Hepatitis B virus surface antigen drives T cell immunity through non-canonical antigen presentation in mice

Abstract Hepatitis B virus (HBV) exclusively infects hepatocytes and produces large amounts of subviral particles containing its surface antigen (HBsAg). T cell immunity is crucial for controlling and clearing HBV infection. However, the intercellular processes underlying HBsAg presentation to T cel...

Full description

Saved in:
Bibliographic Details
Main Authors: Xiaofang Li, Wenxuan Sun, Xiaolan Xu, Qirong Jiang, Yuheng Shi, Huixi Zhang, Weien Yu, Bisheng Shi, Simin Wan, Jiangxia Liu, Wuhui Song, Jiming Zhang, Zhenghong Yuan, Jianhua Li
Format: Article
Language:English
Published: Nature Portfolio 2025-05-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-59985-8
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849309754236600320
author Xiaofang Li
Wenxuan Sun
Xiaolan Xu
Qirong Jiang
Yuheng Shi
Huixi Zhang
Weien Yu
Bisheng Shi
Simin Wan
Jiangxia Liu
Wuhui Song
Jiming Zhang
Zhenghong Yuan
Jianhua Li
author_facet Xiaofang Li
Wenxuan Sun
Xiaolan Xu
Qirong Jiang
Yuheng Shi
Huixi Zhang
Weien Yu
Bisheng Shi
Simin Wan
Jiangxia Liu
Wuhui Song
Jiming Zhang
Zhenghong Yuan
Jianhua Li
author_sort Xiaofang Li
collection DOAJ
description Abstract Hepatitis B virus (HBV) exclusively infects hepatocytes and produces large amounts of subviral particles containing its surface antigen (HBsAg). T cell immunity is crucial for controlling and clearing HBV infection. However, the intercellular processes underlying HBsAg presentation to T cells are incompletely understood. Here, using preclinical mouse models, we show that, following HBsAg expression, the intrahepatic Batf3+XCR1+CCR7- conventional dendritic cell subset cDC1 presents HBsAg by MHC-I cross-dressing, driving CD8+ T cell response. Meanwhile, upon HBsAg access to lymphoid tissues, B cells acquire HBsAg directly in the follicles of lymphoid tissues and initiate CD4+ T cell responses sequentially in the follicular and interfollicular regions, guided by chemoattractant receptors CCR5 and EBI2, respectively. Finally, we identify ALCAM, LFA-1, and CD80 as key co-stimulatory signals essential for optimal T cell responses. Thus, these findings reveal the roadmap of non-canonical antigen presentation that drives T cell immunity against HBsAg, advancing novel therapeutic strategies for chronic HBV infection.
format Article
id doaj-art-bfdbcd42281c41cbbf57a418b9c9c2dd
institution Kabale University
issn 2041-1723
language English
publishDate 2025-05-01
publisher Nature Portfolio
record_format Article
series Nature Communications
spelling doaj-art-bfdbcd42281c41cbbf57a418b9c9c2dd2025-08-20T03:53:58ZengNature PortfolioNature Communications2041-17232025-05-0116112010.1038/s41467-025-59985-8Hepatitis B virus surface antigen drives T cell immunity through non-canonical antigen presentation in miceXiaofang Li0Wenxuan Sun1Xiaolan Xu2Qirong Jiang3Yuheng Shi4Huixi Zhang5Weien Yu6Bisheng Shi7Simin Wan8Jiangxia Liu9Wuhui Song10Jiming Zhang11Zhenghong Yuan12Jianhua Li13Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganisms and Infection, School of Basic Medical Sciences, Shanghai Medical College, Fudan UniversityKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganisms and Infection, School of Basic Medical Sciences, Shanghai Medical College, Fudan UniversityKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganisms and Infection, School of Basic Medical Sciences, Shanghai Medical College, Fudan UniversityDepartment of Infectious Diseases, Huashan Hospital, Fudan UniversityKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganisms and Infection, School of Basic Medical Sciences, Shanghai Medical College, Fudan UniversityKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganisms and Infection, School of Basic Medical Sciences, Shanghai Medical College, Fudan UniversityDepartment of Infectious Diseases, Huashan Hospital, Fudan UniversityKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganisms and Infection, School of Basic Medical Sciences, Shanghai Medical College, Fudan UniversityKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganisms and Infection, School of Basic Medical Sciences, Shanghai Medical College, Fudan UniversityKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganisms and Infection, School of Basic