A groundbreaking Swiss research study has revealed how aging can significantly diminish the effectiveness of CAR-T cell cancer therapy. The research found that immune cells from older subjects demonstrate reduced mitochondrial function and lower anti-tumor capabilities due to decreased NAD levels. Researchers demonstrated that by restoring NAD levels, they could potentially rejuvenate aged CAR-T cells and improve their performance. This study underscores the critical importance of considering biological age in developing personalized cancer treatments.
May 22, 2025
Study shows ageing can reduce effectiveness of CAR-T cell cancer therapy
"CAR-T cells from older individuals are metabolically impaired and
significantly less effective" - Dr. Helen Carrasco Hope
Study shows ageing can reduce effectiveness of CAR-T cell cancer therapy
Age-related decline in the immune system can have a measurable impact on
CAR-T cell therapy -- one of the most advanced forms of cancer immunotherapy,
according to a study.
Key Points
1 Age reduces T cell
mitochondrial function and anti-tumor activity
2 NAD restoration can potentially
rejuvenate immune cells
3 Aging fundamentally reshapes
immune cell metabolism
4 Personalized immunotherapy
needs age-conscious development
CAR-T therapy works by engineering a patient's T cells to recognise and
destroy cancer cells.
The study led by Swiss researchers found that CAR-T cells from aged mice
had poor mitochondrial function, lower "stemness," and reduced
antitumour activity.
It was due to a drop in levels of nicotinamide adenine dinucleotide (NAD)
-- a molecule essential for cellular energy and metabolism of mitochondria,
said the team from the University of Lausanne (UNIL), the Lausanne University
Hospital (CHUV), the Geneva University Hospitals (HUG) and the Ecole
Polytechnique Fédérale de Lausanne (EPFL).
"CAR-T cells from older individuals are metabolically impaired and
significantly less effective. What's exciting is that we were able to
rejuvenate these aged cells by restoring their NAD levels -- reviving their
antitumour function in preclinical models," said Dr. Helen Carrasco Hope.
"Our findings strengthen the growing recognition that ageing
fundamentally reshapes immune cell function and metabolism.
"They highlight the urgent need to model age more accurately in
preclinical studies so that therapies are developed with the real-world cancer
population in mind -- where most patients are older adults," Hope said.
For the study, published in the journal Nature Cancer, the team used
NAD-boosting compounds currently under clinical investigation for other
conditions, demonstrating that this approach is translatable and potentially
applicable in humans.
"This is a major step toward personalised and age-conscious
immunotherapy," said senior author Dr. Nicola Vannini.
"By correcting age-related metabolic defects, we could improve
outcomes for a large segment of cancer patients."
The study adds to a growing body of work showing that age is not just a
chronological number, but a biological factor that can shape therapy response.
The researchers called for age to be systematically considered in the
development and evaluation of cell-based immunotherapies.
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