本研究旨在探讨白细胞介素23(interleukin 23，IL-23)在呼吸道合胞病毒(respiratory syncytial virus，RSV)感染支气管上皮细胞BEAS-2B后对Th1、Th2和Th17细胞分化的影响及作用机制。将RSV感染BEAS-2B后的上清液与淋巴细胞共孵育，并分别阻断IL-23受体(IL-23 receptor，IL-23R)、IL-23p19亚基及p38丝裂原活化蛋白激酶(p38 mitogen-activated protein kinase，p38 MAPK)信号通路。应用酶联免疫吸附试验(enzyme-linked immunosorbent assay，ELISA)检测上清液中细胞因子γ干扰素(interferon γ，IFN-γ)、IL-4、IL-17的浓度。同时，应用实时聚合酶链反应(polymerase chain reaction，PCR)检测相关转录因子(t-bet、gata3、rorγt)和信号转导子(stat4、stat6、stat3)的表达。结果显示，RSV感染后IFN-γ、IL-4和IL-17蛋白表达上调，转录因子及信号转导子的表达也有所增加。阻断IL-23和p38 MAPK信号通路后，Th1、Th2和Th7细胞分泌的细胞因子及转录因子表达均明显下降。结果提示，阻断IL-23后可在基因转导层面抑制RSV感染上皮细胞后诱导的Th1、Th2和Th17细胞分化，此过程可能与p38 MAPK信号通路有关。

The present paper aims to investigate the role of interleukin 23 (IL-23) in facilitating Th1, Th2 and Th17 differentiation during respiratory syncytial virus (RSV) infection of epithelial cells (BEAS-2B). Lymphocytes were treated by supernatants from BEAS-2B cells with RSV or mock infection. Then they were blocked by specific anti-IL-23R antibody, anti-IL-23p19 antibody and p38 mitogen-activated protein kinase (MAPK) inhibitor (SB203580). The concentrations of cytokines such as interferon γ (IFN-γ), IL-4 and IL-17 were detected by enzyme-linked immunosorbent assay (ELISA). The mRNA expressions of transcription factors (t-bet, gata3, rorγt), signal transducers (stat4, stat6, stat3) were determined by real-time polymerase chain reaction (PCR). The results showed that the concentrations of cytokines (IFN-γ， IL-4 and IL-17) were significantly increased after RSV infection, accompanied with the enhanced expressions of transcription factors. However, these cytokines and transcription factors were significantly decreased when IL-23 pathway was blocked by antibodies. The blockage of p38 MAPK signal pathway showed the same results. The results suggest that IL-23 could facilitate Th1, Th2 and Th17 differentiation in RSV-infected BEAS-2B cells, which might be associated with p38 MAPK signal pathway.