Introduction: The Epstein-Barr virus has been associated with a considerable number of autoimmune diseases. We have previously demonstrated that EBV DNA enhances the production of IL-17A, a pro-inflammatory cytokine, via endosomal Toll-like receptor signalling.Methods: We used RNA-seq to analyze the transcriptional profile of mouse immune cells treated with EBV DNA.Results: We observed that EBV DNA upregulates an IL-17A-centric network of mediators. Ensemble Gene Set Enrichment Analysis (EGSEA) showed enriched expression of sets involved in inflammatory responses including IFNγ and TNF-α-associated pathways as well as proinflammatory diseases. On the other hand, while macrophages and B cells were somewhat able to induce an IL-17A response from T cells to EBV DNA, they were less potent than dendritic cells. EBV virions were also capable of eliciting the production of inflammatory mediators from dendritic cell-T cell cultures largely mirroring responses to the viral DNA.Conclusions: Given the wide prevalence of EBV in the population, our analyses reveal a network of mediators and cell types that may serve as therapeutic targets in a large proportion of people affected by autoimmune diseases.

中文翻译：

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树突状细胞-T细胞相互作用介导的以IL-17A为中心的Epstein-Barr病毒DNA反应

简介： EB 病毒与相当多的自身免疫性疾病有关。我们之前已经证明，EBV DNA 通过内体 Toll 样受体信号传导增强促炎细胞因子 IL-17A 的产生。方法：我们使用 RNA-seq 分析用 EBV DNA 处理的小鼠免疫细胞的转录谱。结果：我们观察到 EBV DNA 上调以 IL-17A 为中心的介质网络。整体基因集富集分析 (EGSEA) 显示参与炎症反应的基因集富集表达，包括 IFNγ 和 TNF-α 相关途径以及促炎性疾病。另一方面，虽然巨噬细胞和 B 细胞在一定程度上能够诱导 T 细胞对 EBV DNA 产生 IL-17A 反应，但它们的效力不如树突细胞。 EBV 病毒体还能够从树突状细胞-T 细胞培养物中引发炎症介质的产生，这在很大程度上反映了对病毒 DNA 的反应。结论：鉴于 EBV 在人群中广泛流行，我们的分析揭示了介质和细胞类型的网络，可以作为很大一部分受自身免疫性疾病影响的人的治疗靶点。