Published online Oct 14, 2015. doi: 10.3748/wjg.v21.i38.10721
Peer-review started: April 28, 2015
First decision: June 2, 2015
Revised: June 19, 2015
Accepted: September 2, 2015
Article in press: September 2, 2015
Published online: October 14, 2015
Processing time: 171 Days and 11.9 Hours
Immune-mediated liver injury is widely seen during hepatitis B virus (HBV) infection. Unsuccessful immune clearance of HBV results in chronic hepatitis and increases the risk of liver cirrhosis and hepatocellular carcinoma. HBV-related liver fibrosis (HBVLF), occurring as a result of HBV-induced chronic hepatitis, is a reversible, intermediate stage of chronic hepatitis B (CHB) and liver cirrhosis. Therefore, defining the pathogenesis of HBVLF is of practical significance for achieving better clinical outcomes. Recently, the homeostasis of CD4+ T cells was considered to be pivotal in the process of HBVLF. To better uncover the underlying mechanisms, in this review, we systematically retrospect the impacts of different CD4+ T-cell subsets on CHB and HBVLF. We emphasize CD4+ T-cell homeostasis and the important balance between regulatory T (Treg) and T helper 17 (Th17) cells. We discuss some cytokines associated with Treg and Th17 cells such as interleukin (IL)-17, IL-22, IL-21, IL-23, IL-10, IL-35 and IL-33, as well as surface molecules such as programmed cell death protein 1, cytotoxic T lymphocyte-associated antigen 4, T cell immunoglobulin domain and mucin domain-containing molecule 3 and cannabinoid receptor 2 that have potential therapeutic implications for the homeostasis of CD4+ T cells in CHB and HBVLF.
Core tip: Hepatitis B virus (HBV)-related liver fibrosis (HBVLF) is a reversible, intermediate stage of chronic hepatitis B and liver cirrhosis. The homeostasis of CD4+ T cells, especially the balance between regulatory T (Treg) cells and T helper 17 (Th17) cells is pivotal in HBVLF. Therefore, uncovering the underlying mechanisms of CD4+ T cell homeostasis regulating HBVLF may help achieve better clinical outcomes. We discuss Treg and Th17 cell-related cytokines and surface molecules that may be targeted therapeutically to alter CD4+ T-cell homeostasis in chronic HBV infection.