Review
Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Hepatol. Dec 28, 2015; 7(30): 2980-2991
Published online Dec 28, 2015. doi: 10.4254/wjh.v7.i30.2980
Crosstalk between innate and adaptive immunity in hepatitis B virus infection
Li Wang, Kai Wang, Zhi-Qiang Zou
Li Wang, Zhi-Qiang Zou, Infectious Disease Hospital of Yantai, Yantai 264001, Shandong Province, China
Kai Wang, Hepatology Department, Qilu Hospital Affiliated to Shandong University, Jinan 250012, Shandong Province, China
Author contributions: Wang L, Wang K and Zou ZQ designed and performed literature search; Wang L wrote manuscript.
Supported by Grants of Yantai Science and Technology Plan Project, No. 2012116.
Conflict-of-interest statement: All the authors of the manuscript declare that they have no conflict of interest in connection with this paper
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Li Wang, PhD, Infectious Disease Hospital of Yantai, Huanshan Road 62, Zhifu District, Yantai 264001, Shandong Province, China. liliwang2200@163.com
Telephone: +86-535-6232253 Fax: +86-535-6628542
Received: September 23, 2015
Peer-review started: September 26, 2015
First decision: October 21, 2015
Revised: November 11, 2015
Accepted: December 8, 2015
Article in press: December 11, 2015
Published online: December 28, 2015
Processing time: 94 Days and 17.1 Hours
Core Tip

Core tip: Hepatitis B virus (HBV) is poorly sensed by the innate immune system and can escape innate immune recognition at the early stage of infection. HBV-specific T-cell responses are timely and efficiently induced in acute self-limited infections but are deeply exhausted in chronic hepatitis B. The tolerogenic effect of the liver environment and the persistent exposure of T cells to high antigen loads play a key role in the pathogenesis of T-cell inhibition in chronic HBV infection. Combination of reduction of HBV and virus antigen loads and restoration of the anti-viral T-cell function may represent a strategy to cure chronic HBV infections.