SAMSN1 causes sepsis immunosuppression by inducing macrophages to express coinhibitory molecules that cause T-cell exhaustion via KEAP1–NRF2 signaling
SAMSN1 deletion augmented adaptive T cell immunity and macrophage phagocytic-proliferative dual function. Furthermore, it mediates the KEAP1-NRF2 axis, which affects the expression of coinhibitory molecules on macrophages, leading to T-cell exhaustion. This novel immunosuppression mechanism potentially provides a candidate molecular target for sepsis immunotherapy.
Authors
- Fei Xiao (ORCID: https://orcid.org/0000-0003-1571-0702)
- Yao Li (ORCID: https://orcid.org/0000-0001-5197-8277)
- Xuelian Liao
- Tingting Li (ORCID: https://orcid.org/0000-0002-2303-6394)
- Wei Zhang (ORCID: https://orcid.org/0000-0001-7588-7249)
- Lijun Wang (ORCID: https://orcid.org/0000-0003-1306-7055)
- Yan Kang
Institutions
- Sichuan University (CN)
- West China Second University Hospital of Sichuan University (CN)
- West China Hospital of Sichuan University (CN)
Publication Details
- Journal
- Chinese Medical Journal
- Published
- 2025-04-27
- DOI
- https://doi.org/10.1097/cm9.0000000000003606
- Citations
- 5
- Primary Topic
- Immune cells in cancer
- Type
- article
- Field-Weighted Citation Impact
- 3.99