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Correction published on 26 October 2016, see Int. J. Mol. Sci. 2016, 17(11), 1793.

Open AccessArticle
Int. J. Mol. Sci. 2016, 17(7), 1070; doi:10.3390/ijms17071070

Involvement of the Interleukin-23/Interleukin-17 Axis in Chronic Hepatitis C Virus Infection and Its Treatment Responses

1
Department of Traditional and Western Medical Hepatology, Third Hospital of Hebei Medical University, Shijiazhuang 050000, China
2
Storr Liver Centre, Westmead Institute for Medical Research (WIMR), the University of Sydney at Westmead Hospital, Westmead, NSW 2145, Australia
*
Authors to whom correspondence should be addressed.
Academic Editor: Tatsuo Kanda
Received: 26 April 2016 / Revised: 27 June 2016 / Accepted: 29 June 2016 / Published: 15 July 2016
(This article belongs to the Special Issue Hepatitis Virus Infection and Research)
View Full-Text   |   Download PDF [3125 KB, uploaded 27 October 2016]   |  

Abstract

Interleukin-23 (IL-23) and its downstream factor IL-17 are the key cytokines involved in immune and inflammatory response in chronic liver diseases. This study aimed to investigate the role and molecular mechanisms of the IL-23/Th17 axis in chronic hepatitis C virus (HCV) infection, and the efficacy of IL-23/Th17 modulation in response to anti-HCV therapy. Sixty-six HCV-infected patients and 20 healthy controls were enrolled. The patients received PegIFNa-2a and ribavirin therapy for at least 48 weeks. The plasma level of IL-23 and the number of IL-17A-, IFN-γ-, and IL-21-producing peripheral blood mononuclear cells (PBMCs) at baseline and 12, 24, and 48 weeks following treatment were determined. The mRNA level of Th17 immune-associated molecules in PBMCs was evaluated by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) following treatment with IL-23 agonist or antagonist. Our data showed that, compared to healthy controls, HCV-infected patients had an increased plasma level of IL-23 and increased frequencies of IL-17A- and IFN-γ-producing PBMCs, whereas the HCV patients exhibited a reduced number of IL-21-producing PBMCs. However, the baseline frequencies of IL-21-producing PBMCs were markedly higher in HCV patients who achieved rapid virological response (RVR) than those without RVR. Additionally, the mRNA expressions of IL-21, IFN-γ, myxovirus resistance protein A (MxA), and suppressor of cytokine signaling 3 (SOCS3) were significantly upregulated in PBMCs, while FoxP3 expression was suppressed by IL-23 agonist. Thus, the IL-23/Th17 axis plays an important role in development of chronic HCV infection and antiviral response. IL-23 may enhance the antiviral activity of interferon-based therapy by modulating the expression of Th17 cells-associated molecules in HCV-infected patients. View Full-Text
Keywords: hepatitis C virus; interleukin-23; T helper 17 cells; interferon-γ; myxovirus resistance protein A hepatitis C virus; interleukin-23; T helper 17 cells; interferon-γ; myxovirus resistance protein A
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MDPI and ACS Style

Meng, P.; Zhao, S.; Niu, X.; Fu, N.; Su, S.; Wang, R.; Zhang, Y.; Qiao, L.; Nan, Y. Involvement of the Interleukin-23/Interleukin-17 Axis in Chronic Hepatitis C Virus Infection and Its Treatment Responses. Int. J. Mol. Sci. 2016, 17, 1070.

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