TIGIT impairs NK cell antifibrotic activity through the IFNγ–IFI30 axis in schistosomiasis-induced liver fibrosis
These findings identify TIGIT as a key negative regulator of NK cell antifibrotic activity and reveal an immunoregulatory TIGIT-interferon-γ-IFI30 axis that drives NK cell dysfunction and promotes schistosomiasis-induced liver fibrosis. Targeting this pathway may provide a new immunotherapeutic strategy for fibrotic diseases associated with chronic infection.
Authors
- Yujuan Shen
- Jianping Cao
- Hao Zhou (ORCID: https://orcid.org/0000-0001-7131-3758)
- Shaohong Lu
- Lijun Cui (ORCID: https://orcid.org/0000-0003-2362-8864)
- Feifei Xu (ORCID: https://orcid.org/0000-0003-1946-1520)
- Hongyu Peng (ORCID: https://orcid.org/0009-0009-5123-5380)
- Xiaocheng Zhang (ORCID: https://orcid.org/0009-0008-8996-1858)
- Yuan Hu
- Jianhai Yin
- Jing Zhang
Institutions
- World Health Organization - Pakistan (PK)
- National Institute for Parasitic Diseases (CN)
- Shanghai Jiao Tong University (CN)
- National Health and Family Planning Commission (CN)
- Hangzhou Medical College (CN)
Publication Details
- Journal
- Frontiers in Immunology
- Published
- 2026-02-19
- DOI
- https://doi.org/10.3389/fimmu.2026.1766930
- Primary Topic
- Immune Cell Function and Interaction
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Chinese Center for Disease Control and Prevention