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Increased frequency of Th17 cells in the peripheral blood of children infected with enterovirus 71
Author(s) -
Chen Jianguo,
Tong Jia,
Liu Haibing,
Liu Yingzhao,
Su Zhaoliang,
Wang Shengjun,
Shi Yan,
Zheng Dong,
Sandoghchian Siamak,
Geng Jianzhong,
Xu Huaxi
Publication year - 2012
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.23254
Subject(s) - virology , enterovirus , peripheral blood , enterovirus 71 , peripheral , medicine , enterovirus infections , biology , virus , immunology
Enterovirus 71 (EV71) affects the health of young children globally causing severe neurologic diseases. The relationship between EV71 infection and T helper type 17 (Th17) has not been described, although this new Th subset or interleukin‐17 (IL‐17) has been reported to be associated with other viral infections. The purpose of the current study was to describe the immune profile involving Th17 cells, neutrophils, and related factors and to speculate on the possible immunopathogenesis of EV71 infections. Flow cytometry and an automatic blood cell counter were used to analyze circulating Th17 cells and count neutrophils, respectively. Expression of acid‐related orphan nuclear receptor gamma t (ROR γt) was evaluated by reverse‐transcriptional PCR, and enzyme linked immunosorbent assays (ELISAs) were used for detecting concentrations of IL‐17, IL‐23, and IFN‐γ. The results showed that the frequencies of Th17 cells (1.47 ± 0.87%) and the number of neutrophils (7.4 ± 4.1 × 10 9 /L) in peripheral blood samples from children infected with EV71 were significantly higher compared to controls. In addition, there was a statistically higher expression of ROR γt in peripheral blood mononuclear cells (PBMCs) and elevated concentrations of IL‐17 and IL‐23 in sera, but lower IFN‐γ production during EV71 infections. The findings suggest that Th17 cells are mediators during the immunologic process. J. Med. Virol. 84:763–767, 2012. © 2012 Wiley Periodicals, Inc.