Differential response of HBV envelope-specific CD4+ T cells is related to HBsAg loss after stopping nucleos(t)ide analogue therapy

乙型肝炎表面抗原 医学 中止 乙型肝炎病毒 免疫学 T细胞 乙型肝炎 CD8型 内科学 病毒学 免疫系统 病毒
作者
Yongyin Li,Chunhua Wen,Shuqin Gu,Weibin Wang,Ling Guo,Chris Ka-fai Li,Xuan Yi,Yang Zhou,Zheyu Dong,Xin Fu,Shihong Zhong,Yuhao Wang,Kuiyuan Huang,Junhua Yin,Chun-Xiu Zhong,Xieer Liang,Rong Fan,Haitao Chen,Deke Jiang,Xiaoyong Zhang,Jian Sun,Libo Tang,Jie Peng,Jinlin Hou
出处
期刊:Hepatology [Lippincott Williams & Wilkins]
卷期号:Publish Ahead of Print 被引量:9
标识
DOI:10.1097/hep.0000000000000334
摘要

Background and Aims: Long-term maintenance of viral control, even HBsAg loss, remains a challenge for chronic hepatitis B (CHB) patients undergoing nucleos(t)ide analogue (NA) discontinuation. This study aimed to investigate the relationship between HBV-specific T cell responses targeting peptides spanning the whole proteome and clinical outcomes in CHB patients after NA discontinuation. Approach and Results: Eighty-eight CHB patients undergoing NA discontinuation were classified as responders (remained relapse-free up to 96 wk) or relapsers (relapsed patients who underwent NA re-treatment for up to 48 weeks and re-achieved stable viral control). HBV-specific T cell responses were detected at baseline and longitudinally throughout follow-up. We found responders had a greater magnitude of HBV Polymerase (Pol)-specific T cell responses than relapsers at baseline. After long-term NA discontinuation, simultaneously enhanced HBV Core- and Pol-induced responses were observed in responders. Particularly, responders with HBsAg loss possessed enhanced HBV Envelope (Env)-induced responses after short and long-term follow-up. Notably, CD4+T cells accounted for the predominance of HBV-specific T cell responses. Correspondingly, CD4-deficient mice showed attenuated HBV-specific CD8+T cell responses, reduced HBsAb-producing B cells, and delayed HBsAg loss; in contrast, in vitro addition of CD4+T cells promoted HBsAb production by B cells . Additionally, interleukin (IL)-9, rather than PD-1 blockade, enhanced HBV Pol-specific CD4+T cell responses. Conclusion: HBV-specific CD4+T cell responses induced by the targeted peptide possess specificities for long-term viral control and HBsAg loss in CHB patients undergoing NA discontinuation, indicating that CD4+T cells specific for distinct HBV antigens may endow with divergent antiviral potential. Export
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