Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.
Virology. 2012 Jul 20;429(1):74-90. doi: 10.1016/j.virol.2012.04.005. Epub 2012 May 1.
In vitro studies have shown that enteroviruses employ strategies that may impair the ability of DCs to trigger T cell immunity, but it is unclear how these viruses affect DCs in vivo. Here, we evaluate the effects of wild-type (wt) coxsackievirus B3 on DCs in vitro and in a murine model in vivo. Although CVB3 does not productively infect the vast majority of DCs, virus infection profoundly reduces splenic conventional DC numbers and diminishes their capacity to prime naïve CD8(+) T cells in vitro. In contrast to recombinant CVB3, highly pathogenic wt virus infection significantly diminishes the host's capacity to mount T cell responses, which is temporally associated with the loss of CD8α(+) DCs. Our findings demonstrate that enterovirus infection substantially alters the number, heterogeneity, and stimulatory capacity of DCs in vivo, and these dramatic immunomodulatory effects may weaken the host's capacity to mount antiviral T cell responses.
体外研究表明，肠道病毒采用的策略可能会损害树突状细胞引发 T 细胞免疫的能力，但这些病毒如何在体内影响树突状细胞尚不清楚。在这里，我们评估了野生型（wt）柯萨奇病毒 B3 在体外和体内小鼠模型中的作用。尽管 CVB3 不能有效地感染绝大多数树突状细胞，但病毒感染会显著减少脾脏常规树突状细胞的数量，并降低其在体外激活幼稚 CD8(+) T 细胞的能力。与重组 CVB3 相反，高致病性 wt 病毒感染会显著降低宿主产生 T 细胞反应的能力，这与 CD8α(+) 树突状细胞的丢失具有时间相关性。我们的研究结果表明，肠道病毒感染会在体内显著改变树突状细胞的数量、异质性和刺激能力，这些剧烈的免疫调节作用可能会削弱宿主产生抗病毒 T 细胞反应的能力。
