Journal article
Role of FABP5 in T Cell Lipid Metabolism and Function in the Tumor Microenvironment
Cancers, Vol.15(3), 657
01/20/2023
DOI: 10.3390/cancers15030657
PMCID: PMC9913835
PMID: 36765614
Abstract
To evade immune surveillance, tumors develop a hostile microenvironment that inhibits anti-tumor immunity. Recent immunotherapy breakthroughs that target the reinvigoration of tumor-infiltrating T lymphocytes (TIL) have led to unprecedented success in treating some cancers that are resistant to conventional therapy, suggesting that T cells play a pivotal role in anti-tumor immunity. In the hostile tumor microenvironment (TME), activated T cells are known to mainly rely on aerobic glycolysis to facilitate their proliferation and anti-tumor function. However, TILs usually exhibit an exhausted phenotype and impaired anti-tumor activity due to the limited availability of key nutrients (e.g., glucose) in the TME. Given that different T cell subsets have unique metabolic pathways which determine their effector function, this review introduces our current understanding of T cell development, activation signals and metabolic pathways. Moreover, emerging evidence suggests that fatty acid binding protein 5 (FABP5) expression in T cells regulates T cell lipid metabolism and function. We highlight how FABP5 regulates fatty acid uptake and oxidation, thus shaping the survival and function of different T cell subsets in the TME.
Details
- Title: Subtitle
- Role of FABP5 in T Cell Lipid Metabolism and Function in the Tumor Microenvironment
- Creators
- Rong Jin - University of LouisvilleJiaqing Hao - University of IowaJianyu Yu - University of IowaPingzhang Wang - Peking UniversityEdward R. Sauter - Division of Cancer Prevention, National Institutes of Health/National Cancer Institute, Bethesda, MD 20892, USABing Li - University of Louisville
- Resource Type
- Journal article
- Publication Details
- Cancers, Vol.15(3), 657
- DOI
- 10.3390/cancers15030657
- PMID
- 36765614
- PMCID
- PMC9913835
- NLM abbreviation
- Cancers (Basel)
- ISSN
- 2072-6694
- eISSN
- 2072-6694
- Language
- English
- Date published
- 01/20/2023
- Academic Unit
- Pathology
- Record Identifier
- 9984363420302771
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