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| Role of interleukin 23 in facilitating Th1, Th2 and Th17 differentiation after respiratory syncytial virus infection |
| FENG Jingjing, CHEN Jiajun, WANG Shengmei, JIE Zhijun |
| Department of Respiratory Medicine, Shanghai Fifth People’s Hospital, Fudan University, Shanghai 200240, China |
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Abstract 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.
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Received: 10 February 2017
Published: 25 October 2017
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Corresponding Authors:
JIE Zhijun
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2017, Vol. 12 
