Facultad de Medicina, Universidad Autonoma del Estado de Morelos, 62210 Morelos, Mexico.
J Virol. 2010 Feb;84(4):1856-66. doi: 10.1128/JVI.02640-08. Epub 2009 Dec 9.
This study used an in vivo mouse model to analyze the response of dendritic cells (DCs) in Peyer's patches (PPs) within the first 48 h of infection with the wild-type murine rotavirus EDIM (EDIM(wt)). After the infection, the absolute number of DCs was increased by 2-fold in the PPs without a modification of their relative percentage of the total cell number. Also, the DCs from PPs of infected mice showed a time-dependent migration to the subepithelial dome (SED) and an increase of the surface activation markers CD40, CD80, and CD86. This response was more evident at 48 h postinfection (p.i.) and depended on viral replication, since DCs from PPs of mice inoculated with UV-treated virus did not show this phenotype. As a result of the activation, the DCs showed an increase in the expression of mRNA for the proinflammatory cytokines interleukin-12/23p40 (IL-12/23p40), tumor necrosis factor alpha (TNF-alpha), and beta interferon (IFN-beta), as well as for the regulatory cytokine IL-10. These results suggest that, a short time after rotavirus infection, the DCs from PPs play a critical role in controlling the infection and, at the same time, avoiding an excessive inflammatory immune response.
本研究采用体内小鼠模型,分析感染野生型鼠轮状病毒 EDIM(EDIM(wt))后 48 小时内派尔集合淋巴结(PPs)中树突状细胞(DCs)的反应。感染后,PPs 中 DCs 的绝对数量增加了 2 倍,而其在总细胞数中的相对比例没有改变。此外,来自感染小鼠 PPs 的 DCs 表现出时间依赖性向黏膜下穹窿(SED)迁移,并增加表面激活标志物 CD40、CD80 和 CD86。这种反应在感染后 48 小时更为明显,并且依赖于病毒复制,因为用紫外线处理的病毒接种的小鼠 PPs 中的 DCs 没有表现出这种表型。由于激活,DCs 表达促炎细胞因子白细胞介素-12/23p40(IL-12/23p40)、肿瘤坏死因子 alpha(TNF-alpha)和β干扰素(IFN-beta)以及调节细胞因子 IL-10 的 mRNA 水平增加。这些结果表明,在轮状病毒感染后很短的时间内,PPs 中的 DCs 在控制感染的同时,避免了过度的炎症免疫反应。