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      Lower Expression of MicroRNA-155 Contributes to Dysfunction of Natural Killer Cells in Patients with Chronic Hepatitis B

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          MicroRNAs have been reported to be regulated in different ways in a variety of liver diseases. As a key modulator of cellular function in both innate and adaptive immunity, the role of miR-155 in chronic hepatitis B virus infection remains largely unknown. Here, we investigated the expression and function of miR-155 in chronic hepatitis B (CHB) patients. It was found that miR-155 expression in peripheral blood mononuclear cells (PBMCs) was lower in CHB patients than healthy controls (HC). Among CHB infection, immune-active (IA) patients with abnormal alanine aminotransferase (ALT) levels had relatively higher miR-155 expression in PBMCs and serum than immune-tolerant carriers, but were comparable to inactive carriers. Moreover, there was a positive correlation between miR-155 expression and ALT levels in CHB patients. Particularly, miR-155 expression in natural killer (NK) cells was significantly downregulated in IA patients compared with HC. Inversely, suppressor of cytokine signaling 1 (SOCS1), a target of miR-155, was upregulated in NK cells of IA patients. Overexpression of miR-155 in NK cells from IA patients led to a decrease in SOCS1 expression and an increase of IFN-γ production. Finally, accompanied by the normalization of ALT, miR-155 expression in PBMCs gradually decreased during telbivudine or peg-IFN-α-2a therapy. Interestingly, higher miR-155 expression at baseline was associated with better response to telbivudine therapy, but not peg-IFN-α-2a. In conclusion, our data suggested that miR-155 downregulation in NK cells of IA patients impaired IFN-γ production by targeting SOCS1, which may contribute to immune dysfunction during CHB infection. Additionally, baseline miR-155 expression could predict the treatment response to telbivudine therapy.

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          Most cited references 43

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          MicroRNAs: genomics, biogenesis, mechanism, and function.

           David Bartel (2004)
          MicroRNAs (miRNAs) are endogenous approximately 22 nt RNAs that can play important regulatory roles in animals and plants by targeting mRNAs for cleavage or translational repression. Although they escaped notice until relatively recently, miRNAs comprise one of the more abundant classes of gene regulatory molecules in multicellular organisms and likely influence the output of many protein-coding genes.
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            EASL clinical practice guidelines: Management of chronic hepatitis B virus infection.

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              Requirement of bic/microRNA-155 for normal immune function.

              MicroRNAs are a class of small RNAs that are increasingly being recognized as important regulators of gene expression. Although hundreds of microRNAs are present in the mammalian genome, genetic studies addressing their physiological roles are at an early stage. We have shown that mice deficient for bic/microRNA-155 are immunodeficient and display increased lung airway remodeling. We demonstrate a requirement of bic/microRNA-155 for the function of B and T lymphocytes and dendritic cells. Transcriptome analysis of bic/microRNA-155-deficient CD4+ T cells identified a wide spectrum of microRNA-155-regulated genes, including cytokines, chemokines, and transcription factors. Our work suggests that bic/microRNA-155 plays a key role in the homeostasis and function of the immune system.

                Author and article information

                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                22 September 2017
                : 8
                1State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University , Guangzhou, China
                2Department of Hepatology, Mengchao Haptobiliary Hospital of Fujian Medical University , Fuzhou, China
                3Department of Hepatology, Affiliated Infectious Disease Hospital of Fujian Medical University , Fuzhou, China
                Author notes

                Edited by: Jixin Zhong, Case Western Reserve University, United States

                Reviewed by: Giuseppe Sciume, Sapienza Università di Roma, Italy; Luz Pamela Blanco, National Institutes of Health (NIH), United States; Ka Man Law, University of California, Los Angeles, United States

                *Correspondence: Xiaoyong Zhang, xiaoyzhang@

                These authors have contributed equally to this work.

                Specialty section: This article was submitted to Inflammation, a section of the journal Frontiers in Immunology

                Copyright © 2017 Ge, Huang, Liu, Chen, Xie, Chen, Peng, Sun, Hou and Zhang.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Figures: 5, Tables: 3, Equations: 0, References: 43, Pages: 12, Words: 7706
                Funded by: National Natural Science Foundation of China 10.13039/501100001809
                Award ID: 81301421, 81471952, 81641173, 81670532
                Funded by: Natural Science Foundation of Guangdong Province 10.13039/501100003453
                Award ID: 2014A030313299
                Original Research


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