呼吸道病毒感染很常见，近年来，严重急性呼吸综合征冠状病毒2的爆发凸显了病毒感染对抗病毒先天免疫和炎症反应的影响。许多病毒性呼吸道感染的具体治疗方法尚未确定，主要是对症治疗。因此，了解气道上皮细胞固有免疫系统的细节对于新疗法的开发至关重要。本研究旨在研究暴露于 Toll 样受体 3 激动剂的非癌性支气管上皮 BEAS-2B 细胞中干扰素 (IFN) 刺激基因 (ISG)60 的功能和表达。 BEAS-2B 细胞用合成的 TLR3 配体、聚肌苷-聚胞苷酸 (poly IC) 处理。分别使用逆转录定量 PCR 和蛋白质印迹分析 ISG60 的 mRNA 和蛋白表达水平。使用酶联免疫吸附测定检测 C-X-C 基序趋化因子配体 10 (CXCL10) 的水平，并使用特定的小干扰 RNA 检测 IFN-β、ISG60 和 ISG56 敲低的影响。值得注意的是，ISG60 表达与多聚 IC 浓度成比例增加，重组人 IFN-β 也诱导 ISG60 表达。相比之下，IFN-β和ISG56的敲低降低了ISG60的表达，ISG60的敲低则降低了CXCL10和ISG56的表达。这些发现表明，ISG60 部分涉及 CXCL10 表达，并且 ISG60 可能在支气管上皮细胞的先天免疫反应中发挥作用。本研究强调 ISG60 是针对气道病毒感染的新治疗策略的潜在靶点。

Viral infections in the respiratory tract are common, and, in recent years, severe acute respiratory syndrome coronavirus 2 outbreaks have highlighted the effect of viral infections on antiviral innate immune and inflammatory reactions. Specific treatments for numerous viral respiratory infections have not yet been established and they are mainly treated symptomatically. Therefore, understanding the details of the innate immune system underlying the airway epithelium is crucial for the development of new therapies. The present study aimed to investigate the function and expression of interferon (IFN)‑stimulated gene (ISG)60 in non‑cancerous bronchial epithelial BEAS‑2B cells exposed to a Toll‑like receptor 3 agonist. BEAS‑2B cells were treated with a synthetic TLR3 ligand, polyinosinic‑polycytidylic acid (poly IC). The mRNA and protein expression levels of ISG60 were analyzed using reverse transcription‑quantitative PCR and western blotting, respectively. The levels of C‑X‑C motif chemokine ligand 10 (CXCL10) were examined using an enzyme‑linked immunosorbent assay, and the effects of knockdown of IFN‑β, ISG60 and ISG56 were examined using specific small interfering RNAs. Notably, ISG60 expression was increased in proportion to poly IC concentration, and recombinant human IFN‑β also induced ISG60 expression. By contrast, knockdown of IFN‑β and ISG56 decreased ISG60 expression, and ISG60 knockdown reduced CXCL10 and ISG56 expression. These findings suggested that ISG60 is partly implicated in CXCL10 expression and that ISG60 may serve a role in the innate immune response of bronchial epithelial cells. The present study highlights ISG60 as a potential target for new therapeutic strategies against viral infections in the airway.