Semin Liver Dis 2021; 41(04): 516-524
DOI: 10.1055/s-0041-1731708
Review Article

The Mechanism of Interleukin-35 in Chronic Hepatitis B

Ying Tang
1  Diseases Center, Department of Hepatopancreatobiliary Medicine, The Second Hospital, Jilin University, Changchun, China
,
Tianyi Ma
1  Diseases Center, Department of Hepatopancreatobiliary Medicine, The Second Hospital, Jilin University, Changchun, China
,
Shengnan Jia
1  Diseases Center, Department of Hepatopancreatobiliary Medicine, The Second Hospital, Jilin University, Changchun, China
,
Qian Zhang
1  Diseases Center, Department of Hepatopancreatobiliary Medicine, The Second Hospital, Jilin University, Changchun, China
,
Siqi Liu
1  Diseases Center, Department of Hepatopancreatobiliary Medicine, The Second Hospital, Jilin University, Changchun, China
,
Ling Qi
2  Department of Core Medical Laboratory, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Qingyuan, China
,
Lanlan Yang
1  Diseases Center, Department of Hepatopancreatobiliary Medicine, The Second Hospital, Jilin University, Changchun, China
› Author Affiliations
Funding Information The study is supported in part by grant no. 20190101006JH from the Foundation of Science and Technology, Department of Jilin Province (Jilin, Jilin; to Prof. Ling Qi), no. 20190220 from the Foundation of Qingyuan People's Hospital (Qingyuan, Guangdong; to Prof. Ling Qi), and no. 20200201482JC from the Natural Science Foundation of Jilin Province (Changchun, Jilin; to Prof. Lanlan Yang).

Abstract

Interleukin-35 (IL-35) is a newly identified inhibitory cytokine. It has recently been found to play an extremely important role in chronic hepatitis B disease, which makes it likely to be a target for new therapies for hepatitis B malady. IL-35 modulates a variety of immune mechanisms to cause persistent viral infections, such as affecting the ratio of helper T cells, reducing the activity of cytotoxic T cells, hindering the antigen presentation capacity for dendritic cells, and increasing the transcription level of hepatitis B virus. On the other hand, IL-35 can control the inflammation caused by hepatitis B liver injury. Therefore, to seek a breakthrough in curing hepatitis B disease, the contradictory part of IL-35 in the occurrence and development of this sickness is worthy of further discussion and research. This article will systematically review the biological effects of IL-35 and the specific mechanisms affecting the disease.

Authors' Contribution

Y.T. contributed to manuscript writing; T.M., S.J., and M.W. conducted literature retrieval; and L.Q. and L.Y. revised the manuscript.




Publication History

Publication Date:
07 July 2021 (online)

© 2021. Thieme. All rights reserved.

Thieme Medical Publishers, Inc.
333 Seventh Avenue, 18th Floor, New York, NY 10001, USA