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Interleukin-21 Responses in Patients with Chronic Hepatitis B
To cite this article:
Li Jie, Ren Wanhua, Ma Wei, Zhang Jiao, Shi Jun, and Qin Chengyong. Journal of Interferon & Cytokine Research. February 2015, 35(2): 134-142. doi:10.1089/jir.2013.0119.
Published in Volume: 35 Issue 2: September 22, 2014
Online Ahead of Print: September 22, 2014
Author information
Jie Li,1,* Wanhua Ren,1,* Wei Ma,2,* Jiao Zhang,1 Jun Shi,1 and Chengyong Qin3
1Department of Infectious Disease, Shandong Provincial Hospital Affiliated to Shandong University, Shandong, China.
2Department of Oncological Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Shandong, China.
3Department of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong University, Shandong, China.
*These authors contributed equally to this work.
Address correspondence to:
Dr. Jie Li
Department of Infectious Disease
Provincial Hospital Affiliated to Shandong University
324 Jingwu Road
Ji'nan
Shandong 250021
China
E-mail: [email protected]
Received 3 November 2013
Accepted 24 July 2014
ABSTRACT
Interleukin (IL)-21 has been demonstrated to play a pivotal role in controlling chronic viral infections. However, little is known about the regulatory role of IL-21 in T cell immunity during the process of chronic hepatitis B (CHB). In the present study, the levels of serum IL-21 in 77 patients with various degrees of CHB in immune clearance phase (IC), 25 patients infected with hepatitis B virus (HBV) in immune tolerance phase (IT), and 25 healthy controls (HC) were measured and their potential association with major clinic indexes was examined. Peripheral blood mononuclear cells from CHB patients were stimulated with hepatitis B core antigen (HBcAg) in the presence or absence of anti-IL-21 antibody or recombinant IL-21, and the frequency of HBcAg-specific IL-21+CD4+ and interferon (IFN)-γ+CD8+ T cells was characterized by flow cytometry. Our data indicated that the levels of serum IL-21 were significantly higher in the IC CHB patients than that in the other groups and were positively correlated with the levels of serum HBV DNA and HBeAg in the IC patients. There was a low frequency of HBcAg-specific IL-21+CD4+ T cells in IC CHB patients. Further, IL-21 enhanced HBcAg-specific IFN-γ+CD8+ T cell proliferation, while treatment with anti-IL-21 inhibited antigen-specific IFN-γ+CD8+ T cell expansion in vitro. Our findings imply that IL-21 positively regulates proinflammatory IFN-γ+CD8+ T cell responses during the process of chronic HBV infection in humans.
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