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Updated: Feb 12, 2026

A Protocol for Analyzing Hepatitis C Virus Replication
Published on: June 26, 2014
Immune active cells with 4-1BB signal enhancement inhibit hepatitis B virus replication in noncytolytic manner
Lili Wang1, Yongxiang Yi2, Wenxiu Jiang3
1Cancer Research and Biotherapy Center, The Second Hospital of Nanjing, Affiliated to Medical School of Southeast University, Zhong Fu Road, Gulou District, Nanjing, Jiangsu 210003, PR China.
Immune active cells (IACs) have been shown to be an alternative immunotherapy for CHB patients. However, there is a practical problem of different expansion rate and function of HBV inhibition as individual variability exists. Our previous studies have confirmed that the proliferation and cytolysis of IACs were significantly up-regulated by engineered cells for costimulatory enhancement (ECCE) delivering a 4-1BBζ activating signal. In this study, we aimed to investigate the contribution of ECCE to IACs from CHB patients. We found that ECCE could enhance larger-scale expansion of IACs and the levels of HBV-markers were reduced prominently with minimal cytolysis, in the indirect system which separated ECCE-IACs and HepG2.2.15 by a 0.4-μm membrane. Furthermore, ECCE-IACs produced a lot of IFN-γ and TNF-α. Blockading them, the inhibition was abrogated. These results provide direct evidence that ECCE-IACs efficiently control HBV replication in a noncytolytic manner, and this effect is mediated by IFN-γ and TNF-α.
Immune active cells (IACs) have been shown to be an alternative immunotherapy for CHB patients. However, there is a practical problem of different expansion rate and function of HBV inhibition as individual variability exists. Our previous studies have confirmed that the proliferation and cytolysis of IACs were significantly up-regulated by engineered cells for costimulatory enhancement (ECCE) delivering a 4-1BBζ activating signal. In this study, we aimed to investigate the contribution of ECCE to IACs from CHB patients. We found that ECCE could enhance larger-scale expansion of IACs and the levels of HBV-markers were reduced prominently with minimal cytolysis, in the indirect system which separated ECCE-IACs and HepG2.2.15 by a 0.4-μm membrane. Furthermore, ECCE-IACs produced a lot of IFN-γ and TNF-α. Blockading them, the inhibition was abrogated. These results provide direct evidence that ECCE-IACs efficiently control HBV replication in a noncytolytic manner, and this effect is mediated by IFN-γ and TNF-α.
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