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Elevated Expression of Chemokine CXCL13 in Chronic Hepatitis B Patients Links to Immune Control during Antiviral Therapy

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      Abstract

      C–X–C-chemokine ligand 13 (CXCL13), the ligand for C–X–C chemokine receptor type 5 (CXCR5), is a major regulator of B-cell trafficking and plays an integral role in age-dependent clearance of hepatitis B virus (HBV) in the mouse model. However, the expression and function of CXCL13 in patients with chronic hepatitis B (CHB) remain unknown. By use of liver cell subpopulations isolated from CHB patients, we found that CXCL13 mRNA was abundantly expressed in Kupffer cells (KCs), but not in primary hepatocytes, liver sinusoidal endothelial cells, and hepatic stellate cells. Interestingly, KC isolated from HBV-positive liver had much higher level of CXCL13 expression than non-HBV-infected controls. And its expression was induced by toll-like receptor 3 ligand poly I:C stimulation. Moreover, intense expression of CXCL13 protein and accumulation of CD4 + T and B cells were evident in follicular-like structures in the liver tissue of CHB patients, which indicated its chemotactic effect on CXCR5 + CD4 + cells and B cells. Consistently, the levels of serum CXCL13 were significantly higher in the CHB patients than in healthy controls. Furthermore, CXCL13 concentration was increased in the complete response (CR) group during weeks 0–12 and did not change significantly during the course of telbivudine treatment, compared with the patients who didn’t achieve CR. In conclusion, the HBV-related increase of CXCL13 production in KC and serum CXCL13 level during telbivudine treatment might be associated with immune control of chronic HBV infection.

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      Most cited references 33

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      EASL clinical practice guidelines: Management of chronic hepatitis B virus infection.

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        Global epidemiology of hepatitis B virus infection: new estimates of age-specific HBsAg seroprevalence and endemicity.

        Chronic hepatitis B virus infection is one of the most serious infections and a major risk factor for deaths from cirrhosis and liver cancer. We estimate age-, sex- and region-specific prevalence of chronic HBV infection and calculate the absolute number of persons being chronically infected. A systematic review of the literature for studies reporting HBV infection was conducted and worldwide HBsAg seroprevalence data was collected over a 27-year period (1980-2007). Based on observed data, age-specific prevalence and endemicity were estimated on a global level and for all world regions for 1990 and 2005 using an empirical Bayesian hierarchical model. From 1990 to 2005, the prevalence of chronic HBV infection decreased in most regions. This was particularly evident in Central sub-Saharan Africa, Tropical and Central Latin America, South East Asia and Central Europe. Despite this decrease in prevalence, the absolute number of HBsAg positive persons increased from 223 million in 1990 to 240 million in 2005. Age-specific prevalence varied by geographical region with highest endemicity levels in sub-Saharan Africa and prevalence below 2% in regions such as Tropical and Central Latin America, North America and Western Europe. Asian regions showed distinct prevalence patterns with lower intermediate prevalence in South Asia, but up to 8.6% HBsAg prevalence in East Asia. Strong declines were seen in South East Asian children. Declines in HBV infection prevalence may be related to expanded immunization. The increasing overall number of individuals being chronically infected with HBV, and the widespread global differences in HBV prevalence call for targeted approaches to tackle HBV-related mortality and morbidity. HBV infection prevalence data are needed at country and sub-national level to estimate disease burden and guide health and vaccine policy. Copyright © 2012 Elsevier Ltd. All rights reserved.
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          Hepatitis B virus infection--natural history and clinical consequences.

           M. Prince,  Don Ganem (2004)
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            Author and article information

            Affiliations
            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 Gastroenterology and Hepatology, Essen University Hospital, University of Duisburg-Essen , Essen, Germany
            3Department of Infectious Disease, Guangzhou Eighth People’s Hospital, Guangzhou Medical University , Guangzhou, China
            4Institute of Virology, Essen University Hospital, University of Duisburg-Essen , Essen, Germany
            Author notes

            Edited by: Jixin Zhong, Case Western Reserve University, USA

            Reviewed by: Hui Liu, University of California, San Francisco, USA; Albrecht Piiper, University Hospital Frankfurt, Germany; Junjie Zhang, University of Southern California, USA

            *Correspondence: Jinlin Hou, jlhousmu@ 123456163.com ; Xiaoyong Zhang, xiaoyzhang@ 123456smu.edu.cn

            These authors have contributed equally to this work.

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

            Contributors
            Journal
            Front Immunol
            Front Immunol
            Front. Immunol.
            Frontiers in Immunology
            Frontiers Media S.A.
            1664-3224
            23 March 2017
            2017
            : 8
            5362616 10.3389/fimmu.2017.00323
            Copyright © 2017 Liu, Huang, Werner, Broering, Ge, Li, Liao, Sun, Peng, Lu, 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.

            Counts
            Figures: 6, Tables: 2, Equations: 0, References: 33, Pages: 11, Words: 7039
            Categories
            Immunology
            Original Research

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