Respiratory syncytial virus (RSV) is the leading cause of respiratory viral infection in infants and children. However, little is known about the contribution of monocytes to antiviral responses against RSV infection. We identified the IFN-β production of monocytes using IFN-β/YFP reporter mice. The kinetic analysis of IFN-β-producing cells in in vivo RSV-infected lung cells indicated that monocytes are recruited to the inflamed lung during the early phase of infection. These cells produced IFN-β via the myeloid differentiation factor 88-mediated pathway, rather than the TLR7- or mitochondrial antiviral signaling protein-mediated pathway. In addition, monocyte-ablated mice exhibited decreased numbers of IFN-γ-producing and RSV Ag-specific CD8⁺ T cells. Collectively, these data indicate that monocytes play pivotal roles in cytotoxic T-cell responses and act as type I IFN producers during RSV infection.

中文翻译：

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单核细胞通过依赖 MyD88 的途径和细胞毒性 T 细胞对粘膜呼吸道合胞病毒感染的反应促进 IFN-β 的产生。

呼吸道合胞病毒 (RSV) 是婴儿和儿童呼吸道病毒感染的主要原因。然而，关于单核细胞对抗 RSV 感染的抗病毒反应的贡献知之甚少。我们使用 IFN-β/YFP 报告小鼠鉴定了单核细胞的 IFN-β 产生。在体内RSV 感染的肺细胞中产生 IFN-β 的细胞的动力学分析表明，在感染的早期阶段，单核细胞被募集到发炎的肺。这些细胞通过骨髓分化因子 88 介导的途径产生 IFN-β，而不是 TLR7 或线粒体抗病毒信号蛋白介导的途径。此外，单核细胞消融的小鼠表现出产生 IFN-γ 和 RSV Ag 特异性 CD8 ^{+ 的数量减少}T细胞。总的来说，这些数据表明单核细胞在细胞毒性 T 细胞反应中起关键作用，并在 RSV 感染期间充当 I 型 IFN 生产者。