Health
Why killer T cells lose energy in solid tumors
T cells are sometimes called “assassins” or “killers” because they can organize and carry out tasks that hunt down bacteria, viruses, and cancer cells throughout the body. T cells may be powerful, but recent studies have shown that when they infiltrate the environment of solid tumors, they lose the energy they need to fight cancer.
A research team led by Jessica Thaxton, Ph.D., MSCR, associate professor of cell biology and physiology and co-leader of the Cancer Cell Biology Program at the UNC Lineberger Comprehensive Cancer Center, found that T cells are unable to maintain energy within tumors. We aimed to understand why. Leveraging their expertise in tumor immunity and metabolism, the Thaxton Lab, led by Katie Herst, MPH, and her fourth Graduate student Ellie Hunt discovered that a metabolic enzyme called acetyl-CoA carboxylase (ACC) causes T cells to store fat instead of burning it for energy.
“Our findings fill a long-standing knowledge gap about why T cells in solid tumors do not produce energy properly,” Thaxton said. “When we inhibited ACC expression in a mouse cancer model, we observed that T cells had better survival in solid tumors.”
New discoveries and immunotherapy strategies announced at cell metabolismcould potentially be used to make multiple types of T-cell therapy more effective for patients, including both checkpoint therapy and chimeric antigen receptor (CAR) T-cell therapy.
The field of cancer immunotherapy has long known that T cells cannot produce cellular energy called adenosine triphosphate, or ATP, when they are inside a solid tumor.
In 2019, Thaxton's lab investigated T cells with optimal anti-tumor function.in publications of Cancer immunology researchHurst and Thaxton used a proteomic screen to identify enzymes associated with optimal antitumor metabolism of these T cells. Through this screen, the two discovered that ACC expression can limit the ability of T cells to generate ATP within tumors. ACC is an important molecule involved in many metabolic pathways, preventing cells from breaking down fat and using it as fuel for energy in the mitochondria.
“Acetyl-CoA carboxylase can control the balance between storing lipids and breaking down those lipids to supply energy to the citric acid cycle,” Thaxton said. “When ACC is ‘on,’ cells generally store lipids. When ACC is “off,” cells tend to use lipids within mitochondria to generate ATP. ”
Using Hunt's expertise in confocal imaging, the research team was able to observe lipid storage within T cells isolated from multiple types of cancer. This observation, along with other experiments, supported the team's hypothesis that T cells store lipids rather than breaking them down.
Thaxton's team then used CRISPR Cas9-mediated gene deletion to see what would happen if they “removed” ACC from the images. Lipid stores within the T cells rapidly depleted, and the researchers were able to visualize fat being relocated to the mitochondria and used for energy production.
Thaxton now believes that T cells require a “delicate balance” of lipids to survive within solid tumors, with certain amounts of lipids being dedicated to assassinating cancer cells and lower levels of fat being stored. We hypothesize that this is how it is maintained.
The latest discovery could prove useful in enhancing chimeric antigen receptor (CAR) T-cell therapy. This cutting-edge technology takes her T cells from cancer patients, alters them in the lab to seek out tumor cells, and reinjects the cells to fight the patient's cancer. Preliminary data from Thaxton's lab indicates that his manufactured T cells also contain excess lipid reserves.
The lab has begun studying patient samples to understand how researchers can directly flip the ACC metabolic switch in patients' tumors, eliminating the need to remove cells and put them back into the body. There is. But researchers first need to determine how this might affect other immune cell populations in the body, such as macrophages.
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