Abstract：
Inflammatory monocytes (iMOs) and B cells are the main targets of the poxvirus ectromelia virus (ECTV) in the lymph nodes of mice and play distinct roles in surviving the infection. Infected and bystander iMOs control ECTV\'s systemic spread, preventing early death, while B cells make antibodies that eliminate ECTV. Our work demonstrates that within an infected animal that survives ECTV infection, intrinsic and bystander infection of iMOs and B cells differentially control the transcription of genes important for immune cell function and, perhaps, cell identity. Bystander cells upregulate metabolism, antigen presentation, and interferon-stimulated genes. Infected cells downregulate many cell-type-specific genes and upregulate transcripts typical of non-immune cells. Bystander (Bys) and infected (Inf) iMOs non-redundantly contribute to the cytokine milieu and the interferon response. Furthermore, we uncover how type I interferon (IFN-I) or IFN-γ signaling differentially regulates immune pathways in Inf and Bys iMOs and that, at steady state, IFN-I primes iMOs for rapid IFN-I production and antigen presentation.
摘要：
炎性单核细胞（iMO）和B细胞是小鼠淋巴结中痘病毒异位病毒（ECTV）的主要靶标，并在感染中发挥不同的作用。受感染和旁观者的IMO控制ECTV的系统传播，防止过早死亡,而B细胞产生抗体消除ECTV。我们的工作表明，在ECTV感染中幸存下来的受感染动物中，iMO和B细胞的内在和旁观者感染差异控制对免疫细胞功能重要的基因的转录，也许,细胞身份。旁观者细胞上调新陈代谢，抗原呈递,和干扰素刺激的基因。受感染的细胞下调许多细胞类型特异性基因，并上调非免疫细胞典型的转录本。旁观者（Bys）和感染的（Inf）iMO非冗余地有助于细胞因子环境和干扰素反应。此外，我们揭示了I型干扰素（IFN-I）或IFN-γ信号传导如何差异调节Inf和BysiMO的免疫途径，在稳定状态下，IFN-I启动iMO用于快速IFN-I产生和抗原呈递。