Medical Sciences, Shanghai Medical College, Fudan UniversityKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganisms and Infection, School of Basic Medical Sciences, Shanghai Medical College, Fudan UniversityDepartment of Infectious Diseases, Huashan Hospital, Fudan UniversityKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganisms and Infection, School of Basic Medical Sciences, Shanghai Medical College, Fudan UniversityKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganisms and Infection, School of Basic Medical Sciences, Shanghai Medical College, Fudan UniversityAbstract Hepatitis B virus (HBV) exclusively infects hepatocytes and produces large amounts of subviral particles containing its surface antigen (HBsAg). T cell immunity is crucial for controlling and clearing HBV infection. However, the intercellular processes underlying HBsAg presentation to T cells are incompletely understood. Here, using preclinical mouse models, we show that, following HBsAg expression, the intrahepatic Batf3+XCR1+CCR7- conventional dendritic cell subset cDC1 presents HBsAg by MHC-I cross-dressing, driving CD8+ T cell response. Meanwhile, upon HBsAg access to lymphoid tissues, B cells acquire HBsAg directly in the follicles of lymphoid tissues and initiate CD4+ T cell responses sequentially in the follicular and interfollicular regions, guided by chemoattractant receptors CCR5 and EBI2, respectively. Finally, we identify ALCAM, LFA-1, and CD80 as key co-stimulatory signals essential for optimal T cell responses. Thus, these findings reveal the roadmap of non-canonical antigen presentation that drives T cell immunity against HBsAg, advancing novel therapeutic strategies for chronic HBV infection.https://doi.org/10.1038/s41467-025-59985-8
spellingShingle Xiaofang Li
Wenxuan Sun
Xiaolan Xu
Qirong Jiang
Yuheng Shi
Huixi Zhang
Weien Yu
Bisheng Shi
Simin Wan
Jiangxia Liu
Wuhui Song
Jiming Zhang
Zhenghong Yuan
Jianhua Li
Hepatitis B virus surface antigen drives T cell immunity through non-canonical antigen presentation in mice
Nature Communications
title Hepatitis B virus surface antigen drives T cell immunity through non-canonical antigen presentation in mice
title_full Hepatitis B virus surface antigen drives T cell immunity through non-canonical antigen presentation in mice
title_fullStr Hepatitis B virus surface antigen drives T cell immunity through non-canonical antigen presentation in mice
title_full_unstemmed Hepatitis B virus surface antigen drives T cell immunity through non-canonical antigen presentation in mice
title_short Hepatitis B virus surface antigen drives T cell immunity through non-canonical antigen presentation in mice
title_sort hepatitis b virus surface antigen drives t cell immunity through non canonical antigen presentation in mice
url https://doi.org/10.1038/s41467-025-59985-8
work_keys_str_mv AT xiaofangli hepatitisbvirussurfaceantigendrivestcellimmunitythroughnoncanonicalantigenpresentationinmice
AT wenxuansun hepatitisbvirussurfaceantigendrivestcellimmunitythroughnoncanonicalantigenpresentationinmice
AT xiaolanxu hepatitisbvirussurfaceantigendrivestcellimmunitythroughnoncanonicalantigenpresentationinmice
AT qirongjiang hepatitisbvirussurfaceantigendrivestcellimmunitythroughnoncanonicalantigenpresentationinmice
AT yuhengshi hepatitisbvirussurfaceantigendrivestcellimmunitythroughnoncanonicalantigenpresentationinmice
AT huixizhang hepatitisbvirussurfaceantigendrivestcellimmunitythroughnoncanonicalantigenpresentationinmice
AT weienyu hepatitisbvirussurfaceantigendrivestcellimmunitythroughnoncanonicalantigenpresentationinmice
AT bishengshi hepatitisbvirussurfaceantigendrivestcellimmunitythroughnoncanonicalantigenpresentationinmice
AT siminwan hepatitisbvirussurfaceantigendrivestcellimmunitythroughnoncanonicalantigenpresentationinmice
AT jiangxialiu hepatitisbvirussurfaceantigendrivestcellimmunitythroughnoncanonicalantigenpresentationinmice
AT wuhuisong hepatitisbvirussurfaceantigendrivestcellimmunitythroughnoncanonicalantigenpresentationinmice
AT jimingzhang hepatitisbvirussurfaceantigendrivestcellimmunitythroughnoncanonicalantigenpresentationinmice
AT zhenghongyuan hepatitisbvirussurfaceantigendrivestcellimmunitythroughnoncanonicalantigenpresentationinmice
AT jianhuali hepatitisbvirussurfaceantigendrivestcellimmunitythroughnoncanonicalantigenpresentationinmice