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Updated: Sep 30, 2025

Stem Cell-Derived Viral Ag-Specific T Lymphocytes Suppress HBV Replication in Mice
Published on: September 25, 2019
TIGIT marks exhausted T cells and serves as a target for immune restoration in patients with chronic HBV infection
Yan-Yan Wei1,2, Jing Fan2, Meng-Xuan Shan2
1Department of Infectious Disease, The First Affiliated Hospital of Anhui Medical University Hefei 230022, Anhui, China.
Background:
Chronic HBV infection is a serious worldwide health problem that mainly causes liver cirrhosis and hepatocellular carcinoma (HCC). Few studies have explored how T cell exhaustion helps HBV avoid immune system attack and how to reverse that exhaustion. Recently, T cell immunoglobulin and immune receptor tyrosine-based inhibitory motif (ITIM) domain (TIGIT) have been identified as coinhibitory receptors, similar to PD-1. This study explores the expression of TIGIT and the T cell function changes in patients with chronic HBV infection.
Results:
In this study, we found that the expression of TIGIT on T cells increased significantly in patients with chronic HBV infection. High expression of TIGIT on T cells is associated with functional exhaustion. Importantly, this study demonstrates that blocking TIGIT can reverse T cell exhaustion and restore function in patients with chronic HBV infection.
Conclusions:
HBV induces T cell exhaustion by up-regulating the expression of TIGIT. Blocking the TIGIT/PVR signaling pathway can reverse T cell exhaustion, so this discovery provides an immunotherapy target to battle chronic HBV infection.
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