Interleukin‐23 facilitates Th1 and Th2 cell differentiation in vitro following respiratory syncytial virus infection. Issue 4 (3rd February 2015)

• Record Type: Journal Article
• Authors: Feng, Jingjing; Hu, Yunwen; Song, Zhigang; Liu, Yi; Guo, Xuejun; Jie, Zhijun
• Is Part Of: Journal of medical virology. Volume 87:Issue 4(2015:Apr.)
• Page Start: 708
• Page End: 715
• Publication Date: 2015-02-03
• Subjects: Virology -- Periodicals; 616
• DOI: 10.1002/jmv.24126
• Languages: English
• ISSNs: 0146-6615

Abstract

<abstract abstract-type="main" xml:lang="en"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="jmv24126-sec-0001" sec-type="section"> <p>Respiratory syncytial virus (RSV) infection induces activation and imbalance of the immune system; however, the role of T helper 17 cells (Th17) in the response to RSV infection remains unclear. Interleukin‐23 (IL‐23) is a key cytokine in Th17 cell differentiation. The aim of this study was to explore the function of IL‐23 in determining the distribution of Th lymphocyte subsets (Th1, Th2, and Th17) after RSV infection in vitro. Human bronchial epithelial cell line BEAS‐2B was infected with mock or RSV at various multiplicities of infection (MOI) and transcript expression of IL‐6, IL‐23p19, and transforming growth factor (T<italic>GF‐β</italic>) was detected by real‐time polymerase chain reaction; IL‐6, IL‐23, and TGF‐β in the supernatant were measured by enzyme‐linked immunosorbent assay. The Th subset distribution in lymphocytes was determined by flow cytometry after co‐culture with supernatants from mock and 72‐hr RSV infection cultures. The role of IL‐23 in lymphocytes was assessed by specific receptor blockade (IL‐23R) prior to co‐culture with supernatants from RSV‐infected BEAS‐2B cells, followed by flow cytometry to analyze Th subset differentiation. Cytokine expression increased after RSV infection. IL‐23R blockade suppressed the differentiation of Th1, Th2, and Th17 cells in the presence of supernatants from RSV‐infected BEAS‐2B cells. RSV infection may induce cytokine secretion, thus inducing Th1, Th2, and Th17 differentiation via an IL‐23R‐dependent process. <bold><italic>J. Med. Virol. 87:708–715, 2015</italic>.</bold> © 2015 Wiley Periodicals, Inc.</p> </sec> </abstract>