
Yanlan H
Yanlan H
中科院分区:
医学3区
文献类型:
--
作者:
Qing K;Weifeng W;Fan Y;Yuluan Y;Yu P;Yanlan H

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近年来,一种新的分泌细胞因子白细胞介素-9(IL-9)的辅助性T细胞(Th)被发现,称为Th 9细胞。据报道,它参与组织炎症和自身免疫反应,并诱导不同于Th 17细胞的疾病。Th 17细胞在病毒性心肌炎(viral myocarditis,VMC)中起重要作用,但Th 9细胞是否参与VMC的发病机制尚不清楚。BALB/c小鼠腹腔注射科萨基病毒B3(CVB 3)建立VMC模型。对照组小鼠腹腔注射磷酸盐缓冲液,于注射后0、7、14、21、28、35、42 d,用苏木精-伊红染色观察心肌组织病理学变化。流式细胞术分析脾Th 17和Th 9细胞亚群。采用半定量逆转录聚合酶链反应(RT-PCR)和巢式聚合酶链反应(nestedPCR)检测心肌IL-17、IL-9 mRNA的表达。结果显示,病毒性心肌炎小鼠Th 17细胞和IL-17 mRNA水平在感染后7 d即明显升高,28 d达高峰,并持续至42 d(p < 0.05)。而Th 9细胞和IL-9 mRNA在实验过程中与对照组相比无显著性差异(p > 0.05)。在CVB 3诱导的VMC中,Th 17细胞明显升高,而Th 9细胞无明显升高。VMC的微环境似乎有助于Th 17细胞的分化和增殖,而不是Th 9细胞。我们的初步数据表明,Th 9细胞不能保护VMC,也不能促进疾病。
Recently, a new subset of CD4+T helper(Th) cell that predominantly secret cytokine interleukin-9(IL-9) is identified, termed Th9 cell. It has been reported to participate in tissue inflammation and autoimmune responses, and induce disease which differed from Th17 cells. Th17 cells have been shown to play a critical role in viral myocarditis (VMC), but whether Th9 cells are involved in the pathogenesis of VMC remains unclear. BALB/c mice were intraperitoneally (i.p) injected with coxsackie virus B3(CVB3) for establishing VMC models. Control mice were treated with phosphate-buffered saline i.p. On day 0,7,14,21,28,35,42 after injection, myocardial histopathological changes were evaluated by hematoxylin-eosin staining. Splenic Th17 and Th9 cells subsets were analyzed by flow cytometry. And cardiac IL-17, IL-9 mRNA were measured by semi-quantitative reverse transcription-PCR and nested PCR, respectively. Results showed the levels of Th17 cells and IL-17 mRNA obviously increased in VMC mice on 7 day after infection, peaked on day 28, and highly persisted to at least day 42 (p < 0.05). While the frequencies of Th9 cells and IL-9 mRNA showed no significant difference between VMC and control group throughout the course of the experiment(p > 0.05). It was differentiated Th17 but not Th9 cells significantly elevated in the development of CVB3-induced VMC. The microenvironment of VMC seemed to contribute to the differentiation and proliferation of Th17 rather than Th9 cells. Our preliminary data implied Th9 cells could not protect against VMC nor promote the disease.