期刊
ISCIENCE
卷 25, 期 2, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.isci.2022.103847
关键词
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资金
- NIH
- Doris Duke Charitable Foundation
- Genentech
- American Association for Dental Research
- Deutsche Forschungsgemeinschaft [WA-4610/1-1]
- NIH, NCI [ZIA BC 011345, ZO1 BC010870]
- International Liver Cancer Association (ILCA) Fellowship Award
- Colgate-Palmolive Company
Non-alcoholic fatty liver disease (NAFLD) has a significant impact on liver cancer development and may impair antigen-specific CD8 (+) T cell immunity due to accumulated macrophages in the liver environment.
Non-alcoholic fatty liver disease (NAFLD) has become an important etiology leading to liver cancer. NAFLD alters adaptive T cell immunity and has a profound influence on liver cancer development. However, it is unclear how NAFLD affects tumor antigen-specific T cell response. In this study, we generated a doxycycline-inducible MHC-I and -II antigen-expressing HCC cell line which allowed us to investigate tumor antigen-specific T cell response in two NAFLD mouse models. The system proved to be an effective and efficient way to study tumor antigen-specific T cells. Using this model, it was found that NAFLD impairs antigen-specific CD8(+) T cell immunity against HCC. The effect was not due to reduced generation or intrinsic functional changes of tumor antigen-specific CD8(+) T cells but caused by accumulated macrophages in the liver environment. The findings suggest that targeting macrophages in NAFLD-driven HCC may improve therapeutic outcomes.
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