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IL-35: A potential therapeutic target for controlling hepatitis B virus infection
Xiao Gang Xiang1,2 and
Qing Xie1,2,*
Article first published online: 28 JAN 2015
DOI: 10.1111/1751-2980.12218
© 2014 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Wiley Publishing Asia Pty Ltd
Issue
Journal of Digestive Diseases
Volume 16, Issue 1, pages 1–6, January 2015
Article has an altmetric score of 1
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1 Department of Infectious Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
2 Translational Laboratory of Liver Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China
*Correspondence to: Qing XIE, Department of Infectious Diseases, Translational Laboratory of Liver Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, 197 Ruijin Er Road, Shanghai 200025, China. Email: [email protected]
Interleukin (IL)-35, a recently identified cytokine of the IL-12 family, is a potent immunosuppressive cytokine secreted by regulatory T (Treg) cells and the newly reported regulatory B (Breg) cells. IL-35 functions as a crucial immunosuppressive factor in immune-mediated diseases, and the predominant mechanism of suppression is its ability to suppress T cell proliferation and effector functions. The pathogenic processes of the non-cytopathic hepatitis B virus (HBV) infection-related liver diseases are immune-mediated, including liver damage and viral control. It has been found that IL-35 is detectable in peripheral CD4+ T cells in chronic HBV-infected patients, whereas it is undetectable in healthy individuals. There is growing evidence that cytokine-mediated immune responses play a pivotal role in determining the clinical outcome during HBV infection. It is particularly important to investigate the effects of IL-35 in the immunopathogenesis of chronic HBV infection. In this study, the recent understanding of this issue is discussed.
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