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

Authors

  • 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

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).
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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.




Publikationsverlauf

Artikel online veröffentlicht:
07. Juli 2021

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