Led by Jessica Thaxton, Ph.D, MsCR, an associate professor at UNC Lineberger Comprehensive Cancer Center, a research team delved into why T cells lack sustained energy in tumours. Through their expertise in tumour immunity and metabolism, the Thaxton Lab, under Katie Hurst, MPH, and fourth-year graduate student Ellie Hunt, discovered that a metabolic enzyme, acetyl-CoA carboxylase (ACC), prompts T cells to store fat instead of utilising it for energy. T cells, known as "killers," are instrumental in targeting and eliminating bacteria, viruses, and cancer cells in the body.
“Our discovery fills a long-standing gap in knowledge regarding why T cells in solid tumours don't appropriately generate energy. We inhibited the expression of ACC in mouse cancer models, and we observed that T cells were able to persist much better in solid tumours,” said Thaxton.
Published in Cell Metabolism, the new findings and immunotherapeutic strategies hold promise for enhancing multiple types of T-cell therapies, including checkpoint and chimeric antigen receptor (CAR) T-cell therapies, for patients. In cancer immunotherapy, it's long been understood that T cells struggle to produce adenosine triphosphate (ATP), their cellular energy, within solid tumours.
Utilising Ellie Hunt's expertise in confocal imaging, the research team observed lipid stores in T cells isolated from various cancers. These observations, alongside other experiments, confirmed the team's hypothesis that T cells were storing lipids rather than metabolising them.
